protein
| TYMS |
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inhibiting CDK2, CDK4 complexes |
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inhibiting cycle progression by interacting with G1 cyclin/CDK complexes and PCNA |
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CCNE2 |
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PBK interacts with the DBD domain of tumor suppressor TP53 and modulates expression of transcriptional targets including CDKN1A |
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TFAP2A binds CDKN1A to two regions of the promoter: the proximal region where the AP-2 site lies and upstream near the major TP53 binding site |
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SSBP1 directly binds CDKN1A and this interaction may prevent CDKN1A from ubiquitin-mediated degradation |
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SNW1-associated factors DHX8 and PRPF19 are also selectively required for CDKN1A expression under stress |
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new function of SRSF2 in the process of cellular senescence and CDKN1A is a key target of SRSF2 in this setting |
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acted in part to mediate growth suppression by ARID1A |
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cooperative and interdependent roles for ARID3A and TP53 in the transcriptional activation of CDKN1A in response to DNA damage |
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KDM8 physiologically moderates embryonic cell proliferation through the epigenetic control of CDKN1A expression |
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RNF144B is a potentially critical component of epithelial homeostasis, acting downstream of TP63 to regulate cellular levels of CDKN1A and TP63 |
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HIC1 is a direct transcriptional repressor of CDKN1A and is a key player in the regulation of the DNA damage response |
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KAT5-mediated CDKN1A acetylation is a novel and essential regulatory process required for CDKN1A-dependent DNA damage-induced cell-cycle arrest |
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Aurora B represses CDKN1A, preventing delayed DNA replication, CDK inhibition and premature mitotic exit |
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UCHL5 is also required for high glucose-induced TGFBR1 protein deubiquitination, CDKN1A and fibronectin protein expression and cell hypertrophy |
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RNF114 activates cell cycle progression and suppresses cellular senescence through the RING domain-mediated degradation of CDKN1A |
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unexpected role of MAPK14 in cell cycle regulation in response to Aurora B inhibition, by promoting the transcriptional elongation of the cell cycle inhibitor CDKN1A |
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FMN2 is a crucial protein involved in the control of CDKN1A ( |
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CDKN2A stabilizes the CDKN1A mRNA through negative regulation of the mRNA decay-promoting HNRNPD protein |
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has dual effects under HSPA9-depleted conditions, i.e., mediating cell cycle arrest while limiting cell death |
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transcriptional repression of BMP2 by CDKN1A links quiescence to neural stem cell maintenance |
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TSG101 protein interacts with and down-regulates the promoter of CDKN1A tumor suppressor gene |
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TAF1 is able to phosphorylate TP53 on Thr55, which leads to dissociation of TP53 from the CDKN1A promoter |
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RBM24 is a target gene of the TP53 protein, and can regulate CDKN1A expression via mRNA stability |
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TOP3A binds to the TP53 and CDKN1A promoters and positively regulates their expression, contributing to the TP53-mediated tumor suppression |
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DUX4 might potentially induce proliferation inhibition and G1 phase arrest through upregulation of CDKN1A |
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RASSF6 triggers CDKN1A accumulation to induce G 1 cell cycle arrest and promote apoptosis upon exposure to pro-apoptotic agents |
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TWIST2 directly regulated CDKN1A in hematopoietic cells and whose silence promoted cell proliferation and cell cycle progression, this direct regulation of CDKN1A by TWIST2 has a role in its tumor-suppressor function in AML (acute myeloid leukemia) |
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CDKN1A/CCNE1 pathway is crucial in modulating the anticlastogenic function of BMI1 |
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NR5A2 cooperates with FOXA1 and binds directly to CDKN1A promoter and a distal regulatory region found at -62& |
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8201;kb from its transcriptional start sites, allowing repression of CDKN1A transcription |
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ANKHD1 promotes Multiple myeloma growth by repressing CDKN1A a potent cell cycle regulator |
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MORC2 down-regulated CDKN1A by recruiting HDAC1 to the CDKN1A promoter, in a TP53-independent manner |
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TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two important barriers in the TP53 pathway that prevent oncogenic transformation |
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CDKN1A repression by TBX3 is biologically significant and required for TBX3-induced cell proliferation of chondrosarcoma cells |
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ASPSCR1-TFE3 fusion protein regulates cell cycle progression and induces cellular senescence by up-regulating CDKN1A expression |
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MELK is an interacting partner of CDKN1A (interaction through the cyclin-dependent kinase (CDK) binding region of CDKN1A and the C-terminal domain of MELK) |
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NFIC may contribute to postnatal chondrocyte proliferation by inhibiting CDKN1A expression and by increasing the stability of CCND1 protein |
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CCN3 may in part promote chondrocyte senescence, leading to the degeneration of articular cartilage through the induction of TP53 and CDKN1A |