Affinage

RBL1

Retinoblastoma-like protein 1 · UniProt P28749

Round 2 corrected
Length
1068 aa
Mass
120.8 kDa
Annotated
2026-04-28
130 papers in source corpus 68 papers cited in narrative 62 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RBL1 (p107) is a nuclear pocket protein that restrains cell proliferation by binding and repressing E2F4/5 transcription factors in a cell-cycle-regulated manner, recruiting HDAC1 to silence E2F target genes, and directly inhibiting cyclin A–CDK2 and cyclin E–CDK2 kinase activity with a Ki comparable to p21 (PMID:1833063, PMID:9710622, PMID:9724731). Phosphorylation by cyclin D1–CDK4 at four specific sites dissociates p107 from E2F4 and releases the G1 block, while PP2A holoenzymes containing B55α or PR59 dephosphorylate and reactivate p107 in response to UV, DNA damage, FGF, and oxidative stress (PMID:11884610, PMID:9927208, PMID:9989818, PMID:18927618). Beyond canonical E2F repression, p107 participates in TGFβ-Smad3–mediated c-myc silencing through a preformed cytoplasmic Smad3–E2F4/5–DP1–p107 complex that translocates to the nucleus, represses RNA polymerase III via TFIIIB interaction, contributes to constitutive heterochromatin maintenance through Suv4-20h enzymes, and cooperates with p130 in the DREAM complex to repress G2/M genes after DNA damage (PMID:12150994, PMID:10330166, PMID:15750587, PMID:31667499). In vivo, p107 is functionally redundant with p130 in chondrocyte growth arrest and endochondral bone development, collaborates with RB1 to enforce retinal cell cycle exit—combined loss causes retinoblastoma in mice and Xenopus—and regulates white-to-brown adipocyte fate and neural precursor self-renewal through Hes1 repression (PMID:8682294, PMID:15193257, PMID:27739525, PMID:16271529, PMID:17591923).

Mechanistic history

Synthesis pass · year-by-year structured walk · 11 steps
  1. 1991 High

    Identification of p107 as a second member of the retinoblastoma protein family resolved how viral oncoproteins such as SV40 large T and E1A engage multiple pocket-domain targets, establishing that cell-cycle control involves more than one RB-like repressor.

    Evidence cDNA cloning, chromosomal mapping, and domain-deletion binding assays in human cells

    PMID:1833063

    Open questions at the time
    • No cellular function yet ascribed beyond viral oncoprotein binding
    • No E2F interaction or cell-cycle role demonstrated
  2. 1992 High

    Discovery that p107 forms complexes with cyclin A, cyclin E, CDK2, and E2F at distinct cell-cycle phases—while RB–E2F complexes predominate in G1—established that the two pocket proteins partition E2F regulation temporally through the cell cycle.

    Evidence Reciprocal co-immunoprecipitation, gel mobility shift assays, and cell-cycle synchronization across multiple independent laboratories

    PMID:1398067 PMID:1531040 PMID:1532457

    Open questions at the time
    • Identity of the specific E2F species bound by p107 not yet resolved
    • Mechanism of transcriptional repression unknown
  3. 1994 High

    Identification of E2F-4 as the principal p107-associated E2F, combined with the demonstration that p107 binds and suppresses c-Myc transactivation through a distinct mechanism from RB, revealed that p107 channels growth-suppressive signals through specific transcription factor targets.

    Evidence cDNA cloning of E2F-4, co-immunoprecipitation, transformation assays, c-Myc reporter assays, and growth-arrest rescue experiments

    PMID:7958925 PMID:8146655 PMID:8319904

    Open questions at the time
    • Whether p107–E2F4 and p107–Myc complexes coexist or are mutually exclusive unclear
    • Chromatin-level mechanism of repression not addressed
  4. 1995 High

    Biochemical dissection showed p107 contains two separable growth-suppression domains—a pocket that represses E2F and a p21-like N-terminal domain that directly inhibits cyclin A/E–CDK2 kinase activity—establishing p107 as both a transcriptional repressor and a stoichiometric CDK inhibitor.

    Evidence In vitro kinase assays with Ki determination, domain-deletion structure–function analysis, competitive binding with p21, growth-suppression assays

    PMID:7622038 PMID:7743997 PMID:9710622

    Open questions at the time
    • Structural basis for simultaneous CDK inhibition and E2F repression unknown
    • Relative contribution of each domain in physiological contexts untested
  5. 1996 High

    Cyclin D1–CDK4 was identified as the kinase that phosphorylates p107 in mid-G1 to dissociate E2F-4, while p107/p130 double-knockout mice revealed functional redundancy in limb development and showed that single knockouts are viable—defining CDK4 as the upstream activating kinase and p130 as the primary compensating family member.

    Evidence Cell synchronization, kinase assays, dominant-negative CDK4, and gene-targeted knockout mice with histological analysis

    PMID:7797074 PMID:8682293 PMID:8682294

    Open questions at the time
    • Specific phosphorylation sites not yet mapped
    • Redundancy versus specificity in non-skeletal tissues unresolved
  6. 1998 High

    Discovery that p107 recruits HDAC1 through an LXCXE-like motif to repress E2F-4 target genes provided the first chromatin-modifying mechanism through which p107 silences transcription, explaining how viral E1A displaces HDAC1 to de-repress targets.

    Evidence Co-immunoprecipitation, E1A competition assays, TSA treatment, and E2F-4-dependent reporter assays

    PMID:9724731

    Open questions at the time
    • Whether additional chromatin remodelers are recruited alongside HDAC1 unknown
    • Genome-wide target specificity of HDAC1 recruitment not tested
  7. 1999 High

    Identification of PP2A as the phosphatase that dephosphorylates and reactivates p107 in response to UV irradiation—independently of p53/p21—and the discovery of the p107-specific PP2A subunit PR59 established a CDK-opposing phosphatase axis that rapidly reactivates p107 under stress.

    Evidence UV irradiation in p53/p21-null cells, phosphatase inhibitors (okadaic acid, calyculin A), in vitro dephosphorylation with purified PP2A, PR59 co-immunoprecipitation and overexpression

    PMID:9927208 PMID:9989818

    Open questions at the time
    • Whether PR59-PP2A is the UV-responsive holoenzyme or another B subunit is involved not determined
    • Structural basis for PR59 selectivity for p107 over RB unknown
  8. 2002 High

    The finding that a preformed cytoplasmic Smad3–E2F4/5–DP1–p107 complex translocates to the nucleus upon TGFβ signaling to repress c-myc placed p107 as a direct signal transducer of TGFβ upstream of CDK regulation, while concurrent mapping of four CDK4 phosphorylation sites (T369, S640, S964, S975) defined the molecular switch for p107 inactivation.

    Evidence Co-immunoprecipitation, subcellular fractionation, ChIP on c-myc promoter, in vitro kinase assays with site-directed mutagenesis and mass spectrometry

    PMID:11884610 PMID:12150994

    Open questions at the time
    • How cytoplasmic pre-assembly is regulated prior to TGFβ stimulation unknown
    • Whether phosphorylation at all four sites is required simultaneously or sequentially untested in vivo
  9. 2004 High

    Demonstration that RB-family proteins including p107 recruit Suv4-20h methyltransferases to maintain H4K20me3 at pericentric and telomeric heterochromatin—independently of E2F—expanded p107's role beyond E2F-dependent gene regulation to constitutive heterochromatin maintenance.

    Evidence Triple-knockout MEFs, ChIP for histone modifications, co-immunoprecipitation with Suv4-20h1/h2

    PMID:15750587

    Open questions at the time
    • Relative contribution of p107 versus RB versus p130 to heterochromatin maintenance not individually resolved
    • Whether this function is dispensable in p107-single-null cells unclear due to redundancy
  10. 2005 Medium

    In vivo genetic studies revealed tissue-specific roles: p107 loss converts white adipose to brown adipose with elevated PGC-1α/UCP-1, while p107 represses Hes1 to limit neural precursor self-renewal—demonstrating that p107 controls fate decisions beyond generic cell-cycle arrest.

    Evidence p107-knockout mice, adipogenesis assays, Hes1/p107 compound knockout, neurosphere assays, BrdU labeling

    PMID:16271529 PMID:17591923

    Open questions at the time
    • Whether PGC-1α repression is direct or indirect through pRb level changes not fully resolved
    • Molecular mechanism linking p107 to Hes1 promoter repression (direct binding vs. E2F) not defined
  11. 2019 High

    Genome-wide expression profiling after individual and combined RB-family knockdowns in DNA-damaged human fibroblasts established that p107 specifically represses G2/M genes through the DREAM complex (with p130), while G1/S gene repression depends on p130 and RB—resolving the division of labor among pocket proteins in the DNA-damage response.

    Evidence shRNA knockdown of individual RB family members in primary human fibroblasts, doxorubicin treatment, genome-wide gene expression profiling

    PMID:31667499

    Open questions at the time
    • Whether DREAM complex composition shifts during prolonged damage signaling untested
    • ChIP-seq for p107-DREAM occupancy at G2/M promoters in damage conditions not performed

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for p107's simultaneous CDK inhibition and E2F repression, the relative in vivo contributions of individual PP2A holoenzymes to p107 reactivation in different stress contexts, and whether p107's heterochromatin and DREAM functions are mechanistically linked.
  • No crystal structure of full-length p107 or p107–E2F4–CDK2 ternary complex
  • Genome-wide ChIP-seq for endogenous p107 across cell-cycle phases in primary cells lacking
  • Tissue-specific tumor suppressor function of p107 independent of RB not demonstrated in human cancers

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0098772 molecular function regulator activity 3 GO:0042393 histone binding 1
Localization
GO:0005634 nucleus 4 GO:0005654 nucleoplasm 2 GO:0005829 cytosol 1
Pathway
R-HSA-1640170 Cell Cycle 8 R-HSA-74160 Gene expression (Transcription) 5 R-HSA-1266738 Developmental Biology 3 R-HSA-73894 DNA Repair 3 R-HSA-162582 Signal Transduction 2 R-HSA-4839726 Chromatin organization 2
Partners
CCNA2CDK2E2F4HDAC1MYBL2MYCPPP2CASMAD3
Complex memberships
DREAM complexSmad3–E2F4/5–DP1–p107p107–E2F4/5–DP1

Evidence

Reading pass · 62 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1991 p107 (RBL1) was molecularly cloned; its cDNA maps to chromosome 20q11.2 and encodes a 936-residue protein with a major region of homology to RB spanning 564 residues. The homologous pocket region of p107 independently binds SV40 large T antigen and adenovirus E1A, establishing p107 as a structurally and functionally related RB family member. cDNA cloning, chromosomal mapping (FISH), domain-deletion binding assays Cell High 1833063
1992 p107 forms a complex with cyclin A in cells independently of viral oncoproteins; the unique spacer sequence between the A and B sub-segments of the p107 pocket (absent in RB) is required for cyclin A interaction, explaining why cyclin A binds p107 but not RB. Co-immunoprecipitation, domain deletion mutants, in vitro binding with reticulocyte-translated proteins Science High 1532457 1532458
1992 p107 and RB independently bind the transcription factor E2F at distinct cell cycle phases: RB–E2F complexes predominate in G1, while a p107–cyclin A–p33cdk2–E2F complex appears in S phase, establishing that the two pocket proteins regulate E2F activity at different cell cycle stages. Co-immunoprecipitation, gel mobility shift assays, cell cycle synchronization Cell / Nature / Genes & development High 1398067 1530885 1531040
1992 The p107–E2F complex in S phase also contains p33cdk2 and cyclin E (in G1) or cyclin A (in S), and these two kinase complexes associate with p107 in a temporally distinct manner during the cell cycle. Immunoprecipitation with cyclin- and cdk2-specific antisera, cell cycle synchronization Genes & development High 1398067
1993 p107 represses E2F-dependent transcription; adenovirus E1A overcomes p107-mediated transcriptional repression. This repression is cell-type dependent and inversely correlates with a cellular E1A-like activity in F9 embryonal carcinoma cells. Transient transfection reporter assays, co-transfection in multiple cell lines including F9 EC cells Molecular biology of the cell High 7685208
1993 p107-associated proteins identified in ML-1 cells include cyclin A, cyclin E, cdk2, and a 62–65 kDa E2F-like phosphoprotein that is immunologically distinct from pRB-associated E2F-1, indicating p107 preferentially associates with a specific E2F species. Monoclonal antibody panel, co-immunoprecipitation, biochemical characterization Journal of virology High 8230483
1993 p107 inhibits E2F-dependent transcription in a co-transfection assay. The E2F–p107 interaction (unlike E2F–RB) persists through the G1/S transition into S phase, providing a distinct regulatory mechanism from RB. Gel mobility shift assay, co-transfection transcriptional repression assays The EMBO journal High 8458319
1993 Distinct regions of E2F1 mediate regulation by RB versus p107: point mutations within the C-terminal acidic domain of E2F1 can distinguish RB from p107 binding, and the leucine repeat element required for E4 regulation is not required for p107-mediated inhibition. E2F1 mutagenesis, co-transfection, functional reporter assays Molecular and cellular biology Medium 8413230
1993 HPV16 E7 associates with p107 through sequences overlapping with but distinct from those required for RB binding; this association correlates with E7's transformation-competent activities and its interaction with a histone H1 kinase at G2/M. Co-immunoprecipitation, E7 point mutant analysis, kinase assays Journal of virology Medium 8386265
1993 Cyclin A–p107 and p33cdk2 complexes bind to a 25-bp element of the human thymidine kinase promoter in an S-phase-specific manner, and mutation of this element reduces both in vitro complex binding and S-phase-regulated promoter activity in vivo. Electrophoretic mobility shift assay, promoter mutagenesis, S-phase synchronization Proceedings of the National Academy of Sciences Medium 8475104
1994 E2F-4 is a p107-binding E2F family member; p107 binds E2F-4 in vivo and suppresses E2F-4's ability to transform immortalized rodent cells. E2F-4 is a differentially phosphorylated p107-binding partner present throughout the cell cycle. cDNA cloning, co-immunoprecipitation, transformation assays, reporter assays Genes & development High 7958924 7958925
1994 p107 binds to the N-terminal transactivation domain of c-Myc in vivo (but RB does not), and this binding suppresses c-Myc transactivation activity. Expression of c-Myc releases cells from p107-induced growth arrest but not from pRB-induced arrest, placing c-Myc as a specific downstream target of p107. cDNA expression library screen with Myc fusion protein, co-immunoprecipitation, co-transfection reporter assays, growth arrest rescue experiments Science / The EMBO journal High 8076603 8146655
1994 p107 overexpression is a potent inhibitor of E2F-mediated trans-activation and can inhibit cell proliferation causing G1 arrest in certain cell lines. Growth inhibition by p107 and pRB occurs through distinct mechanisms: p107 can arrest C33A cells (which are resistant to pRB), certain p107 mutants unable to bind E1A still inhibit proliferation, and growth arrest by each is rescued differentially by cell cycle regulators. Overexpression, cell growth assays, FACS cell cycle analysis, E1A binding mutant analysis Genes & development High 8319904
1994 HPV16 E7 deregulates B-myb expression by targeting p107/E2F complexes; E7 transcriptionally activates B-myb during G1 and causes its constitutive over-expression, and analysis of E7 mutants confirms that B-myb regulation in NIH3T3 cells occurs through p107 rather than pRB. Transfection with E7 mutants, Northern blot, E2F reporter assays, gel-shift with specific antisera The EMBO journal Medium 8112300
1995 p107 contains a p21CIP1-related cyclin/cdk-binding domain; p107 inhibits phosphorylation of target substrates by cyclin A/cdk2 and cyclin E/cdk2, and binding of p107 or p21 to cyclin/cdk2 is mutually exclusive. In cells treated with DNA-damaging agents, elevated p21 displaces p107 from cyclin/cdk2 complexes. Activation of p107-bound kinases leads to dissociation of p107 from E2F. In vitro kinase assays, competitive binding assays, cell treatment with DNA-damaging agents, co-immunoprecipitation Genes & development High 7622038
1995 p107 contains two independent growth-suppression domains: one mediating interaction with E2F and another mediating interaction with cyclin A/E complexes. The cyclin-binding domain alone is sufficient for growth suppression in C33A cells (resistant to pRB), while both domains are functional in untransformed fibroblasts. Structure-function analysis, deletion mutants, co-expression growth arrest assays, FACS The EMBO journal High 7743997
1995 Phosphorylation of p107 by cyclin D1/cdk4 (but not cyclin E/cdk2) is cell-cycle regulated, beginning ~8 hours after serum stimulation coinciding with cyclin D1 induction. Phosphorylation of p107 causes loss of association with E2F-4, and dominant-negative cdk4 abolishes p107 phosphorylation. A p107-induced cell cycle block can be released by cyclin D1/cdk4 but not cyclin E/cdk2. Cell synchronization, kinase assays, dominant-negative cdk4 overexpression, co-immunoprecipitation, growth arrest rescue Genes & development High 7797074
1995 p107 represses the E2F-site–dependent transcription of the cyclin A promoter, and adenovirus 12S E1A activates cyclin A transcription by counteracting p107 repression through conserved region 2 (which binds p107) but not through CR1 or the N-terminus (which bind p300/pRB). Adenovirus deletion mutant infection, reporter assays, quiescent fibroblast model Journal of virology Medium 8642699
1995 p107 associates with the transcription factor Sp1 in vivo independently of the pocket domain; p107 represses Sp1-dependent transcription through a region distinct from the pocket domain used for E2F regulation, demonstrating two separable transcriptional repression mechanisms. Co-immunoprecipitation, transient transfection reporter assays with Gal4-Sp1 chimeras, domain deletion analysis Molecular and cellular biology Medium 7565695
1995 The human p107 promoter is TATA-less and contains tandem E2F sites with differential roles: RB and p107 itself repress the p107 promoter through the 5' E2F site but not the 3' (initiation site) copy, revealing autoregulatory feedback and functional asymmetry between tandem E2F elements. Promoter deletion analysis, site-directed mutagenesis, luciferase reporter assays, transfection of RB and p107 Molecular and cellular biology Medium 7791762
1995 The ability of p107 to suppress E2F-dependent transcription is not dependent on its ability to associate with cyclin A/cdk2; p107 mutants that fail to bind E2F cannot repress E2F transcription, while mutants deficient in cyclin A/cdk2 binding still repress E2F. Both E2F-dependent and E2F-independent activities correlate with cell growth suppression. p107 deletion mutants, co-transfection reporter assays, growth suppression assays Molecular and cellular biology Medium 7799940
1995 Cyclin A-cdk2 phosphorylation disrupts both E2F–pRB and E2F–p107 complexes, releasing free E2F; cyclin D1-cdk4 and cyclin E-cdk2 also disrupt E2F–pRB complexes. These results directly demonstrate that CDK-mediated phosphorylation of pRB and p107 regulates their E2F complex formation. Purified recombinant pRB, purified cyclin/cdk complexes, gel mobility shift assay with nuclear extracts from pRB-defective cells Oncogene High 7753545
1995 Lymphoma-derived MYC mutant alleles with missense mutations in the transactivation domain are resistant to p107-mediated transcriptional suppression; p107-cyclin A-CDK complex phosphorylates Thr-58 of wild-type c-Myc in a manner dependent on prior Ser-62 phosphorylation, but this phosphorylation is absent in lymphoma Myc mutants. In vitro and in vivo phosphorylation assays, transformation assays, c-Myc mutant binding/transcription analysis Molecular and cellular biology Medium 7623799
1996 p107 and p130 share overlapping biological roles in limb development: mice doubly deficient in p107 and p130 exhibit deregulated chondrocyte growth, defective endochondral bone development, shortened limbs, and neonatal lethality, while single knockouts are viable, demonstrating functional redundancy in vivo. Gene targeting (homologous recombination), mouse knockout, histological analysis Genes & development High 8682294
1996 Targeted disruption of mouse p107 alone yields viable, fertile mice with no obvious abnormalities; however, Rb+/−;p107−/− mice show growth retardation and increased mortality, and Rb−/−;p107−/− embryos die ~2 days earlier than Rb−/− embryos with accelerated apoptosis in liver and CNS, demonstrating overlapping in vivo functions between p107 and RB. Homologous recombination gene targeting, double-knockout mouse generation, histological/pathological analysis Genes & development High 8682293
1996 E2F-4 associates with p130 in arrested/quiescent cells but switches to p107 and pRB as cells re-enter the cell cycle and pass G1/S; E2F-4 accounts for the majority of endogenous E2F activity and the majority of free E2F in G1 cells. Cell synchronization, specific antisera immunoprecipitation, gel mobility shift assay Molecular and cellular biology High 8657117
1996 p107 contains a functional transcriptional repressor domain within its pocket (A and B conserved domains) that functions as a general repressor when tethered to a promoter via E2F or via a Gal4 DNA-binding domain fusion, independently of E2F binding. The two pocket sub-domains can function even when co-expressed as separate proteins. Gal4 fusion tethering assay, domain deletion mutants, co-transfection reporter assays Molecular and cellular biology Medium 8668177
1996 p107 binds B-MYB in vivo through its pocket and C-terminal domain, and suppresses B-MYB's autoregulatory transcriptional activation; overexpression of B-myb can overcome p107-induced growth arrest, placing B-MYB as a downstream effector of p107-mediated growth suppression. Co-immunoprecipitation, co-transfection reporter assays, p107 deletion constructs, growth arrest rescue The Journal of biological chemistry Medium 8910512
1996 Regulation of p107 by G1 cyclin-associated kinases: p107 phosphorylation begins in mid-G1 and is driven by cyclin D-associated kinases. Hypophosphorylated p107 selectively binds E2F-4, and G1 cyclin-dependent phosphorylation of p107 leads to dissociation of p107–E2F-4 complexes and inactivation of the p107 G1 block. Cell synchronization, kinase assays, co-immunoprecipitation, CDK inhibitor analysis Proceedings of the National Academy of Sciences High 8643455
1997 SV40 large T antigen alters phosphorylation state of p107 and p130 through its J-domain (DnaJ homology region) in addition to LXCXE binding; the N-terminal 147 amino acids including the LXCXE domain plus additional N-terminal residues are required. A heterologous J-domain from human DnaJ can substitute for the TAg N-terminus in altering p107/p130 phosphorylation. The J-domain effect confers growth advantage via p107/p130 inactivation. TAg mutant analysis, transient expression assays, fibroblasts from p107/p130 double-knockout mice, heterologous J-domain rescue Molecular and cellular biology / Journal of virology High 8627752 9271376
1997 pRB and p107/p130 regulate distinct sets of E2F-responsive genes: loss of pRB deregulates one set of E2F targets while loss of both p107 and p130 deregulates a completely different set. Neither p107 nor p130 single knockouts show changes in E2F target gene expression. Primary cells from single and double knockout mice, RNA analysis of E2F target gene expression Genes & development High 9192872
1997 p107 and p130 both repress RNA polymerase III transcription by physically interacting with TFIIIB (a subunit of the Pol III initiation factor); endogenous TFIIIB co-immunoprecipitates and co-fractionates with p107 and p130, and Pol III activity is deregulated in p107/p130 double-knockout fibroblasts. GST pull-down, co-immunoprecipitation with recombinant components and endogenous proteins, Pol III transcription assays in cell extracts, double-knockout MEFs Molecular and cellular biology High 10330166
1997 p107 and p130 accumulate in cells by distinct mechanisms: p107 levels are regulated transcriptionally through E2F-dependent repression in quiescent cells (p107 mRNA is low in quiescence), while p130 is controlled post-translationally via CDK-mediated phosphorylation and proteasome-mediated degradation. Cell synchronization, RNA blotting, proteasome inhibitor treatment, protein stability assays Cell growth & differentiation Medium 9563849
1997 p130 and p107 use a conserved amino-terminal domain to inhibit cyclin A-cdk2 and cyclin E-cdk2 kinase activities; reconstituted p107-cyclin-cdk2 complexes with purified recombinant proteins exhibit stoichiometric kinase inhibition not due to substrate competition or cdk2 activation loss. Endogenous p130-cyclin A-cdk2 complexes purified from human cells also show low kinase activity augmented by dissociation of p130. Reconstitution with purified recombinant proteins, in vitro kinase assays, purification of endogenous complexes from human cells Molecular and cellular biology High 9199292
1998 p107 is a bona fide inhibitor of cyclin A-cdk2 and cyclin E-cdk2 with a Ki comparable to p21/WAF1; a second cyclin-binding site maps to the N-terminal domain of p107 (and p130). The N-terminal domain inhibits but is not a good kinase substrate, while the C-terminal cyclin-binding domain is an excellent substrate but not an inhibitor; both domains are needed for full inhibitory activity. In vitro kinase assays with Ki determination, domain deletion mutants, peptide competition assays, growth suppression assays Molecular and cellular biology High 9710622
1998 HDAC1 interacts with p107 (and p130) through an LXCXE-like motif; adenovirus E1A competes with HDAC1 for p107 interaction. p107 can simultaneously interact with HDAC1 and E2F-4, and histone deacetylase activity is required for p107-induced repression of E2F-4, indicating p107 represses E2F through HDAC1 recruitment. Co-immunoprecipitation in live cells, competition assays with E1A, histone deacetylase inhibitor treatment, reporter assays Proceedings of the National Academy of Sciences High 9724731
1999 A novel PP2A regulatory subunit PR59 specifically associates with p107 (not pRB) in vivo and is a genuine PP2A holoenzyme component. Elevated PR59 expression causes p107 dephosphorylation (not pRB dephosphorylation) and G1 arrest, identifying a p107-specific PP2A holoenzyme that targets p107 for dephosphorylation and activation. Co-immunoprecipitation, isolation of PR59 by virtue of p107 association, over-expression, cell cycle analysis (FACS) Oncogene High 9927208
1999 C/EBPalpha controls the composition of E2F complexes by interacting with p107 and disrupting p107-containing S-phase E2F complexes; a region of C/EBPalpha with E2F sequence similarity is sufficient for disruption. This occurs through protein–protein interaction (not DNA binding), and purified His-C/EBPalpha can directly disrupt p107/E2F complexes in vitro. Co-immunoprecipitation, in vitro complex disruption with purified proteins, C/EBPalpha knockout mouse liver analysis, gel mobility shift assay Molecular and cellular biology High 10082561
1999 UV irradiation induces rapid dephosphorylation of p107 and an increase in p107/E2F repressor complexes in a PP2A-dependent manner; phosphatase inhibitors (calyculin A, okadaic acid) abolish UV-mediated dephosphorylation, overexpression of specific PP2A B subunits interferes with dephosphorylation, and p107 can be dephosphorylated in vitro with PP2A. This occurs independently of p53 and p21. UV irradiation, phosphatase inhibitor treatment, PP2A B-subunit overexpression, in vitro dephosphorylation with purified PP2A, p53/p21 knockout cells Oncogene High 9989818
1999 HCMV IE1-72 protein binds to the N-terminal portion of p107 (not the C-terminal pocket) through exons 2 and 3 of IE1-72, and this interaction relieves p107-mediated transcriptional repression of E2F-responsive promoters but not Rb-mediated repression. IE1-72 alone can overcome p107-mediated growth arrest in a manner dependent on the physical interaction. Co-immunoprecipitation, in vitro reconstitution with reticulocyte-translated proteins, domain deletion mutants, reporter assays, growth arrest assays Journal of virology / Journal of general virology High 10355776 8892909
2000 E2F and pRB-family protein occupancy at target gene promoters is dynamically regulated in vivo: in quiescent cells, promoters are occupied by E2F-4 and p130; by late G1, p130 and E2F-4 are replaced by E2F-1 and E2F-3. p107 appears at promoters associated with activation. Low histone acetylation correlates with p130/E2F-4 repression; histone acetylation increases with gene activation. Chromatin immunoprecipitation (ChIP) in synchronized living cells, histone acetylation analysis Genes & development High 10766737
2000 pRB and p107 have opposing roles in adipocyte differentiation: p107 loss lowers the requirement for the differentiation factor PPARgamma and pRB-deficient cells exhibit differentiation defects. pRB (not p107) is required for cell cycle exit and potentiates C/EBPalpha activity, while p107 does not affect C/EBPalpha-driven transcription. 3T3 fibroblasts from single and double knockout mice, adipogenesis assays, overexpression experiments, reporter assays Proceedings of the National Academy of Sciences Medium 10995476
2002 Smad3 mediates TGFbeta-induced repression of c-myc through a pre-formed cytoplasmic complex containing Smad3, E2F4/5, DP1, and the corepressor p107. In response to TGFbeta, this complex translocates to the nucleus, associates with Smad4, and recognizes a composite Smad-E2F site on the c-myc promoter for repression, revealing p107 as a TGFbeta signal transducer upstream of CDK. Co-immunoprecipitation, subcellular fractionation, chromatin immunoprecipitation, reporter assays, dominant-negative experiments Cell High 12150994
2002 Cyclin D1/Cdk4 directly phosphorylates p107 at four specific sites (Thr-369, Ser-640, Ser-964, Ser-975) identified by in vitro and in vivo phosphorylation mapping; mutation of these four sites renders p107 refractory to inactivation by cyclin D1/Cdk4. The RXL motif of p107 is required for Cdk4-mediated phosphorylation of S640 by facilitating phosphorylation of nonconsensus Cdk substrates. In vitro phosphorylation with purified kinases, site-directed mutagenesis, cell cycle arrest assays, mass spectrometry phosphopeptide mapping Molecular and cellular biology High 11884610
2002 p107 and p130 coordinately regulate chondrocyte proliferation, Cbfa1 expression, and hypertrophic differentiation during endochondral bone development; p107 is required in prechondrogenic condensations for cell cycle withdrawal, while both p107 and p130 contribute to chondrocyte cell cycle exit and Cbfa1-dependent terminal differentiation. Cbfa1 expression and hypertrophic differentiation occur only in cells that have undergone p107/p130-mediated proliferative arrest. Analysis of p107/p130 knockout mice, immunohistochemistry, in situ hybridization, BrdU labeling Developmental biology Medium 12086466
2002 FGF signaling targets p107 and p130 (but not pRB) to induce chondrocyte growth arrest: FGF causes rapid dephosphorylation of all three Rb-family proteins, but p107/p130-double-null chondrocytes fail to respond to FGF growth inhibition while Rb-null chondrocytes respond normally. A PyLT mutant that binds pRB but not p107/p130 cannot rescue FGF resistance. Chondrocyte cell lines, PyLT mutant expression, p107/p130 knockout MEF micromass cultures, metatarsal organ culture, BrdU labeling The Journal of cell biology High 12177046
2003 Oxidative stress (H2O2) induces rapid dephosphorylation of pRB, p107, and p130 via protein phosphatase 2A (PP2A); PP2A core enzyme physically interacts with pRB and p107 in both treated and untreated cells, pRB-associated PP2A activity is enhanced by H2O2, and SV40 small t antigen (PP2A inhibitor) blocks H2O2-induced dephosphorylation and prevents DNA synthesis inhibition. Phosphatase inhibitor treatment (okadaic acid, calyculin A), SV40 small t antigen overexpression (wild-type and PP2A-binding mutant), co-immunoprecipitation of PP2A with p107 The Journal of biological chemistry High 12621062
2004 A dynamic equilibrium between CDKs and PP2A modulates phosphorylation of p107 throughout the cell cycle; PP2A catalytic subunit specifically interacts with p107 and p130 (co-immunoprecipitation), and PP2A inhibition (by SV40 small t, okadaic acid at PP2A-selective concentrations, or calyculin A) prevents cycloheximide- and flavopiridol-induced dephosphorylation of pocket proteins. CDK inhibitor treatment (flavopiridol), cycloheximide, phosphatase inhibitors, PP2A holoenzyme manipulation, SV40 small t overexpression, co-immunoprecipitation Cell cycle High 15467457
2004 RBL1 (p107) together with RB1 and RBL2 is required for constitutive heterochromatin formation; triple-knockout (TKO) MEFs show decreased DNA methylation, increased H3 acetylation, and decreased H4K20 trimethylation at pericentric and telomeric chromatin. RB1 family proteins directly interact with the H4K20 tri-methylating enzymes Suv4-20h1 and Suv4-20h2, independent of E2F function. Triple-knockout MEFs, chromatin immunoprecipitation, co-immunoprecipitation with Suv4-20h enzymes, histone modification analysis Nature cell biology High 15750587
2004 Rb/p107 loss in the retina does not affect progenitor proliferation or cell specification but perturbs cell cycle exit in all seven retinal precursor types; only three precursors survive and arrest via terminal differentiation, while tumors arise from intrinsically death-resistant precursors with extended (not infinite) proliferative capacity. Conditional Cre-mediated knockout of Rb/p107, BrdU labeling, retinal cell-type marker analysis, apoptosis assays Cancer cell Medium 15193257
2005 p107 regulates white versus brown adipocyte fate by repressing PGC-1alpha: p107-null mice exhibit uniform replacement of white adipose tissue with brown adipose tissue containing elevated PGC-1alpha and UCP-1. p107−/− WAT contains reduced pRb levels. pRb (but not p107) directly binds the PGC-1alpha promoter and represses its transcription. p107-knockout mice, ChIP for pRb at PGC-1alpha promoter, Cre-mediated Rb deletion in primary preadipocytes, differentiation assays Cell metabolism Medium 16271529
2005 p107 inhibits G1-to-S-phase progression by down-regulating expression of the F-box protein Skp2, leading to p27 stabilization and Cdk2 inhibition; reciprocally, Skp2 accumulates to higher levels in p107-null fibroblasts, and ectopic Skp2 rescues the p27 and DNA synthesis defects caused by p107 overexpression. p107 overexpression and p107-knockout fibroblasts, Skp2 re-expression rescue, p27 stability assays, Cdk2 activity assays, FACS The Journal of cell biology Medium 15631990
2005 p130 and p107 play a key role in transcriptional repression of G2/M genes following DNA damage; p130/p107 loss partially abrogates repression of plk1 after adriamycin treatment, and loss of all three RB-family proteins abolishes G2 arrest, indicating p107 specifically contributes to G2/M gene repression and cell cycle exit from G2 in response to DNA damage. RB-family knockout MEFs, gene expression profiling after DNA damage, FACS for G2 arrest, adriamycin treatment Journal of cell science Medium 15827088
2007 Mammalian Mip/LIN-9 forms a repressor complex with E2F4 and p107 (or p130) in G0/early G1, and in late G1/S switches to associating with B-Myb; CDK4-mediated phosphorylation of p107/p130 drives the separation. p107 within the Mip/LIN-9 complex blocks cyclin B promoter activation by B-Myb and Mip/LIN-9, taking functional precedence over the transcriptional activation complex. Co-immunoprecipitation in cell-cycle-synchronized cells, reporter assays with dominant-negative CDK4 Oncogene Medium 17563750
2007 p107 represses transcription at the Hes1 promoter, which normally promotes neural precursor self-renewal; p107-null mice show enhanced Hes1 levels and an expanded neural precursor pool but with reduced cortical neuron numbers and reduced neurogenesis rate. Loss of one Hes1 allele rescues neural precursor numbers and neurogenesis in p107-null brains. p107-knockout mice, Hes1/p107 compound knockout, neurosphere assays, neuronal birthdating (BrdU/EdU), reporter assays for Hes1 promoter The Journal of cell biology Medium 17591923
2008 PP2A mediates p107 dephosphorylation as a key event in FGF-induced chondrocyte growth arrest; overexpression of cyclin D1/cdk4 prevents FGF-induced p107 dephosphorylation and growth arrest; SV40 small T antigen expression or siRNA knockdown of PP2A catalytic subunit also prevents p107 dephosphorylation and FGF-induced arrest; FGF treatment induces an association between p107 and PP2A. Cyclin D1/cdk4 overexpression, SV40 small T antigen expression, siRNA knockdown of PP2A, co-immunoprecipitation of p107 and PP2A, growth arrest assays PloS one High 18927618
2009 p107 and p130 associate with E2F target gene promoters by chromatin immunoprecipitation; GFP-tagged pRB shows similar nuclear dynamics to p107 and p130 by live-cell fluorescence imaging. Using anti-GFP antibody ChIP, RB association with target promoters is demonstrable, and direct RB phosphorylation disrupts promoter association, analogous to p107/p130 regulation. GFP-tagged protein live-cell imaging, FRAP, chromatin immunoprecipitation with multiple antibody approaches, phosphorylation mutant analysis The Journal of biological chemistry Medium 19279001
2010 B55alpha-containing PP2A holoenzymes play a major role in restricting p107 phosphorylation and inducing p107 activation; targeted selectivity exists in the interaction of pocket proteins with distinct PP2A holoenzymes, with B55alpha specifically targeting p107 over pRB. PP2A holoenzyme purification, co-immunoprecipitation, overexpression and knockdown of B55alpha, phosphorylation state analysis of p107 The Journal of biological chemistry Medium 20663872
2013 MAGE-A11 interacts with p107 and inhibits p107 ubiquitination to stabilize it; MAGE-A11 links p107 to hypophosphorylated E2F1, stabilizing and activating E2F1. At low MAGE-A11, this interaction causes transcriptional repression; at higher MAGE-A11 (as in prostate cancer), p107 is converted from a transcriptional repressor to a transcriptional activator of androgen receptor and E2F1 targets. Co-immunoprecipitation, ubiquitination assays, siRNA knockdown, reporter assays, p107/MAGE-A11 interaction domain mapping The Journal of biological chemistry Medium 23853093
2016 CRISPR/Cas9-mediated knockout of rb1 and rbl1 (p107) together (but not either alone) in Xenopus tropicalis causes rapid development of retinoblastoma, confirming that the cooperative tumor suppressor function of RB1 and RBL1 demonstrated in mice is conserved in a non-mammalian vertebrate and validating Xenopus as a retinoblastoma model. CRISPR/Cas9 mosaic knockout in Xenopus tropicalis, tumor histopathology, ophthalmoscopy Scientific reports Medium 27739525
2019 Following p53 activation by DNA damage, p130 and RB cooperate to repress G1/S genes, while G2/M genes are repressed specifically by p130 and p107 (not RB) through the DREAM complex (p107-DREAM and p130-DREAM); p107 contributes to G1/S gene repression only in the absence of RB and p130, demonstrating distinct and specific roles for each family member in damage-induced gene repression. Gene expression profiling in primary human fibroblasts, shRNA knockdown of individual RB family members, DNA damage treatment (doxorubicin), cell cycle analysis Nucleic acids research High 31667499
2011 A systematic screen identified p107 as a CDK4/6 substrate; the DREAM complex containing p107 mediates cell cycle gene repression. CDK4/6 phosphorylate p107 along with FOXM1 to control cell cycle entry and senescence suppression. Systematic CDK4/6 substrate screen, mass spectrometry phosphoproteomics Cancer cell Low 22094256

Source papers

Stage 0 corpus · 130 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2005 Towards a proteome-scale map of the human protein-protein interaction network. Nature 2090 16189514
2002 Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. Proceedings of the National Academy of Sciences of the United States of America 1479 12477932
2015 The BioPlex Network: A Systematic Exploration of the Human Interactome. Cell 1118 26186194
2017 Architecture of the human interactome defines protein communities and disease networks. Nature 1085 28514442
2018 VIRMA mediates preferential m6A mRNA methylation in 3'UTR and near stop codon and associates with alternative polyadenylation. Cell discovery 829 29507755
2021 Dual proteome-scale networks reveal cell-specific remodeling of the human interactome. Cell 705 33961781
2011 Phylogenetic-based propagation of functional annotations within the Gene Ontology consortium. Briefings in bioinformatics 656 21873635
1992 The transcription factor E2F interacts with the retinoblastoma product and a p107-cyclin A complex in a cell cycle-regulated manner. Cell 604 1531040
1993 Inhibition of cell proliferation by p107, a relative of the retinoblastoma protein. Genes & development 550 8319904
2000 Analysis of promoter binding by the E2F and pRB families in vivo: distinct E2F proteins mediate activation and repression. Genes & development 517 10766737
2011 A systematic screen for CDK4/6 substrates links FOXM1 phosphorylation to senescence suppression in cancer cells. Cancer cell 460 22094256
1991 Molecular cloning, chromosomal mapping, and expression of the cDNA for p107, a retinoblastoma gene product-related protein. Cell 459 1833063
1992 Cyclin E/cdk2 and cyclin A/cdk2 kinases associate with p107 and E2F in a temporally distinct manner. Genes & development 455 1398067
2004 The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). Genome research 438 15489334
2022 OpenCell: Endogenous tagging for the cartography of human cellular organization. Science (New York, N.Y.) 432 35271311
2013 The DREAM complex: master coordinator of cell cycle-dependent gene expression. Nature reviews. Cancer 431 23842645
2000 Id2 is a retinoblastoma protein target and mediates signalling by Myc oncoproteins. Nature 421 11034201
2002 E2F4/5 and p107 as Smad cofactors linking the TGFbeta receptor to c-myc repression. Cell 399 12150994
1997 pRB and p107/p130 are required for the regulated expression of different sets of E2F responsive genes. Genes & development 390 9192872
1992 Independent binding of the retinoblastoma protein and p107 to the transcription factor E2F. Nature 384 1530885
1996 Shared role of the pRB-related p130 and p107 proteins in limb development. Genes & development 372 8682294
2002 Isolating human transcription factor targets by coupling chromatin immunoprecipitation and CpG island microarray analysis. Genes & development 371 11799066
1994 Reversal of terminal differentiation mediated by p107 in Rb-/- muscle cells. Science (New York, N.Y.) 358 8197461
1994 E2F-4, a new member of the E2F gene family, has oncogenic activity and associates with p107 in vivo. Genes & development 352 7958925
1996 Reverse two-hybrid and one-hybrid systems to detect dissociation of protein-protein and DNA-protein interactions. Proceedings of the National Academy of Sciences of the United States of America 345 8816797
1994 E2F-4, a new member of the E2F transcription factor family, interacts with p107. Genes & development 345 7958924
1992 Homologous sequences in adenovirus E1A and human papillomavirus E7 proteins mediate interaction with the same set of cellular proteins. Journal of virology 343 1331501
2007 Evolutionarily conserved multisubunit RBL2/p130 and E2F4 protein complex represses human cell cycle-dependent genes in quiescence. Molecular cell 341 17531812
1995 E2F-4 and E2F-5, two members of the E2F family, are expressed in the early phases of the cell cycle. Proceedings of the National Academy of Sciences of the United States of America 326 7892279
1998 Substrate recruitment to cyclin-dependent kinase 2 by a multipurpose docking site on cyclin A. Proceedings of the National Academy of Sciences of the United States of America 322 9724724
2012 Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins. Nature 319 22810586
1996 E2F-4 switches from p130 to p107 and pRB in response to cell cycle reentry. Molecular and cellular biology 313 8657117
2005 Mitf cooperates with Rb1 and activates p21Cip1 expression to regulate cell cycle progression. Nature 307 15716956
1996 Targeted disruption of p107: functional overlap between p107 and Rb. Genes & development 293 8682293
2011 Mapping a dynamic innate immunity protein interaction network regulating type I interferon production. Immunity 286 21903422
1998 Role of the retinoblastoma protein family, pRB, p107 and p130 in the negative control of cell growth. Oncogene 277 9916999
2005 Role of the RB1 family in stabilizing histone methylation at constitutive heterochromatin. Nature cell biology 266 15750587
2011 A directed protein interaction network for investigating intracellular signal transduction. Science signaling 258 21900206
1993 Interactions of the p107 and Rb proteins with E2F during the cell proliferation response. The EMBO journal 255 8458319
1995 Regulation of the retinoblastoma protein-related p107 by G1 cyclin complexes. Genes & development 252 7797074
1995 p107 uses a p21CIP1-related domain to bind cyclin/cdk2 and regulate interactions with E2F. Genes & development 248 7622038
2004 Native E2F/RBF complexes contain Myb-interacting proteins and repress transcription of developmentally controlled E2F target genes. Cell 244 15479636
2004 Cell-specific effects of RB or RB/p107 loss on retinal development implicate an intrinsically death-resistant cell-of-origin in retinoblastoma. Cancer cell 237 15193257
1996 A unique role for the Rb protein in controlling E2F accumulation during cell growth and differentiation. Proceedings of the National Academy of Sciences of the United States of America 235 8622916
2007 Human papillomavirus type 16 E7 oncoprotein associates with the cullin 2 ubiquitin ligase complex, which contributes to degradation of the retinoblastoma tumor suppressor. Journal of virology 230 17609271
1998 The three members of the pocket proteins family share the ability to repress E2F activity through recruitment of a histone deacetylase. Proceedings of the National Academy of Sciences of the United States of America 229 9724731
1995 In vivo association of E2F and DP family proteins. Molecular and cellular biology 229 7739537
1992 Interaction of p107 with cyclin A independent of complex formation with viral oncoproteins. Science (New York, N.Y.) 229 1532457
1992 Interaction between human cyclin A and adenovirus E1A-associated p107 protein. Science (New York, N.Y.) 220 1532458
1994 Binding and suppression of the Myc transcriptional activation domain by p107. Science (New York, N.Y.) 218 8146655
1994 p130/pRb2 has growth suppressive properties similar to yet distinctive from those of retinoblastoma family members pRb and p107. Cancer research 215 7923196
2001 p107 and p130: versatile proteins with interesting pockets. Experimental cell research 198 11237530
1993 Human papillomavirus type 16 E7 associates with a histone H1 kinase and with p107 through sequences necessary for transformation. Journal of virology 195 8386265
2005 Rb and p107 regulate preadipocyte differentiation into white versus brown fat through repression of PGC-1alpha. Cell metabolism 181 16271529
1997 The retinoblastoma gene family pRb/p105, p107, pRb2/p130 and simian virus-40 large T-antigen in human mesotheliomas. Nature medicine 179 9256285
1997 Inactivation of pRB-related proteins p130 and p107 mediated by the J domain of simian virus 40 large T antigen. Molecular and cellular biology 157 9271376
1995 The pRB-related protein p107 contains two growth suppression domains: independent interactions with E2F and cyclin/cdk complexes. The EMBO journal 137 7743997
1994 Interaction of c-Myc with the pRb-related protein p107 results in inhibition of c-Myc-mediated transactivation. The EMBO journal 137 8076603
1993 Molecular characterization of the proteinase-encoding gene, prb1, related to mycoparasitism by Trichoderma harzianum. Molecular microbiology 135 8326868
1994 HPV16 E7 oncoprotein deregulates B-myb expression: correlation with targeting of p107/E2F complexes. The EMBO journal 132 8112300
1995 A link between increased transforming activity of lymphoma-derived MYC mutant alleles, their defective regulation by p107, and altered phosphorylation of the c-Myc transactivation domain. Molecular and cellular biology 127 7623799
1997 Regulation and expression of retinoblastoma proteins p107 and p130 during 3T3-L1 adipocyte differentiation. The Journal of biological chemistry 124 9092557
2004 Tissue-specific tumor suppressor activity of retinoblastoma gene homologs p107 and p130. Genes & development 121 15574596
2000 Opposing roles of pRB and p107 in adipocyte differentiation. Proceedings of the National Academy of Sciences of the United States of America 119 10995476
1995 Differential roles of two tandem E2F sites in repression of the human p107 promoter by retinoblastoma and p107 proteins. Molecular and cellular biology 117 7791762
1996 Activity of the retinoblastoma family proteins, pRB, p107, and p130, during cellular proliferation and differentiation. Critical reviews in biochemistry and molecular biology 116 8817077
1993 A genetic analysis of the E2F1 gene distinguishes regulation by Rb, p107, and adenovirus E4. Molecular and cellular biology 115 8413230
1993 Analysis of p107-associated proteins: p107 associates with a form of E2F that differs from pRB-associated E2F-1. Journal of virology 113 8230483
1996 Human papillomavirus E7 oncoproteins bind a single form of cyclin E in a complex with cdk2 and p107. Virology 112 8553588
1993 Transcriptional repression by the Rb-related protein p107. Molecular biology of the cell 112 7685208
1996 The human cytomegalovirus IE1-72 protein interacts with the cellular p107 protein and relieves p107-mediated transcriptional repression of an E2F-responsive promoter. Journal of virology 103 8892909
2003 Oxidative stress induces protein phosphatase 2A-dependent dephosphorylation of the pocket proteins pRb, p107, and p130. The Journal of biological chemistry 102 12621062
1997 p130 and p107 use a conserved domain to inhibit cellular cyclin-dependent kinase activity. Molecular and cellular biology 101 9199292
1996 Regulation of the retinoblastoma protein-related protein p107 by G1 cyclin-associated kinases. Proceedings of the National Academy of Sciences of the United States of America 100 8643455
2007 Mammalian Mip/LIN-9 interacts with either the p107, p130/E2F4 repressor complex or B-Myb in a cell cycle-phase-dependent context distinct from the Drosophila dREAM complex. Oncogene 99 17563750
1997 Improved biocontrol activity of Trichoderma harzianum by over-expression of the proteinase-encoding gene prb1. Current genetics 98 9000378
2008 An FTS/Hook/p107(FHIP) complex interacts with and promotes endosomal clustering by the homotypic vacuolar protein sorting complex. Molecular biology of the cell 95 18799622
1999 C/EBPalpha regulates formation of S-phase-specific E2F-p107 complexes in livers of newborn mice. Molecular and cellular biology 94 10082561
1986 Purification, characterization, and structural properties of a single protein from rat basophilic leukemia (RBL-1) cells possessing 5-lipoxygenase and leukotriene A4 synthetase activities. Molecular pharmacology 94 3785138
1995 Association of p107 with Sp1: genetically separable regions of p107 are involved in regulation of E2F- and Sp1-dependent transcription. Molecular and cellular biology 93 7565695
2000 Combinatorial roles for pRB, p107, and p130 in E2F-mediated cell cycle control. Proceedings of the National Academy of Sciences of the United States of America 92 10995475
1995 MDM2 transformation in the absence of p53 and abrogation of the p107 G1 cell-cycle arrest. Oncogene 90 8570197
1996 Simian virus 40 large T antigen alters the phosphorylation state of the RB-related proteins p130 and p107. Journal of virology 89 8627752
1999 Functional interaction between a novel protein phosphatase 2A regulatory subunit, PR59, and the retinoblastoma-related p107 protein. Oncogene 86 9927208
2005 p130/p107/p105Rb-dependent transcriptional repression during DNA-damage-induced cell-cycle exit at G2. Journal of cell science 83 15827088
2004 Alterations of pRb1-cyclin D1-cdk4/6-p16(INK4A) pathway in endometrial carcinogenesis. Cancer letters 75 14670612
2002 Reversal of growth suppression by p107 via direct phosphorylation by cyclin D1/cyclin-dependent kinase 4. Molecular and cellular biology 75 11884610
1994 Evidence for a protein domain superfamily shared by the cyclins, TFIIB and RB/p107. Nucleic acids research 73 8152925
1987 Protease B of Saccharomyces cerevisiae: isolation and regulation of the PRB1 structural gene. Genetics 73 3549451
1998 Distinct mechanisms control the accumulation of the Rb-related p107 and p130 proteins during cell growth. Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research 72 9563849
1998 p130 is dispensable in peripheral T lymphocytes: evidence for functional compensation by p107 and pRB. Molecular and cellular biology 70 9418868
2002 Distinct phosphorylation events regulate p130- and p107-mediated repression of E2F-4. The Journal of biological chemistry 67 12006580
1993 Temporal regulation of cyclin A-p107 and p33cdk2 complexes binding to a human thymidine kinase promoter element important for G1-S phase transcriptional regulation. Proceedings of the National Academy of Sciences of the United States of America 67 8475104
1998 Dual cyclin-binding domains are required for p107 to function as a kinase inhibitor. Molecular and cellular biology 65 9710622
2003 Mullerian Inhibiting Substance inhibits cervical cancer cell growth via a pathway involving p130 and p107. Proceedings of the National Academy of Sciences of the United States of America 62 14671316
2019 RB, p130 and p107 differentially repress G1/S and G2/M genes after p53 activation. Nucleic acids research 61 31667499
2002 p107 and p130 Coordinately regulate proliferation, Cbfa1 expression, and hypertrophic differentiation during endochondral bone development. Developmental biology 59 12086466
1995 The interactions of E2F with pRB and with p107 are regulated via the phosphorylation of pRB and p107 by a cyclin-dependent kinase. Oncogene 56 7753545
1995 Viral oncoprotein binding to pRB, p107, p130, and p300. Virus research 56 7762286
1995 The Rb-related p107 protein can suppress E2F function independently of binding to cyclin A/cdk2. Molecular and cellular biology 55 7799940
2016 CRISPR/Cas9 mediated knockout of rb1 and rbl1 leads to rapid and penetrant retinoblastoma development in Xenopus tropicalis. Scientific reports 54 27739525
1999 RNA polymerase III transcription factor IIIB is a target for repression by pocket proteins p107 and p130. Molecular and cellular biology 54 10330166
1996 Transcriptional repression and growth suppression by the p107 pocket protein. Molecular and cellular biology 52 8668177
2002 FGF signaling targets the pRb-related p107 and p130 proteins to induce chondrocyte growth arrest. The Journal of cell biology 51 12177046
1996 B-myb promotes S phase and is a downstream target of the negative regulator p107 in human cells. The Journal of biological chemistry 51 8621601
2003 Abnormal epidermal differentiation and impaired epithelial-mesenchymal tissue interactions in mice lacking the retinoblastoma relatives p107 and p130. Development (Cambridge, England) 50 12702649
2004 A dynamic equilibrium between CDKs and PP2A modulates phosphorylation of pRB, p107 and p130. Cell cycle (Georgetown, Tex.) 49 15467457
1997 Enterocyte differentiation is compatible with SV40 large T expression and loss of p53 function in human colonic Caco-2 cells. Status of the pRb1 and pRb2 tumor suppressor gene products. FEBS letters 49 9136893
1994 pRB, p107 and the regulation of the E2F transcription factor. Journal of cell science. Supplement 49 7883798
1998 p130, p107, and pRb are differentially regulated in proliferating cells and during cell cycle arrest by alpha-interferon. The Journal of biological chemistry 47 9726970
1999 E2F/p107 and E2F/p130 complexes are regulated by C/EBPalpha in 3T3-L1 adipocytes. Nucleic acids research 45 10446255
2010 p107 in the public eye: an Rb understudy and more. Cell division 44 20359370
1980 Mapping of the proteinase b structural gene PRB1, in Saccharomyces cerevisiae and identification of nonsense alleles within the locus. Genetics 41 7009321
2002 Multiple environmental signals determine the transcriptional activation of the mycoparasitism related gene prb1 in Trichoderma atroviride. Molecular genetics and genomics : MGG 40 12207218
1996 The retinoblastoma family member p107 binds to B-MYB and suppresses its autoregulatory activity. The Journal of biological chemistry 40 8910512
2002 The cancer preventive flavonoid silibinin causes hypophosphorylation of Rb/p107 and Rb2/p130 via modulation of cell cycle regulators in human prostate carcinoma DU145 cells. Cell cycle (Georgetown, Tex.) 39 12429923
1999 Rapid dephosphorylation of p107 following UV irradiation. Oncogene 39 9989818
1999 Domain mapping of the human cytomegalovirus IE1-72 and cellular p107 protein-protein interaction and the possible functional consequences. The Journal of general virology 38 10355776
1990 Consequences of growth media, gene copy number, and regulatory mutations on the expression of the PRB1 gene of Saccharomyces cerevisiae. Genetics 38 2407604
2005 p107 inhibits G1 to S phase progression by down-regulating expression of the F-box protein Skp2. The Journal of cell biology 37 15631990
2007 The Retinoblastoma family member p107 regulates the rate of progenitor commitment to a neuronal fate. The Journal of cell biology 36 17591923
2013 Proto-oncogene activity of melanoma antigen-A11 (MAGE-A11) regulates retinoblastoma-related p107 and E2F1 proteins. The Journal of biological chemistry 35 23853093
2009 Retinoblastoma/p107/p130 pocket proteins: protein dynamics and interactions with target gene promoters. The Journal of biological chemistry 34 19279001
1999 Retinoblastoma-related p107 and pRb2/p130 proteins in malignant lymphomas: distinct mechanisms of cell growth control. Clinical cancer research : an official journal of the American Association for Cancer Research 34 10632341
1995 In-vivo analysis of hpv e7 protein association with prb, p107 and p130. International journal of oncology 34 21556519
2010 B55alpha PP2A holoenzymes modulate the phosphorylation status of the retinoblastoma-related protein p107 and its activation. The Journal of biological chemistry 33 20663872
2008 PP2A-mediated dephosphorylation of p107 plays a critical role in chondrocyte cell cycle arrest by FGF. PloS one 33 18927618
1996 Adenovirus E1A activates cyclin A gene transcription in the absence of growth factors through interaction with p107. Journal of virology 33 8642699
1998 pRb and p107 regulate E2F activity during lens fiber cell differentiation. Oncogene 32 9467965
1996 PRB1, PRB2, and PRB4 coded polymorphisms among human salivary concanavalin-A binding, II-1, and Po proline-rich proteins. American journal of human genetics 30 8554050