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Human CDKN1A Protein expressed in HEK-293 Cells - ABIN2713874
Porter, Farmaki, Altilia, Schools, West, Chen, Chang, Puzyrev, Lim, Rokow-Kittell, Friedhoff, Papavassiliou, Kalurupalle, Hurteau, Shi, Baran, Gyorffy, Wentland, Broude, Kiaris, Roninson: Cyclin-dependent kinase 8 mediates chemotherapy-induced tumor-promoting paracrine activities. in Proceedings of the National Academy of Sciences of the United States of America 2012
We characterized the effect of the novel loci through pathway analysis and found that pathways involved are not entirely distinct as assumed so far. Further, we identified a novel association between CDKN1A and POAG. Using a zebrafish model we show that six6b (associated with POAG and optic nerve head variation) alters the expression of cdkn1a
intestinal clock controls the expression of key cell cycle regulators, such as cdc2 (show CDK1 Proteins), wee1 (show WEE1 Proteins), p21, PCNA (show PCNA Proteins) and cdk2 (show CDK2 Proteins), but only weakly influences cyclin B1 (show CCNB1 Proteins), cyclin B2 (show CCNB2 Proteins) and cyclin E1 (show CCNE1 Proteins) expression.
Results show that p21 expression is downregulated by LincRNAFEZF1-AS1 (show PTGDR Proteins) which epigenetically repress the expression of P21 via binding with LSD1 (show KDM1A Proteins).
Data suggest that KLF4 (show KLF4 Proteins) could promote cell senescence through a complex network: miR (show MLXIP Proteins)-203, survivin (show BIRC5 Proteins), and p21, which were all regulated by overexpression of KLF4 (show KLF4 Proteins) and contributed to cell senescence.
High CIP1 expression is associated with melanoma.
ZNF224 (show ZNF224 Proteins) increases cell survival and decreases apoptosis by decreasing the expression of p53 (show TP53 Proteins) and p21 via miR (show MLXIP Proteins)-663a as a transcriptional activator.
Nurr1 (show NR4A2 Proteins) was induced during intestinal regeneration after I/R injury. Nurr1 (show NR4A2 Proteins) promoted proliferation of intestinal epithelial cells after H/R injury. Nurr1 (show NR4A2 Proteins) inhibited p21 expression in a p53 (show TP53 Proteins)-independent manner. Nurr1 (show NR4A2 Proteins) inhibited p21 gene transcription by binding to p21 promoter directly.
Germline mutations in TERT (show TERT Proteins) (rs2736100, n = 33) and CDKN1A (rs2395655, n = 27) associated with idiopathic pulmonary fibrosis risk were detected in most samples.
methylation at m6A (show GPM6A Proteins) by METTL3 (show METTL3 Proteins)/METTL14 (show METTL14 Proteins) facilitates the methylation of m5C by NSUN2 (show NSUN2 Proteins), and vice versa. NSUN2 (show NSUN2 Proteins)-mediated m5C and METTL3 (show METTL3 Proteins)/METTL14 (show METTL14 Proteins)-mediated m6A (show GPM6A Proteins) methylation synergistically enhance p21 expression at the translational level
Data show that co-treated with vincristine and XL019, a inhibitor of JAK2 and P-glycoprotein (P-gp), up-regulated expression of p21 and phosphorylated H2A histone family, member X (pH2AX).
Results show that p21CIP1 expression is regulated by IL9 (show IL9 Proteins) in diffuse large B-cell lymphoma.
Results demonstrated that dsRNA-mediated p21 induction in human cell lines is a common phenomenon. This process occurs at the transcriptional level, and the complementary p21 promoter is the intended dsRNA target.
p21 expression reports on Bovine herpesvirus 4 replication and could represent a host cell defensive response to infection-associated cellular damage.
our genetic and biochemical data show an important function of p21 in the regulation of growth-related processes in the heart.
The Smad3 (show SMAD3 Proteins) and Bmal1 (show ARNTL Proteins) regulate p21 and S100A4 (show S100A4 Proteins) expression in myocardial stromal fibroblasts through TNF-alpha (show TNF Proteins).
Data suggest BAF180 (show PBRM1 Proteins) protein as a critical regulator of cellular senescence and HSC (show FUT1 Proteins) homeostasis, which is at least partially regulated through BAF180 (show PBRM1 Proteins)-mediated suppression of cell cycle regulator p21 expression.
Histone methyltransferase Suv39h1 (show SUV39H1 Proteins) attenuates high glucose-induced fibronectin (show FN1 Proteins) and p21(WAF1) in mesangial cells
It has been observed that even in tissues with no detectable Linc-p21 transcript, deletion of the locus significantly affects local gene expression, including of the cell cycle regulator Cdkn1a.
The findings suggest that p21 facilitates the development of cardiac hypertrophy, and regulating the expression of p21 may be an approach to attenuate hypertrophic growth of cardiomyocytes.
Ad-p21 inhibits RNV in OIR. A potential underlying mechanism for this may be that overexpression of p21 arrests the cell cycle at the G1- to S-phase transition via inhibition of CDK2 (show CDK2 Proteins) activity.
The study demonstrates an essential role of Setd2 in myoblast proliferation and differentiation, and uncovers Setd2-mediated molecular mechanism through regulating MyoG (show MYOG Proteins) and p21.
Schistosoma japonicum egg antigen p40 (show LANCL1 Proteins) through action on the STAT3 (show STAT3 Proteins)/p53 (show TP53 Proteins)/p21 pathway triggered cellular senescence, while knockdown of p53 (show TP53 Proteins) or STAT3 (show STAT3 Proteins) partly restored cell senescence.
Data show that Emu-Myc (show MYC Proteins) mice lacking both p21 and PUMA (show BBC3 Proteins) developed lymphoma at a rate considerably longer latency than Emu-Myc (show MYC Proteins);p53 (show TP53 Proteins)(+/-)mice.
This gene encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, and thus functions as a regulator of cell cycle progression at G1. The expression of this gene is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. This protein can interact with proliferating cell nuclear antigen (PCNA), a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation. Multiple alternatively spliced variants have been found for this gene.
cyclin dependent kinase inhibitor p16Xic2
, cyclin-dependent kinase inhibitor 1
, cyclin D1
, cyclin-dependent kinase inhibitor 1A (p21, Cip1)
, cyclin-dependent kinase inhibitor 1A
, cyclin-dependent kinase inhibitor 1A (P21)
, CDK-interacting protein 1
, CDK-interaction protein 1
, DNA synthesis inhibitor
, melanoma differentiation associated protein 6
, wild-type p53-activated fragment 1
, melanoma differentiation-associated protein