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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.
HOXA11 (show HOXA11 Proteins)-AS could simultaneously interact with enhancer of zeste homolog 2 (show EZH2 Proteins) to suppress its target p21 protein (show NRAS Proteins) expression
The intensity of p21 and Bcl-2 (show BCL2 Proteins) expressions in different grades of OSCC indicates a key role in progression of oral neoplasia.
The findings identify that CHD4 (show CHD4 Proteins) deficiency preferentially impairs cell survival via increasing the level of p21.
Glyoxalase 2 expression in prostate cancer was dependent on androgen receptor (show AR Proteins) and was aimed at stimulating cell proliferation and eluding apoptosis through a mechanism involving the p53 (show TP53 Proteins)-p21 axis
data suggest that PUMA (show BBC3 Proteins) cooperates with p21 to regulate normal acinus (show ACIN1 Proteins) formation and epithelial-to-mesenchymal transition.
LASS5 (show LASS5 Proteins) interacts with SDHB (show SDHB Proteins) and synergistically represses p53 (show TP53 Proteins) and p21 activity.
Schistosoma japonicum egg antigen p40 (show IL9 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.
No mutations in CDKN1A coding region were detected in 39 probands from families with criteria for Li-Fraumeni and Li-Fraumeni like syndromes.
Results suggest that the simultaneous evaluation of SRY (sex determining region Y)-box 2 (show SOX2 Proteins) protein (SOX2 (show SOX2 Proteins)) and cyclin dependent kinase inhibitor 1A (p21) in advanced endometrial cancer patients provides more accurate information for patient prognosis than either alone.
p21 adjusts the equilibrium between p65 (show GORASP1 Proteins)-p50 (show CD40 Proteins) and p50-p50 NF-kappaB (show NFKB1 Proteins) pathways to mediate macrophage plasticity in LPS (show IRF6 Proteins) tolerance
p21 expression reports on Bovine herpesvirus 4 replication and could represent a host cell defensive response to infection-associated cellular damage.
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.
Study reports that p27 (show CDKN1B Proteins) normally exerts a negative feedback on p21 expression: p27 (show CDKN1B Proteins) directly represses the expression of the transcription factor Pitx2 (show PITX2 Proteins) which in turn maintains decreased p21 levels. Consequently, in cells lacking p27 (show CDKN1B Proteins), de-repression of Pitx2 (show PITX2 Proteins) causes the up-regulation of p21 showing a new mechanism by which p27 (show CDKN1B Proteins) regulates cell cycle progression by transcriptionally regulating the expression of Pitx2 (show PITX2 Proteins) and p21.
p21-associated inhibition of early-stage malignant progression and the intense expression in papilloma outgrowths, identifies a novel, significant antagonism between p21 and ras(Ha)/ROCK2 (show ROCK2 Proteins)/NF-kappaB (show NFKB1 Proteins) signalling in skin carcinogenesis.these data show that ROCK2 (show ROCK2 Proteins) activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 (show TP53 Proteins) loss and novel NF-kappaB (show NFKB1 Proteins) expression
In this study, we found upregulation of several hemostasis-related genes, including the thrombin (show F2 Proteins)-activatable receptor PAR-1 (protease-activated receptor-1 (show F2R Proteins)), in Runx1 (show RUNX1 Proteins)/Cbfb (show CBFB Proteins)-deleted MLL (show MLL Proteins)-AF9 (show MLLT3 Proteins) cells. Similar to the effect of Runx1 (show RUNX1 Proteins)/Cbfb (show CBFB Proteins) deletion, PAR-1 (show MARK2 Proteins) overexpression induced CDKN1A/p21 expression and attenuated proliferation in MLL (show MLL Proteins)-AF9 (show MLLT3 Proteins) cells
both in vitro and in vivo studies proved that CypD (show CYPD Proteins) inhibitor-based treatment was able to efficiently impair this interaction, leading to a tumor formation reduction. All together, these findings indicate that the countering effect of CypD (show CYPD Proteins) on the p53 (show TP53 Proteins)-p21 pathway participates in oncogene (show RAB1A Proteins)-dependent transformation.
FLT3 (show FLT3 Proteins)-ITD is capable of inhibiting FLT3 (show FLT3 Proteins)-ITD+ cell proliferation through the p21/Pbx1 (show PBX1 Proteins) axis
These data reveal a novel role for p21/waf1 in the resolution of inflammation via its ability to control neutrophil apoptosis.
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