CDK inhibitor p21 is degraded by a proliferating cell nuclear antigen-coupled Cul4-DDB1Cdt2 pathway during S phase and after UV irradiation
about
CRL4(Cdt2) E3 ubiquitin ligase monoubiquitinates PCNA to promote translesion DNA synthesisSelective ubiquitylation of p21 and Cdt1 by UBCH8 and UBE2G ubiquitin-conjugating enzymes via the CRL4Cdt2 ubiquitin ligase complex.A mouse model uncovers LKB1 as an UVB-induced DNA damage sensor mediating CDKN1A (p21WAF1/CIP1) degradationDifferential regulation of p53 and p21 by MKRN1 E3 ligase controls cell cycle arrest and apoptosisThe expanding regulatory universe of p53 in gastrointestinal cancerMotif co-regulation and co-operativity are common mechanisms in transcriptional, post-transcriptional and post-translational regulationThe role and mechanism of CRL4 E3 ubiquitin ligase in cancer and its potential therapy implicationsRegulation of Unperturbed DNA Replication by UbiquitylationSequential replication-coupled destruction at G1/S ensures genome stability.Examination of the expanding pathways for the regulation of p21 expression and activity.Distinct and overlapping functions of the cullin E3 ligase scaffolding proteins CUL4A and CUL4BSET8 is degraded via PCNA-coupled CRL4(CDT2) ubiquitylation in S phase and after UV irradiationCUL4A abrogation augments DNA damage response and protection against skin carcinogenesisThe ability of TRIM3 to induce growth arrest depends on RING-dependent E3 ligase activityKSP inhibitor SB743921 inhibits growth and induces apoptosis of breast cancer cells by regulating p53, Bcl-2, and DTLThe E3 Ligase CHIP Mediates p21 Degradation to Maintain Radioresistance.Degradation of p12 subunit by CRL4Cdt2 E3 ligase inhibits fork progression after DNA damage.Regulation of TGF-β signaling, exit from the cell cycle, and cellular migration through cullin cross-regulation: SCF-FBXO11 turns off CRL4-Cdt2.Efficient parvovirus replication requires CRL4Cdt2-targeted depletion of p21 to prevent its inhibitory interaction with PCNACRL1-FBXO11 promotes Cdt2 ubiquitylation and degradation and regulates Pr-Set7/Set8-mediated cellular migration.CRL4(Cdt2) regulates cell proliferation and histone gene expression by targeting PR-Set7/Set8 for degradationCRL4Cdt2: master coordinator of cell cycle progression and genome stabilityp21 in cancer: intricate networks and multiple activitiesDNA damage during S-phase mediates the proliferation-quiescence decision in the subsequent G1 via p21 expression.CUL4A contributes to the biology of basal-like breast tumors through modulation of cell growth and antitumor immune response.The DNA unwinding element binding protein DUE-B interacts with Cdc45 in preinitiation complex formation.14-3-3Tau regulates ubiquitin-independent proteasomal degradation of p21, a novel mechanism of p21 downregulation in breast cancer.Proliferating cell nuclear antigen-dependent rapid recruitment of Cdt1 and CRL4Cdt2 at DNA-damaged sites after UV irradiation in HeLa cells.Regulation of the histone H4 monomethylase PR-Set7 by CRL4(Cdt2)-mediated PCNA-dependent degradation during DNA damage.Lung tumourigenesis in a conditional Cul4A transgenic mouse model.Damaged DNA-binding protein 1 (DDB1) interacts with Cdh1 and modulates the function of APC/CCdh1.PCNA-coupled p21 degradation after DNA damage: The exception that confirms the rule?The CRL4Cdt2 ubiquitin ligase mediates the proteolysis of cyclin-dependent kinase inhibitor Xic1 through a direct association with PCNACRL4(Cdt2)-mediated destruction of the histone methyltransferase Set8 prevents premature chromatin compaction in S phase.Cell type-dependent requirement for PIP box-regulated Cdt1 destruction during S phase.Cullins and cancer.Cables1 controls p21/Cip1 protein stability by antagonizing proteasome subunit alpha type 3.Checkpoint kinase ATR phosphorylates Cdt2, a substrate receptor of CRL4 ubiquitin ligase, and promotes the degradation of Cdt1 following UV irradiation.Pharmacological targeting of miR-155 via the NEDD8-activating enzyme inhibitor MLN4924 (Pevonedistat) in FLT3-ITD acute myeloid leukemia.CUL4A overexpression enhances lung tumor growth and sensitizes lung cancer cells to erlotinib via transcriptional regulation of EGFR.
P2860
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P2860
CDK inhibitor p21 is degraded by a proliferating cell nuclear antigen-coupled Cul4-DDB1Cdt2 pathway during S phase and after UV irradiation
description
2008 nî lūn-bûn
@nan
2008 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
2008 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
name
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@ast
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@en
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@nl
type
label
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@ast
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@en
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@nl
prefLabel
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@ast
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@en
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@nl
P2093
P2860
P3181
P356
P1476
CDK inhibitor p21 is degraded ...... phase and after UV irradiation
@en
P2093
Hiroka Iida
Masato Michishita
Toshihiro Takami
Toshiki Tsurimoto
Yasushi Shiomi
P2860
P304
29045-29052
P3181
P356
10.1074/JBC.M806045200
P407
P577
2008-08-14T00:00:00Z