| 1999 |
β-TrCP directly binds phosphorylated β-catenin through its WD40 repeat domain in a GSK3β phosphorylation-dependent manner, forming part of an SCF E3 ubiquitin ligase complex (with Skp1 and Cul1) that targets β-catenin for proteasomal degradation; overexpression of wild-type β-TrCP promotes β-catenin downregulation, while a dominant-negative deletion mutant upregulates β-catenin and activates Tcf-dependent signaling. |
Direct binding assay, Co-IP from mammalian cells, dominant-negative overexpression, β-catenin stability assay |
Current biology : CB |
High |
10074433
|
| 1999 |
FWD1 (mouse homolog of β-TrCP) forms a multi-molecular complex with β-catenin, Axin, GSK-3β, and APC; phosphorylation at the N-terminal signal-induced sites of β-catenin is required for FWD1 association; FWD1 facilitates ubiquitination and proteasomal degradation of β-catenin as part of the SCF(FWD1) ubiquitin ligase. |
Co-immunoprecipitation, in vitro ubiquitination assay, dominant-negative overexpression, β-catenin stability assay |
The EMBO journal |
High |
10228155
|
| 1999 |
Human β-TrCP associates with Skp1 and Cul1 to form a novel SCF ubiquitin ligase complex, and interacts with β-catenin in vivo; expression of a dominant-negative β-TrCP stabilizes β-catenin. |
Co-immunoprecipitation, dominant-negative overexpression |
Oncogene |
High |
10023660
|
| 1999 |
β-TrCP (FWD1) specifically recognizes the doubly phosphorylated DSGψXS motif in IκBα; an F-box-deleted β-TrCP inhibits IκBα degradation; β-TrCP mediates ubiquitination of phosphorylated IκBα in vitro and in cells, enabling NF-κB nuclear translocation. |
Co-IP (phosphorylation-dependent), dominant-negative overexpression, in vitro ubiquitination, NF-κB reporter assay |
Proceedings of the National Academy of Sciences of the United States of America |
High |
10097128
|
| 1999 |
β-TrCP interacts specifically with phosphorylated IκBα (Ser32/Ser36) but not unmodified or phosphorylation-deficient IκBα; F-box deletion abolishes ability to ubiquitinate IκBα; β-TrCP is the adaptor for IκBα recognition by SCFβTrCP E3 complex. |
Co-IP (phosphorylation-dependent), dominant-negative expression, NF-κB transcription assay |
The Journal of biological chemistry |
High |
10075690
|
| 1999 |
β-Trcp negatively regulates Wnt/β-catenin signaling and dorsal axis formation in Xenopus; phosphorylated β-catenin is specifically recognized by β-Trcp; inhibition of endogenous β-Trcp by dominant-negative mutant stabilizes β-catenin, activates Wnt signaling, and induces axis duplication. |
Xenopus embryo injection, dominant-negative overexpression, co-IP |
Proceedings of the National Academy of Sciences of the United States of America |
High |
10339577
|
| 1999 |
FWD1/β-TrCP recognizes the conserved DSGψXS phospho-motif in IκBα, IκBβ, and IκBε; phosphorylation of both conserved serines is required for FWD1-mediated ubiquitination of all three IκB proteins; the D31A mutation in IκBα abolishes FWD1 binding without affecting phosphorylation. |
Co-IP, in vitro ubiquitination, site-directed mutagenesis, degradation assay |
The Journal of biological chemistry |
High |
10497169 10514433
|
| 1999 |
β-TrCP interacts specifically with IκBβ in a manner dependent on phosphorylation of serines 19 and 23; F-box deletion abolishes β-TrCP-mediated ubiquitination of IκBβ. |
Co-IP, ubiquitination assay, dominant-negative mutant |
The Journal of biological chemistry |
Medium |
10514424
|
| 2001 |
β-TrCP controls ATF4 stability by binding ATF4 in a phosphorylation-dependent manner (requiring Ser219 in a DSGXXXS motif); an F-box-deleted β-TrCP acts as dominant-negative to inhibit ATF4 ubiquitination and degradation, thereby enhancing ATF4-dependent cAMP-mediated transcription; β-TrCP and ATF4 are co-localized in the nucleus. |
Co-IP, dominant-negative overexpression, ubiquitination assay, luciferase reporter, subcellular localization |
Molecular and cellular biology |
Medium |
11238952
|
| 2001 |
IKKβ directly phosphorylates NF-κB1 p105 at C-terminal serines 923 and 927 (within a DSGψ-like motif), and this phosphorylation recruits both β-TrCP1 and β-TrCP2 for polyubiquitination and complete proteasomal degradation of p105. |
In vitro kinase assay, Co-IP, RNAi knockdown, ubiquitination assay |
Molecular and cellular biology |
High |
11158290
|
| 2003 |
Crystal structure (3.0 Å) of a β-TrCP1-Skp1-β-catenin complex reveals the basis of substrate recognition by the β-TrCP1 WD40 domain binding the doubly phosphorylated DpSGφXpS destruction motif; ubiquitination efficiency is determined by lysine-to-destruction motif spacing, confirmed by in vitro ubiquitination of mutant β-catenin peptides. |
X-ray crystallography, in vitro ubiquitination assay with mutant peptides |
Molecular cell |
High |
12820959
|
| 2003 |
β-TrCP is the F-box protein of SCF that targets phosphorylated Cdc25A for ubiquitin-mediated proteasomal degradation during S phase and in response to DNA damage; siRNA knockdown of both β-TrCP1 and β-TrCP2 prevents Cdc25A degradation induced by ionizing radiation and causes radioresistant DNA synthesis, indicative of an intra-S-phase checkpoint defect. |
siRNA knockdown, ubiquitination assay, DNA damage checkpoint assay (radioresistant DNA synthesis) |
Nature |
High |
14603323
|
| 2003 |
β-TrCP1 knockout mice display defects in meiotic progression (accumulation of metaphase I spermatocytes) and mitotic defects in MEFs including centrosome overduplication, multipolar spindles, and misaligned chromosomes; Emi1 is a bona fide substrate of β-TrCP1; stabilization of β-catenin and IκBα requires silencing of both β-TrCP1 and β-TrCP2. |
Gene knockout mice, siRNA, substrate stability assay, cell biology (centrosome counting) |
Developmental cell |
High |
12791266
|
| 2003 |
Emi1 is phosphorylated by Cdc2 on a DSGxxS consensus site and is subsequently recognized and ubiquitinated by SCF(βTrCP/Slimb), leading to its destruction in prophase; failure of βTrCP-dependent Emi1 destruction stabilizes APC substrates and results in mitotic catastrophe including centrosome overduplication. |
Co-IP, ubiquitination assay, phospho-mutant analysis, centrosome overduplication assay |
Developmental cell |
High |
12791267
|
| 2003 |
β-TrCP1-deficient MEFs show impaired (but not abolished) degradation of IκBα and IκBβ, reduced NF-κB nuclear translocation and transcriptional activity, and altered β-catenin subcellular localization; β-TrCP1 knockout MEFs display reduced proliferation, increased cell size, and increased polyploidy. |
Gene knockout mice, immunofluorescence, NF-κB reporter, FACS |
Proceedings of the National Academy of Sciences of the United States of America |
High |
12843402
|
| 2003 |
FWD1/β-TrCP mediates ubiquitination and proteasomal degradation of the circadian clock protein FREQUENCY (FRQ) in Neurospora; FRQ and FWD1 interact physically in vivo; fwd1 disruption results in accumulation of hyperphosphorylated FRQ and abolishes circadian rhythms. |
Co-IP in vivo, genetic disruption, circadian reporter assay, FRQ stability assay |
The EMBO journal |
High |
12941694
|
| 2003 |
β-TrCP binding and processing of NF-κB1 p105 requires IKK-mediated phosphorylation at serines 927 and 932; βTrCP RNAi blocks TNF-α-induced p105 ubiquitination and proteolysis; βTrCP affinity for doubly phosphorylated p105 is substantially lower than for IκBα, contributing to delayed p105 proteolysis. |
RNAi knockdown, phosphopeptide competition, in vitro kinase assay, ubiquitination assay |
Molecular and cellular biology |
High |
12482991
|
| 2003 |
HIV-1 Vpu sequesters β-TrCP in the cytoplasm by binding through its phosphorylated DS52GXXS56 motif, acting as a competitive inhibitor that prevents β-TrCP-mediated degradation of endogenous substrates (β-catenin, IκBα, ATF4, Emi1, Cdc25A) and excludes β-TrCP from the nucleus. |
GFP fusion imaging, substrate stability assay, dominant-negative competition |
The Journal of biological chemistry |
Medium |
14561767
|
| 2004 |
Hierarchical phosphorylation of Cdc25A commits it to β-TrCP-dependent degradation: Chk1-dependent phosphorylation at Ser76 is a priming step required for subsequent phosphorylation at Ser82 within the DSG motif, which anchors Cdc25A to β-TrCP. |
Phospho-site mutagenesis, Co-IP, degradation assay |
Cell cycle (Georgetown, Tex.) |
Medium |
14752276
|
| 2004 |
SCF(β-TrCP1) ubiquitinates and destabilizes Smad4; β-TrCP1 interacts with Smad4 in yeast two-hybrid and mammalian cells but not Smad2, and weakly with Smad3 only through Smad4; ectopic SCF(β-TrCP1) induces Smad4 ubiquitination and degradation, inhibiting TGF-β transcriptional responses. |
Yeast two-hybrid, Co-IP, ubiquitination assay, siRNA, TGF-β reporter |
The Journal of biological chemistry |
Medium |
14988407
|
| 2005 |
β-TrCP binding and ubiquitination of NF-κB2/p100 requires NIK/IKKα-dependent phosphorylation of p100 at serines 866 and 870; mutation of either serine abolishes β-TrCP recruitment and ubiquitination of p100. |
Co-IP, phospho-mutant analysis, in vivo ubiquitination assay |
Cellular signalling |
Medium |
16303288
|
| 2006 |
β-TrCP2 directly binds Gli2 and promotes its ubiquitination and degradation; single amino acid substitution in the Gli2 β-TrCP binding site abolishes interaction, ubiquitination, and stabilizes Gli2 protein, leading to enhanced Gli-dependent transcription. |
Co-IP, ubiquitination assay, site-directed mutagenesis, transcriptional reporter |
The Journal of biological chemistry |
Medium |
16651270
|
| 2006 |
S6K1-mediated phosphorylation of PDCD4 on Ser67 in response to mitogens recruits SCF(βTRCP) E3 ligase for ubiquitin-mediated proteasomal degradation of PDCD4; expression of a stable PDCD4 mutant unable to bind βTRCP inhibits translation of mRNAs with structured 5'UTRs, reduces cell size, and slows cell cycle progression. |
Kinase assay, Co-IP, ubiquitination assay, translation reporter, stable mutant overexpression, cell size measurement |
Science (New York, N.Y.) |
High |
17053147
|
| 2006 |
Wnt/β-catenin/Tcf signaling elevates βTrCP mRNA and protein expression in a Tcf-dependent manner, creating a negative feedback loop: increased βTrCP accelerates wild-type β-catenin degradation while also upregulating NF-κB transactivation without affecting IKK activity. |
Tcf reporter, mRNA analysis, β-catenin degradation assay, NF-κB reporter |
Molecular cell |
Medium |
10882123
|
| 2007 |
β-TrCP (as part of SCF) mediates ubiquitination and proteasomal degradation of the erythropoietin receptor (Epo-R); β-TrCP binds via its WD40 domain to a novel recognition motif (the ubiquitin-dependent endocytosis motif) in Epo-R; mutation of Ser462 abolishes β-TrCP binding, Epo-R ubiquitination, and degradation, causing prolonged Epo-R signaling and hypersensitivity to Epo. |
Co-IP, siRNA knockdown, site-directed mutagenesis, receptor degradation/endocytosis assay |
Blood |
Medium |
17327410
|
| 2007 |
GSK-3β associates with and phosphorylates Mcl-1 at Ser155/Ser159/Thr163, leading to association with β-TrCP and SCF(β-TrCP)-mediated ubiquitination and degradation of Mcl-1; a triple-alanine Mcl-1 mutant (3A) resists phosphorylation, is not ubiquitinated by β-TrCP, is more stable, and blocks GSK-3β-induced apoptosis. |
Co-IP, in vitro kinase assay, ubiquitination assay, phospho-mutant analysis, apoptosis assay |
Molecular and cellular biology |
High |
17387146
|
| 2007 |
β-TrCP1 degradation of PER2 is required for mammalian circadian rhythm generation; β-TrCP1-interaction-deficient PER2 variants are dramatically stabilized and disrupt circadian rhythmicity when expressed; β-TrCP1 and β-TrCP2 both target PER2 via the m2 degron site in vitro. |
Dominant-negative β-TrCP, siRNA, PER2 mutant expression, circadian reporter assay |
Journal of biological rhythms |
Medium |
17876059
|
| 2008 |
Plk1, following Cdk1-dependent recruitment, phosphorylates a SCF(βTrCP) recognition site on hBora to trigger its ubiquitin-mediated destruction; Plk1 depletion causes massive hBora accumulation, Aurora A mislocalization, and centrosome maturation defects; co-depletion of hBora partially restores Aurora A localization and bipolar spindle formation. |
Co-IP, siRNA co-depletion, ubiquitination assay, immunofluorescence, epistasis |
Chromosoma |
Medium |
18521620
|
| 2008 |
ERK-mediated phosphorylation of STAT1 at Ser727 targets it for proteasomal degradation by SCF(βTRCP); βTRCP binds wild-type STAT1 but not the non-phosphorylatable STAT1(S727A) mutant; silencing βTRCP or inhibiting ERK stabilizes STAT1. |
Co-IP, phospho-mutant analysis, siRNA, pharmacological ERK inhibition, STAT1 stability assay |
The Journal of biological chemistry |
Medium |
18378670
|
| 2009 |
IKK2 phosphorylates p53 at Ser362 and Ser366, leading to p53 recruitment to and ubiquitination by β-TrCP1; this p53 degradation is independent of Mdm2; siRNA-mediated reduction of β-TrCP1 or dominant-negative β-TrCP1 enhances p53 stability; p53-S362A/S366A mutations reduce IKK2-mediated phosphorylation and β-TrCP1 association. |
Co-IP, siRNA, dominant-negative overexpression, phospho-mutant analysis, p53 stability assay, cell-cycle analysis |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
19196987
|
| 2009 |
BimEL is phosphorylated on three serine residues in a conserved degron by Rsk1/2 (promoted by prior Erk1/2-mediated phosphorylation of Ser69), enabling binding and degradation via βTrCP; a BimEL phosphorylation mutant unable to bind βTrCP is stabilized and potently induces apoptosis by the intrinsic mitochondrial pathway. |
Co-IP, phospho-mutant analysis, kinase assay, apoptosis assay, siRNA |
Molecular cell |
High |
19150432
|
| 2009 |
USP47 is a novel interactor of both β-Trcp1 and β-Trcp2; binding requires the β-Trcp WD-repeat region (point mutations abolish binding); unlike canonical β-TrCP substrates, USP47 protein levels are not affected by β-Trcp silencing; depletion of USP47 causes Cdc25A accumulation and decreased cell survival. |
Co-IP, WD-repeat point mutagenesis, siRNA knockdown, cell viability assay |
Oncogene |
Medium |
19966869
|
| 2010 |
Human Plk4 undergoes βTrCP-dependent proteasomal degradation; Plk4 trans-autophosphorylation within homodimers creates the βTrCP binding/recognition site, promoting Plk4's own degradation; kinase-dead Plk4 disrupts trans-autophosphorylation, shielding endogenous Plk4 from βTrCP recognition and causing centriole overduplication. |
Protein stability assay, Co-IP, kinase-dead mutant overexpression, centriole counting |
Journal of cell science |
Medium |
20516151
|
| 2011 |
DEPTOR is a physiological substrate of SCF(βTrCP); upon growth factor stimulation, RSK1 and S6K1 phosphorylate DEPTOR's degron sequence, enabling βTrCP binding and ubiquitination/degradation; blocking βTrCP-dependent DEPTOR degradation (via knockdown or stable mutant) inhibits mTOR and activates AKT. |
Co-IP, siRNA, stable degron mutant, mTOR/AKT activity assay |
Molecular cell |
High |
22017876 22017877
|
| 2011 |
mTOR auto-amplification loop: mTORC1/2-mediated priming phosphorylation followed by CK1α phosphorylation of a conserved degron in DEPTOR facilitates βTrCP binding and degradation; blocking this pathway via βTrCP knockdown or stable DEPTOR mutant results in mTOR inhibition. |
Co-IP, siRNA, stable degron mutant, CK1α kinase assay |
Molecular cell |
High |
22017877
|
| 2011 |
β-TrCP1 is mislocalized to the nucleus in glioblastoma (vs. cytoplasm in astrocytoma and normal brain), spatially separating it from its cytoplasmic substrate PHLPP1; restoring β-TrCP1 to the cytoplasm rescues the Akt-PHLPP1 negative feedback loop and β-catenin degradation. |
Subcellular fractionation, immunofluorescence, pharmacological/genetic manipulation of localization, functional Akt/PHLPP1 assay |
The Journal of biological chemistry |
Medium |
21454620
|
| 2011 |
βTrCP regulates BMI1 ubiquitination and proteasome-mediated degradation; overexpression of wild-type βTrCP but not ΔF mutant promotes BMI1 ubiquitination; BMI1 recognition motif mutation stabilizes BMI1, increases its pro-oncogenic activity. |
Co-IP, ubiquitination assay, ΔF mutant, recognition motif mutagenesis, cellular senescence assay |
Cell cycle (Georgetown, Tex.) |
Medium |
21430439
|
| 2012 |
SCF(βTrCP) mediates proteasomal destruction of the deubiquitinase USP37 at the G2/M transition in a Plk1-dependent phosphorylation-dependent manner; USP37 interacts with βTrCP in a phospho-dependent manner; stabilization of a phospho-site mutant USP37 hinders the G2/M transition. |
Co-IP, siRNA, phospho-mutant analysis, cell-cycle analysis, Plk1 kinase assay |
The Journal of biological chemistry |
Medium |
23027877
|
| 2012 |
β-TrCP1 targets HuR for ubiquitin-mediated proteasomal degradation upon metabolic stress (glycolysis inhibition); targeting requires PKCα-mediated Ser318 phosphorylation-dependent cytoplasmic translocation of HuR and IKKα-mediated phosphorylation at Ser304 in an unconventional β-TrCP1 recognition motif (EEAMAIAS). |
Co-IP, GST pull-down, ubiquitination assay, dominant-negative β-TrCP1, mutagenesis, subcellular fractionation |
The Journal of biological chemistry |
Medium |
23115237
|
| 2013 |
SCFβ-TRCP mediates ubiquitination and proteasomal degradation of MTSS1; CK1δ phosphorylates Ser322 in the DSGXXS degron of MTSS1 to trigger β-TRCP interaction; depletion of Cullin 1 or β-TRCP1 increases MTSS1 levels; non-degradable MTSS1(S322A) shows stronger inhibition of cancer cell proliferation and migration. |
Co-IP, ubiquitination assay, CK1δ kinase assay, siRNA knockdown, functional migration/proliferation assay |
Oncotarget |
Medium |
24318128
|
| 2014 |
βTrCP controls lysosome-mediated degradation of CDK1; CDK1 is ubiquitinated by SCFβTrCP; DNA damage regulates βTrCP-induced CDK1 degradation in a cell-type-dependent manner. |
Ubiquitination assay, siRNA, lysosome inhibitor, DNA damage treatment |
Oncotarget |
Low |
25149538
|
| 2015 |
DNA damage triggers β-TRCP-dependent degradation of CReP (a PP1 regulatory subunit targeting eIF2α); depletion of CReP is required for full induction of eIF2α phosphorylation after DNA damage, reducing cap-dependent translation during recovery. |
Ligase Trapping (ubiquitin ligase-ubiquitin binding domain fusion), stable mutant CReP, eIF2α phosphorylation assay, translation assay |
PLoS genetics |
Medium |
26091241
|
| 2016 |
SAG/RBX2-CUL5 E3 ligase (with E2s UBCH10/UBE2S) ubiquitylates β-TrCP1 via atypical K11-linked polyubiquitin chains for proteasomal degradation; SAG and β-TrCP1 levels are inversely correlated; silencing UBCH10 or UBE2S (but not UBCH5C) causes β-TrCP1 accumulation. |
Co-IP, ubiquitination assay with linkage specificity, siRNA knockdown, protein stability assay |
Scientific reports |
Medium |
27910872
|
| 2017 |
β-TrCP targets DMRT1 for ubiquitylation and proteasomal degradation to control the mitosis-meiosis transition in mouse male germ cells; DMRT1 contains a consensus β-TrCP degron; conditional inactivation of β-TrCP2 in β-TrCP1 KO male germ cells results in sterility, failure to enter meiosis, and apoptosis; heterozygous deletion of Dmrt1 in β-TrCP-deficient spermatogonia partially rescues meiotic entry. |
Conditional knockout, Co-IP, ubiquitination assay, genetic epistasis (heterozygous Dmrt1 deletion), in vivo spermatogenesis analysis |
Development (Cambridge, England) |
High |
28982686
|
| 2018 |
β-TrCP recognizes cyclin F through a non-canonical TSGXXS degron (phosphorylated by casein kinase II) and mediates its degradation at the G2/M transition; this degradation is required for timely mitotic progression. |
Co-IP, phospho-mutant analysis, siRNA, CK2 kinase assay, cell-cycle analysis |
Cell reports |
Medium |
30257202
|
| 2018 |
FOXN2 is ubiquitinated and degraded by β-Trcp in a manner requiring RSK2-mediated phosphorylation of Ser365 and Ser369 in a conserved DSGYAS motif; β-Trcp/RSK2-mediated FOXN2 degradation promotes tumorigenesis and radioresistance in lung cancer. |
Co-IP, ubiquitination assay, RSK2 kinase assay, phospho-mutant analysis, gain/loss-of-function in vitro and in vivo |
Cell death and differentiation |
Medium |
29396548
|
| 2018 |
TSPAN15 interacts specifically with BTRC to promote ubiquitination and proteasomal degradation of phosphorylated IκBα, triggering NF-κB nuclear translocation and transcription of metastasis-related genes (ICAM1, VCAM1, MMP9, etc.) in esophageal squamous cell carcinoma. |
Co-IP, ubiquitination assay, siRNA, NF-κB nuclear translocation assay, functional metastasis assay |
Nature communications |
Medium |
29650964
|
| 2019 |
PARP11 mono-ADP-ribosylates β-TrCP; mono-ADP-ribosylation of β-TrCP promotes IFNAR1 ubiquitination and degradation, attenuating IFN-I antiviral signaling; PARP11 is upregulated by viral infection to promote this immune evasion mechanism. |
Co-IP, ADP-ribosylation assay, IFNAR1 stability assay, siRNA, mouse viral infection model |
Nature microbiology |
High |
30988430
|
| 2019 |
ERAP1 binds USP47, displaces USP47-associated βTrCP, and promotes βTrCP degradation, leading to modulation of Gli transcription factors and enhancement of Hedgehog pathway activity; pharmacological inhibition of ERAP1 suppresses Hh-dependent tumor growth in vitro and in vivo. |
Co-IP, βTrCP stability assay, Gli reporter assay, pharmacological inhibition, in vivo tumor model |
Nature communications |
Medium |
31341163
|
| 2019 |
β-TrCP1 and β-TrCP2 are physiological substrates of SCF E3 ligase and mutually target each other for ubiquitination and degradation via their respective β-TrCP degron sequences; AMPK activated by glucose deprivation phosphorylates β-TrCP1, promoting its degradation by β-TrCP2 (but not vice versa); β-TrCP2 preferentially degrades DEPTOR and REDD1 (mTORC1 inhibitors) to activate mTORC1 and inhibit autophagy. |
Co-IP, ubiquitination assay, AMPK kinase assay, degron mutant analysis, autophagy assay |
Cell death and differentiation |
Medium |
31406304
|
| 2021 |
βTrCP is the E3 ligase for ubiquitination of transferrin receptor (TFRC); TRIB2 desensitizes cells to ferroptosis by facilitating βTrCP-mediated TFRC ubiquitination and degradation to decrease labile iron pools; βTrCP knockout abolishes TRIB2-mediated iron reduction and ferroptosis resistance. |
Co-IP, ubiquitination assay, βTrCP knockout, labile iron pool measurement, ferroptosis assay |
Cell death discovery |
Medium |
34315867
|
| 2008 |
Alternative splicing of β-TrCP1 produces isoforms where exon III insertion prevents Skp1 interaction and causes nuclear (vs. cytoplasmic) localization; exon-III-containing isoforms show reduced ability to antagonize Wnt/β-catenin signaling in Xenopus. |
Yeast two-hybrid, immunofluorescence of isoforms, Xenopus axis assay |
Cellular signalling |
Low |
18929646
|
| 2005 |
FGD1 (a Cdc42 GEF) is a substrate of SCF(FWD1/β-TrCP); recognition requires phosphorylation of conserved serines in the DSGIDS motif; a phosphorylation-deficient FGD1(SA) mutant does not interact with FWD1/β-TrCP, is more stable, and shows enhanced cell motility; co-expression of SCF(FWD1/β-TrCP) reduces FGD1(WT)-induced morphological changes but not those of FGD1(SA). |
Co-IP, ubiquitination assay, phospho-mutant analysis, cell morphology and motility assay |
Genes to cells : devoted to molecular & cellular mechanisms |
Medium |
15743413
|
| 2002 |
CK2-dependent phosphorylation of the E2 ubiquitin-conjugating enzyme UBC3B at Ser233 induces its interaction with β-TrCP; co-transfection of CK2α' with UBC3B (but not a C-terminal deletion) enhances β-catenin degradation. |
Yeast two-hybrid, Co-IP, in vitro phosphorylation, β-catenin degradation assay |
Oncogene |
Low |
12037680
|
| 2016 |
RVFV NSs interacts with both FBXW11 (β-TrCP2) and β-TrCP1 and recruits SCF E3 ligase complexes containing these F-box proteins to target the antiviral kinase PKR for proteasomal degradation; siRNA depletion of both paralogs is required for maximal PKR protection. |
siRNA screen of ~70 F-box proteins, Co-IP, PKR stability assay, viral replication assay |
Journal of virology |
Medium |
27122577
|