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NOP53

Ribosome biogenesis protein NOP53 · UniProt Q9NZM5

Length
478 aa
Mass
54.4 kDa
Annotated
2026-04-29
49 papers in source corpus 28 papers cited in narrative 28 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NOP53 (PICT1/GLTSCR2) is a nucleolar protein that serves as a critical nexus linking ribosome biogenesis, the p53 tumor suppressor pathway, and nucleolar stress sensing. In its core ribosome biogenesis function, NOP53 acts as an adaptor recruiting the MTR4 helicase and RNA exosome to pre-60S ribosomal particles via its arch-interacting motif (AIM), mediating both early 32S pre-rRNA cleavage (AIM-independent) and late 5.8S rRNA maturation (AIM-dependent), while also stabilizing the pre-60S foot structure during nuclear export (PMID:36403484, PMID:31662437, PMID:34125911, PMID:28883156). NOP53 retains RPL11 in the nucleolus under unstressed conditions, preventing RPL11–MDM2 interaction; upon nucleolar stress or DNA damage, ATM-dependent phosphorylation at S233/T289 triggers ubiquitin-independent 20S proteasomal degradation of NOP53, releasing RPL11 to inhibit MDM2 and stabilize p53 (PMID:21804542, PMID:27829214, PMID:24923447). Beyond ribosome biogenesis, NOP53 stabilizes PTEN to suppress PI3K/AKT signaling, inhibits the NPM–MYC transcriptional axis, promotes ARF degradation via ULF/TRIP12, suppresses autophagy through ZKSCAN3 activation and histone H3 dephosphorylation, maintains chromosomal stability during mitosis, and—when translocated to the cytoplasm during viral infection—attenuates RIG-I/IFN-β antiviral signaling by facilitating USP15-mediated deubiquitination of RIG-I (PMID:16971513, PMID:25956029, PMID:27323397, PMID:34502226, PMID:30421090, PMID:27824081).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2006 High

    The first functional role for NOP53 was established as a stabilizer of the tumor suppressor PTEN, linking it to PI3K/AKT signaling control — answering whether this nucleolar protein had tumor-suppressive signaling functions.

    Evidence RNAi knockdown with PTEN-null controls, Western blot, and AKT phosphorylation readouts in cell lines

    PMID:16971513

    Open questions at the time
    • Mechanism of PTEN stabilization (direct vs. indirect) not determined
    • Whether PTEN interaction occurs in the nucleolus or nucleoplasm unresolved
  2. 2009 Medium

    Discovery that NOP53 can sequester viral Bcl-2 to the nucleolus established the principle that NOP53 functions as a nucleolar tethering factor, a theme recurrent in its biology.

    Evidence Yeast two-hybrid, Co-IP, confocal imaging of KSHV KS-Bcl-2 localization, siRNA knockdown

    PMID:20042497

    Open questions at the time
    • Physiological relevance during KSHV infection not tested in vivo
    • Whether sequestration applies to cellular Bcl-2 family members unknown
  3. 2011 High

    Two key advances in 2011 defined NOP53 as a central mediator of the ribosomal protein–MDM2–p53 axis and as a participant in the DNA damage response, answering how nucleolar integrity communicates with p53 surveillance.

    Evidence Pict1 knockout mice/ES cells with Co-IP and ubiquitination rescue (RPL11–MDM2 axis); siRNA knockdown with DDR kinase phosphorylation readouts and G2/M checkpoint analysis

    PMID:21741933 PMID:21804542

    Open questions at the time
    • Whether RPL11 retention and DDR functions are mechanistically separable was unclear
    • Identity of the stress signals triggering NOP53 degradation not yet known
  4. 2012 High

    Demonstration that NOP53 translocates to the nucleoplasm under ribosomal stress where it directly stabilizes p53 in an ARF-independent manner established a second, direct route to p53 activation beyond RPL11 release, and mapping of nucleolar localization sequences defined the structural basis for compartmentalization.

    Evidence Co-IP, subcellular fractionation, xenograft model, EGFP fusion deletion mapping

    PMID:22292050 PMID:22522597

    Open questions at the time
    • Relative contribution of direct p53 stabilization vs. RPL11-MDM2 pathway not quantified
    • Whether the two NoLS are differentially regulated unknown
  5. 2014 High

    Three discoveries established the biochemical properties of NOP53 itself and its metabolic connections: homo-oligomerization via the C-terminal domain, ubiquitin-independent 20S proteasomal degradation as the mechanism of stress-induced turnover, and a role in Myc-dependent mitochondrial metabolism.

    Evidence FRET, gel filtration, cross-linking (oligomerization); in vitro 20S proteasome reconstitution with nucleoplasmic mutant (degradation); overexpression screen with C. elegans ortholog validation (metabolism)

    PMID:24556985 PMID:24735870 PMID:24923447

    Open questions at the time
    • Whether oligomerization state changes upon stress not tested
    • How 20S proteasome recognizes NOP53 without ubiquitin unclear
    • Direct Myc targets mediating metabolic effects uncharacterized
  6. 2015 Medium

    NOP53 was shown to regulate the NPM–MYC oncogenic axis by competitively binding NPM to disrupt NPM–MYC complex formation at target promoters, and separately to induce NPM proteasomal degradation, establishing NOP53 as a multilayered NPM antagonist.

    Evidence Co-IP, ChIP at MYC target promoters, luciferase reporters, ubiquitination assays with proteasome inhibitors

    PMID:25818168 PMID:25956029

    Open questions at the time
    • Whether NPM regulation occurs in physiological stress contexts or only upon overexpression not established
    • Structural basis of NOP53–NPM interaction unknown
  7. 2016 High

    Multiple 2016 studies resolved upstream regulation and downstream effector mechanisms: JNK/c-Jun signaling maintains nucleolar retention and stability of NOP53; NOP53 binds rDNA and UBF to suppress RNA Pol I transcription and trigger pro-death autophagy; NOP53 promotes ARF degradation via ULF/TRIP12; and ATM-dependent phosphorylation at S233/T289 triggers NOP53 degradation linking DNA damage to p53 activation via RPL11.

    Evidence JNK inhibitor and c-Jun peptide treatment (JNK axis); ChIP at rDNA promoter with CX-5461 comparison (Pol I); Co-IP and ubiquitination assays (ARF); ATM inhibitors with phosphosite mutagenesis (S233A/T289A, S233D/T289D) and Co-IP (ATM axis)

    PMID:26903295 PMID:27323397 PMID:27729611 PMID:27829214

    Open questions at the time
    • How JNK-mediated nucleolar retention and ATM-mediated degradation are coordinately regulated unknown
    • Whether rDNA binding is direct or UBF-dependent not resolved
    • Whether ARF degradation occurs under physiological nucleolar stress unclear
  8. 2017 High

    The 3.2 Å crystal structure of yeast Mtr4 KOW domain bound to the Nop53 AIM peptide revealed the molecular basis for exosome recruitment to pre-ribosomes, and NMR showed simultaneous RNA and protein binding, resolving how Nop53/NOP53 bridges rRNA substrate and processing machinery.

    Evidence X-ray crystallography at 3.2 Å, NMR, mutagenesis of binding interfaces in S. cerevisiae

    PMID:28883156

    Open questions at the time
    • Human NOP53–MTR4 structure not yet determined
    • Whether AIM–KOW binding is regulated by post-translational modifications unknown
  9. 2018 Medium

    NOP53 was implicated in viral exploitation strategies: HSV-1 γ₁34.5 induces cytoplasmic translocation of NOP53 to facilitate PP1α recruitment for eIF2α dephosphorylation, and NOP53 knockdown impairs HSV-1 virulence in vivo, establishing NOP53 as a host factor co-opted by viruses.

    Evidence Co-IP, eIF2α phosphorylation assays, shRNA knockdown, mouse infection model

    PMID:29367603

    Open questions at the time
    • Whether cytoplasmic NOP53 functions in antiviral RIG-I attenuation and viral eIF2α dephosphorylation are coordinated unknown
    • Generalizability to other DNA viruses untested
  10. 2019 High

    Proteomic analysis in yeast established Nop53 as the primary adaptor recruiting the RNA exosome and Rrp6 to pre-60S particles and showed exosome association occurs earlier in ribosome maturation than previously appreciated.

    Evidence Co-IP/mass spectrometry, yeast genetics, sucrose gradient sedimentation in S. cerevisiae

    PMID:31662437

    Open questions at the time
    • Whether human NOP53 recruits exosome at the same maturation stage unconfirmed at this point
    • Stoichiometry of exosome–Nop53–pre-60S complex not determined
  11. 2021 Medium

    Three advances clarified distinct NOP53 functions: a structural role in pre-60S foot stabilization separable from AIM-dependent exosome recruitment (yeast); autophagy suppression via dual ZKSCAN3-dependent and histone H3 S10 dephosphorylation-dependent pathways; and maintenance of chromosomal stability during mitosis.

    Evidence Nop53 depletion vs. AIM mutant with polysome profiling and mass spectrometry (foot stabilization); siRNA, ChIP, histone phosphorylation assays (autophagy); shRNA with rescue, live-cell imaging, micronucleus scoring (chromosomal stability)

    PMID:30421090 PMID:34125911 PMID:34502226

    Open questions at the time
    • Mechanism by which NOP53 promotes H3 S10 dephosphorylation (phosphatase identity) unknown
    • Whether chromosomal instability phenotype is secondary to ribosome biogenesis defects not excluded
    • Foot stabilization shown only in yeast
  12. 2022 High

    Two studies in human cells resolved the dual pre-rRNA processing function of NOP53 (AIM-independent early 32S cleavage and AIM-dependent late 5.8S maturation) and demonstrated that NOP53 undergoes liquid-liquid phase separation via its IDR1, with distinct M-R motifs governing nucleolar localization.

    Evidence AIM mutant complementation with Northern blot for pre-rRNA intermediates (processing); in vitro droplet formation, FRAP, 1,6-hexanediol, IDR1/M-R mutagenesis (LLPS)

    PMID:36316314 PMID:36403484

    Open questions at the time
    • Whether LLPS is required for exosome recruitment or ribosome assembly function not tested
    • How the two processing steps are coordinated mechanistically unclear
  13. 2024 Medium

    Identification of MRE11 as a NOP53 interactor connected NOP53 directly to DNA damage repair, with NOP53 deletion causing ROS accumulation, mitochondrial dysfunction, and impaired DNA repair in alveolar type II cells.

    Evidence Co-IP/mass spectrometry identifying MRE11, PICT1 conditional deletion, ROS and comet assays, mitochondrial respiration measurement

    PMID:39578839

    Open questions at the time
    • Whether NOP53–MRE11 interaction is direct or bridged by other factors unknown
    • Mechanism linking NOP53 to mitochondrial ROS control not established
    • Single cell type studied

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include: how NOP53's ribosome biogenesis, p53 surveillance, and signaling functions are hierarchically organized; whether LLPS regulates its stress-sensing switch; the structural basis of human NOP53–MTR4 and NOP53–RPL11 interactions; and how cytoplasmic translocation during viral infection is mechanistically triggered and whether it represents a general innate immune regulatory mechanism.
  • No integrated model connecting ribosome biogenesis defects to the multiple signaling outputs
  • Human NOP53 structure not available
  • In vivo validation of many signaling axes limited to single labs

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0060090 molecular adaptor activity 3 GO:0003723 RNA binding 2 GO:0003677 DNA binding 1 GO:0042393 histone binding 1
Localization
GO:0005730 nucleolus 4 GO:0005654 nucleoplasm 3 GO:0005829 cytosol 2
Pathway
R-HSA-8953854 Metabolism of RNA 4 R-HSA-162582 Signal Transduction 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-5357801 Programmed Cell Death 3 R-HSA-73894 DNA Repair 3 R-HSA-1640170 Cell Cycle 2 R-HSA-9612973 Autophagy 2 R-HSA-168256 Immune System 1
Partners
MRE11MTR4NPM1PTENRIG-IRPL11UBFUSP15
Complex memberships
RNA exosomepre-60S ribosomal particle

Evidence

Reading pass · 28 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2011 PICT1 (NOP53) binds RPL11 and retains it in the nucleolus; loss of PICT1 releases RPL11 to the nucleoplasm where it binds MDM2 and blocks MDM2-mediated ubiquitination of p53, leading to p53 accumulation and G1 arrest/apoptosis even without DNA damage. Pict1 knockout mice and ES cells, co-immunoprecipitation, ubiquitination assays, genetic rescue experiments Nature medicine High 21804542
2006 PICT-1 (NOP53) binds and stabilizes PTEN protein; RNAi knockdown of PICT-1 downregulates endogenous PTEN, activates PI3K/AKT signaling, promotes cell proliferation, and reduces apoptosis in a PTEN-dependent manner. RNAi knockdown, Western blot, PIP3 downstream effector phosphorylation assays, anchorage-independent growth assay Molecular biology of the cell High 16971513
2007 GLTSCR2 (NOP53) is a nucleus-localized protein that induces caspase-independent, PTEN-modulated apoptotic cell death when overexpressed, through a mechanism divergent from PTEN-induced death pathways. Overexpression, co-immunoprecipitation, cell death assays, caspase activity assays Cell death and differentiation Medium 17657248
2012 Under ribosomal stress, GLTSCR2 (NOP53) translocates from the nucleolus to the nucleoplasm where it directly interacts with and stabilizes p53, inhibiting cell cycle progression in an ARF-independent manner. Co-immunoprecipitation, subcellular fractionation, immunofluorescence, xenograft tumor model, siRNA knockdown Cell death and differentiation High 22522597
2017 The crystal structure of S. cerevisiae Mtr4 bound to Nop53 at 3.2 Å resolution reveals that the KOW domain of Mtr4 recognizes the arch-interacting motif (AIM) of Nop53 through hydrophobic and electrostatic interactions; NMR shows the KOW domain can simultaneously bind AIM-containing protein and structured RNA at adjacent surfaces. X-ray crystallography (3.2 Å), NMR, mutagenesis RNA (New York, N.Y.) High 28883156
2011 GLTSCR2 (NOP53) is involved in the DNA damage response; its expression increases under genotoxic conditions, it mobilizes to the nucleoplasm, and its knockdown attenuates phosphorylation of ATM, ATR, Chk1, Chk2, and H2AX, delays DNA repair, and abolishes G2/M checkpoint activation. siRNA knockdown, immunofluorescence, Western blot for DDR kinase phosphorylation, flow cytometry, colony survival assay The American journal of pathology Medium 21741933
2014 Nucleolar stress induces ubiquitin-independent, 20S proteasome-mediated degradation of PICT1 (NOP53); nucleolar localization is required for stress-induced degradation, as a nucleoplasmic mutant is resistant to stress-induced but not in vitro degradation. Proteasome inhibitors, E1 ubiquitin-activating enzyme inhibitor, genetic inactivation, in vitro 20S proteasome degradation assay, nucleoplasmic localization mutant The Journal of biological chemistry High 24923447
2016 DNA damage triggers ATM-dependent phosphorylation of PICT-1 at S233 and T289, leading to its proteasomal degradation, release of RPL11 from the nucleolus, increased RPL11-MDM2 binding, and p53 accumulation/apoptosis. ATM inhibitors (wortmannin, KU55933), phosphosite mutagenesis (S233A/T289A alanine and S233D/T289D phosphomimetic mutants), co-immunoprecipitation, immunofluorescence Oncotarget High 27829214
2010 PICT-1 (NOP53) localizes to the nucleolus and interacts with Ser518-dephosphorylated merlin (growth-inhibitory form) in the nucleolus; the PICT-1 C-terminal truncation mutant (1-356) that loses merlin binding has markedly reduced inhibitory effects on cell cycle and proliferation. Co-immunoprecipitation, confocal microscopy, siRNA knockdown of merlin, overexpression of truncation mutants, flow cytometry The international journal of biochemistry & cell biology Medium 21167305
2016 PICT-1 (NOP53) overexpression triggers pro-death autophagy by directly binding ribosomal DNA (rDNA) gene loci and interacting with UBF to inhibit phosphorylation of UBF and recruitment of RNA Pol I to the rDNA promoter, suppressing rRNA transcription and inactivating AKT/mTOR/p70S6K signaling. ChIP (chromatin immunoprecipitation), co-immunoprecipitation, deletion mutant analysis, Pol I inhibitor CX-5461 comparison, Western blot for mTOR pathway components Oncotarget Medium 27729611
2009 PICT-1 (NOP53) interacts with KSHV KS-Bcl-2 and sequesters it from mitochondria to the nucleolus; this nucleolar targeting correlates with reduction of KS-Bcl-2 antiapoptotic activity, and knockdown of PICT-1 abolishes nucleolar localization of KS-Bcl-2. Yeast two-hybrid, co-immunoprecipitation, confocal microscopy, siRNA knockdown, deletion mapping of interaction domains Journal of virology Medium 20042497
2012 PICT-1/GLTSCR2 (NOP53) nucleolar localization is mediated by two independent nucleolar localization sequences (NoLS) containing arginine and leucine clusters; its nucleolar distribution resembles rRNA processing factors but does not precisely colocalize with UBF1 or Fibrillarin. Confocal microscopy of EGFP and myc-tagged fusion proteins, deletion mapping PloS one Medium 22292050
2014 PICT-1 (NOP53) forms homo-oligomers (primarily dimers) mediated by its carboxy-terminal domain, as shown by yeast two-hybrid, co-immunoprecipitation, FRET, microfluidic affinity binding, glutaraldehyde cross-linking, and gel filtration. Yeast two-hybrid, co-immunoprecipitation, FRET, in vitro microfluidic affinity binding, glutaraldehyde cross-linking, gel filtration Journal of molecular biology High 24735870
2015 GLTSCR2 (NOP53) inhibits the NPM-MYC oncogenic axis: redistributed GLTSCR2 in the nucleoplasm competitively binds NPM, inhibiting formation of the NPM-MYC binary complex and reducing NPM-MYC recruitment to MYC target gene promoters, thereby suppressing MYC transcriptional activity. Co-immunoprecipitation, chromatin immunoprecipitation (ChIP), luciferase reporter assay, colony formation assay The American journal of pathology Medium 25956029
2015 GLTSCR2 (NOP53) acts as an upstream negative regulator of nucleophosmin (NPM): it induces nucleoplasmic translocation and proteasomal polyubiquitination-dependent degradation of NPM, and decreases NPM-mediated transforming activity. Co-immunoprecipitation, immunofluorescence, ubiquitination assay, proteasome inhibitor treatment, shRNA knockdown Journal of cellular and molecular medicine Medium 25818168
2017 GLTSCR2 (NOP53) promotes translocation of ARF from the nucleolus to the nucleoplasm, increases ARF binding to the E3 ubiquitin ligase ULF/TRIP12, and enhances ARF degradation through the polyubiquitination pathway. Co-immunoprecipitation, immunofluorescence, ubiquitination assay, overexpression and knockdown Oncotarget Medium 27323397
2016 Viral infection induces cytoplasmic translocation of GLTSCR2 (NOP53), where it interacts with RIG-I and USP15; this triple interaction promotes USP15-mediated removal of K63-linked ubiquitination from RIG-I, attenuating RIG-I signaling and type I IFN-β production to support viral replication. Deletion of the nuclear export sequence (NES) abolishes this activity. Co-immunoprecipitation, ubiquitination assays, NES deletion mutant, RIG-I activation assays, IFN-β reporter assay Scientific reports Medium 27824081
2018 HSV-1 viral protein γ34.5 induces cytoplasmic translocation of NOP53; cytoplasmic NOP53 facilitates γ34.5 recruitment of protein phosphatase PP1α to dephosphorylate eIF2α, enabling efficient viral translation. NOP53 knockdown disrupts the γ34.5-PP1α interaction and impairs HSV-1 virulence in vivo. Co-immunoprecipitation, eIF2α phosphorylation assays, viral yield assays, NOP53 knockdown (shRNA), in vivo mouse infection model Cell death & disease Medium 29367603
2016 JNK phosphorylation of c-Jun is required for nucleolar retention and protein stability of GLTSCR2 (NOP53); inhibition of JNK (with SP600125) or addition of c-Jun peptide induces nucleoplasmic translocation of GLTSCR2 and its proteasomal polyubiquitination-dependent degradation, possibly by reducing GLTSCR2 monomer binding affinity. Kinase inhibitor treatment, immunocytochemistry, immunoblot, cycloheximide chase, ubiquitination assay, co-immunoprecipitation Biochemical and biophysical research communications Medium 26903295
2014 GLTSCR2/PICT1 (NOP53) enhances mitochondrial function and maintains oxygen consumption; it controls cellular proliferation and metabolism via the transcription factor Myc, and is induced by mitochondrial stress. High-throughput overexpression screen, flow cytometry, RNAi in C. elegans (ortholog), respiration assays Proceedings of the National Academy of Sciences of the United States of America Medium 24556985
2019 Yeast Nop53 (ortholog of NOP53) acts as an adaptor recruiting the RNA exosome to pre-60S particles; it interacts with the 25S rRNA, the exosome catalytic subunit Rrp6, and the helicase Mtr4; proteomic analysis shows the exosome binds pre-ribosomal complexes earlier during ribosome maturation than previously thought. Co-immunoprecipitation, mass spectrometry (proteomics), yeast genetics, sucrose gradient sedimentation The Journal of biological chemistry High 31662437
2021 Yeast Nop53 (ortholog of NOP53) has a structural role in stabilizing the pre-60S foot interface and facilitating transition from nucleolar state E particle to nuclear stages; Nop53 depletion (unlike AIM-motif mutants) causes retention of unprocessed foot in late pre-60S intermediates and impairs late maturation events including Yvh1 recruitment. Yeast Nop53 depletion, AIM-motif mutant analysis, polysome profiling, mass spectrometry, Northern blot for pre-rRNA intermediates Nucleic acids research Medium 34125911
2022 Human PICT1/NOP53 interacts with MTR4 and the RNA exosome in an arch-interacting motif (AIM)-dependent manner and is required for two distinct pre-rRNA processing steps: early cleavage of 32S intermediate RNA and late maturation of 12S precursor into 5.8S rRNA; only the late step requires AIM-dependent recruitment of MTR4 and exosome. Depletion of PICT1 or MTR4 (but not exosome catalytic subunits RRP6/DIS3) induces p53 stabilization. Co-immunoprecipitation, siRNA depletion, AIM-sequence mutant overexpression, Northern blot for pre-rRNA intermediates, Western blot for p53 Biochemical and biophysical research communications High 36403484
2021 NOP53 suppresses autophagy through two divergent pathways: (1) a ZKSCAN3-dependent pathway where NOP53 transcriptionally activates autophagy suppressor ZKSCAN3 to inhibit LC3B induction; (2) a ZKSCAN3-independent pathway where NOP53 physically interacts with histone H3 and promotes dephosphorylation of H3 at S10, transcriptionally downregulating ATG7 and ATG12. siRNA knockdown, co-immunoprecipitation, chromatin immunoprecipitation, luciferase reporter assay, histone H3 phosphorylation assay, autophagy flux assays International journal of molecular sciences Medium 34502226
2022 NOP53 undergoes liquid-liquid phase separation (LLPS) in vivo and in vitro; the intrinsically disordered region 1 (IDR1) is required for LLPS, while multivalent arginine-rich linear motifs (M-R motifs) are essential for nucleolar localization but dispensable for LLPS. NOP53 silencing sensitizes colorectal cancer cells to radiotherapy and negatively regulates the p53 pathway. In vitro droplet formation assay, FRAP, 1,6-hexanediol sensitivity, IDR1 deletion mutant, M-R motif mutagenesis, shRNA knockdown, clonogenic survival assay Cell death discovery Medium 36316314
2018 NOP53 knockdown causes abnormal nuclear morphology (large/irregular nuclei, multinucleated cells), aberrant chromosome congression in metaphase, spindle checkpoint activation, delayed mitosis, and chromosomal instability (micronuclei, nuclear buds); re-expression of NOP53 rescues these defects. shRNA knockdown, rescue by re-expression, immunofluorescence, live-cell imaging, Giemsa staining, flow cytometry Pathology oncology research : POR Medium 30421090
2024 PICT1 (NOP53) interacts with MRE11, a DNA damage repair factor; PICT1 deletion in alveolar type II cells leads to mitochondrial and nuclear ROS accumulation, cell cycle arrest, mitochondrial and nuclear DNA damage, decreased mitochondrial respiration, and impaired DNA damage repair. Co-immunoprecipitation followed by mass spectrometry (identifying MRE11 as novel interactor), PICT1 deletion, ROS assay, mitochondrial respiration assay, comet assay Cell communication and signaling : CCS Medium 39578839
2021 PICT1 (NOP53) overexpression in medullary thyroid (TT) cells induces production of p53β (a p53 splice variant lacking C-terminus), decreases p21 expression, elevates cell viability, and reduces PTEN expression while increasing phospho-Akt-Ser47, suggesting a role in spliceosome regulation and mTOR pathway modulation. Lentiviral overexpression, Western blot, cell viability assay, mTOR pathway protein analysis Journal of neuroendocrinology Low 36306198

Source papers

Stage 0 corpus · 49 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Regulation of the MDM2-P53 pathway and tumor growth by PICT1 via nucleolar RPL11. Nature medicine 153 21804542
2006 Critical role of PICT-1, a tumor suppressor candidate, in phosphatidylinositol 3,4,5-trisphosphate signals and tumorigenic transformation. Molecular biology of the cell 72 16971513
2007 The putative tumor suppressor gene GLTSCR2 induces PTEN-modulated cell death. Cell death and differentiation 62 17657248
2012 Nucleolar protein GLTSCR2 stabilizes p53 in response to ribosomal stresses. Cell death and differentiation 57 22522597
2008 Suppression of putative tumour suppressor gene GLTSCR2 expression in human glioblastomas. The Journal of pathology 47 18729076
2017 Structural insights into the interaction of the nuclear exosome helicase Mtr4 with the preribosomal protein Nop53. RNA (New York, N.Y.) 37 28883156
2011 Involvement of GLTSCR2 in the DNA Damage Response. The American journal of pathology 32 21741933
2013 PICT1 regulates TP53 via RPL11 and is involved in gastric cancer progression. British journal of cancer 30 24045667
2018 The pre-rRNA processing factor Nop53 regulates fungal development and pathogenesis via mediating production of reactive oxygen species. Environmental microbiology 27 29488307
2015 The Nucleolar Protein GLTSCR2 Is an Upstream Negative Regulator of the Oncogenic Nucleophosmin-MYC Axis. The American journal of pathology 23 25956029
2012 Nucleolar localization of GLTSCR2/PICT-1 is mediated by multiple unique nucleolar localization sequences. PloS one 22 22292050
2019 NOP53 as A Candidate Modifier Locus for Familial Non-Medullary Thyroid Cancer. Genes 20 31703244
2016 PICT-1 triggers a pro-death autophagy through inhibiting rRNA transcription and AKT/mTOR/p70S6K signaling pathway. Oncotarget 20 27729611
2010 Moesin-ezrin-radixin-like protein (merlin) mediates protein interacting with the carboxyl terminus-1 (PICT-1)-induced growth inhibition of glioblastoma cells in the nucleus. The international journal of biochemistry & cell biology 20 21167305
2009 GLTSCR2/PICT-1, a putative tumor suppressor gene product, induces the nucleolar targeting of the Kaposi's sarcoma-associated herpesvirus KS-Bcl-2 protein. Journal of virology 18 20042497
2022 NOP53 undergoes liquid-liquid phase separation and promotes tumor radio-resistance. Cell death discovery 17 36316314
2016 The nucleolar protein GLTSCR2 is required for efficient viral replication. Scientific reports 15 27824081
2015 Arabidopsis SMALL ORGAN 4, a homolog of yeast NOP53, regulates cell proliferation rate during organ growth. Journal of integrative plant biology 15 26310197
2014 GLTSCR2/PICT1 links mitochondrial stress and Myc signaling. Proceedings of the National Academy of Sciences of the United States of America 15 24556985
2018 Downregulation of NOP53 Ribosome Biogenesis Factor Leads to Abnormal Nuclear Division and Chromosomal Instability in Human Cervical Cancer Cells. Pathology oncology research : POR 14 30421090
2020 The HMGB1-2 Ovarian Cancer Interactome. The Role of HMGB Proteins and Their Interacting Partners MIEN1 and NOP53 in Ovary Cancer and Drug-Response. Cancers 13 32867128
2021 PICT1 is critical for regulating the Rps27a-Mdm2-p53 pathway by microtubule polymerization inhibitor against cervical cancer. Biochimica et biophysica acta. Molecular cell research 12 34166715
2018 Multifunctional viral protein γ34.5 manipulates nucleolar protein NOP53 for optimal viral replication of HSV-1. Cell death & disease 12 29367603
2016 PICT-1 is a key nucleolar sensor in DNA damage response signaling that regulates apoptosis through the RPL11-MDM2-p53 pathway. Oncotarget 12 27829214
2013 Downregulation of GLTSCR2 expression is correlated with breast cancer progression. Pathology, research and practice 12 24054033
2015 GLTSCR2 is an upstream negative regulator of nucleophosmin in cervical cancer. Journal of cellular and molecular medicine 11 25818168
2014 Nucleolar stress induces ubiquitination-independent proteasomal degradation of PICT1 protein. The Journal of biological chemistry 11 24923447
2019 The ribosome assembly factor Nop53 controls association of the RNA exosome with pre-60S particles in yeast. The Journal of biological chemistry 10 31662437
2017 GLTSCR2 promotes the nucleoplasmic translocation and subsequent degradation of nucleolar ARF. Oncotarget 9 27323397
2014 The nucleolar PICT-1/GLTSCR2 protein forms homo-oligomers. Journal of molecular biology 9 24735870
2013 Clinical significance of PICT1 in patients of hepatocellular carcinoma with wild-type TP53. Annals of surgical oncology 9 23532381
2010 The expression of GLTSCR2, a candidate tumor suppressor, is reduced in seborrheic keratosis compared to normal skin. Pathology, research and practice 9 20185249
2021 The ribosome assembly factor Nop53 has a structural role in the formation of nuclear pre-60S intermediates, affecting late maturation events. Nucleic acids research 8 34125911
2017 Cellular protein GLTSCR2: A valuable target for the development of broad-spectrum antivirals. Antiviral research 8 28286234
2012 GLTSCR2 contributes to the death resistance and invasiveness of hypoxia-selected cancer cells. FEBS letters 8 22850112
2021 NOP53 Suppresses Autophagy through ZKSCAN3-Dependent and -Independent Pathways. International journal of molecular sciences 6 34502226
2013 Down-regulation and aberrant cytoplasmic expression of GLTSCR2 in prostatic adenocarcinomas. Cancer letters 6 23920125
2007 GLTSCR2 sensitizes cells to hypoxic injury without involvement of mitochondrial apoptotic cascades. Pathobiology : journal of immunopathology, molecular and cellular biology 6 17890897
2016 c-Jun N-terminal kinase regulates the nucleoplasmic translocation and stability of nucleolar GLTSCR2 protein. Biochemical and biophysical research communications 5 26903295
2013 Expression of GLTSCR2/Pict-1 in squamous cell carcinomas of the skin. Archives of dermatological research 5 23942755
2024 Mitochondrial dysfunction and impaired DNA damage repair through PICT1 dysregulation in alveolar type II cells in emphysema. Cell communication and signaling : CCS 3 39578839
2022 The role of PICT1 in RPL11/Mdm2/p53 pathway-regulated inhibition of cell growth induced by topoisomerase IIα inhibitor against cervical cancer cell line. Biochemical pharmacology 3 35605655
2022 MTR4 adaptor PICT1 functions in two distinct steps during pre-rRNA processing. Biochemical and biophysical research communications 3 36403484
2018 Abnormal Expression of PICT-1 and Its Codon 389 Polymorphism Is a Risk Factor for Human Endometrial Cancer. Oncology 3 29617699
2016 Role of GLTSCR2 in the regulation of telomerase activity and chromosome stability. Molecular medicine reports 3 27357325
2018 Cytoplasmic Translocation of Nucleolar Protein NOP53 Promotes Viral Replication by Suppressing Host Defense. Viruses 2 29677136
2014 The expression of GLTSCR2 in cervical intra-epithelial lesion and cancer. Archives of gynecology and obstetrics 2 25118835
2022 PICT-1 regulates p53 splicing and sensitivity of medullary thyroid carcinoma cells to everolimus. Journal of neuroendocrinology 1 36306198
2015 Suppression of GLTSCR2 expression in renal cell carcinomas. Pathology, research and practice 1 26724143