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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 (显示 CDK1 ELISA试剂盒), wee1 (显示 WEE1 ELISA试剂盒), p21, PCNA (显示 PCNA ELISA试剂盒) and cdk2 (显示 CDK2 ELISA试剂盒), but only weakly influences cyclin B1 (显示 CCNB1 ELISA试剂盒), cyclin B2 (显示 CCNB2 ELISA试剂盒) and cyclin E1 (显示 CCNE1 ELISA试剂盒) expression.
MiR-17-5p promoted cell growth in vivo and in vitro by directly targeting p21.
These findings suggest that vitamin C can promote the proliferation and cell cycle progression in the adipose-derived stem cells possibly through regulation of p53 (显示 TP53 ELISA试剂盒)-p21 signal pathway.
The BRG1 (显示 SMARCA4 ELISA试剂盒)/SIRT1 (显示 SIRT1 ELISA试剂盒)/p53 (显示 TP53 ELISA试剂盒) signal axis is a novel mechanism of cell senescence in CRC (显示 CALR ELISA试剂盒).
The p21's PCNA (显示 PCNA ELISA试剂盒) interacting region (PIR (显示 PIR ELISA试剂盒)), and not its cyclin-dependent kinase (显示 CDK1 ELISA试剂盒) binding domain, is needed to prevent the replication defects and the genomic instability caused by p21 depletion.
KDM6A (显示 KDM6A ELISA试剂盒) and p21CIP1 expression are essential to curb E7 induced replication stress to levels that do not markedly interfere with cell viability
HOXA11 (显示 HOXA11 ELISA试剂盒)-AS could simultaneously interact with enhancer of zeste homolog 2 (显示 EZH2 ELISA试剂盒) to suppress its target p21 protein (显示 NRAS ELISA试剂盒) expression
The intensity of p21 and Bcl-2 (显示 BCL2 ELISA试剂盒) expressions in different grades of OSCC indicates a key role in progression of oral neoplasia.
The findings identify that CHD4 (显示 CHD4 ELISA试剂盒) deficiency preferentially impairs cell survival via increasing the level of p21.
Glyoxalase 2 expression in prostate cancer was dependent on androgen receptor (显示 AR ELISA试剂盒) and was aimed at stimulating cell proliferation and eluding apoptosis through a mechanism involving the p53 (显示 TP53 ELISA试剂盒)-p21 axis
data suggest that PUMA (显示 BBC3 ELISA试剂盒) cooperates with p21 to regulate normal acinus (显示 ACIN1 ELISA试剂盒) formation and epithelial-to-mesenchymal transition.
p21 expression reports on Bovine herpesvirus 4 replication and could represent a host cell defensive response to infection-associated cellular damage.
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 (显示 CDK2 ELISA试剂盒) activity.
The study demonstrates an essential role of Setd2 in myoblast proliferation and differentiation, and uncovers Setd2-mediated molecular mechanism through regulating MyoG (显示 MYOG ELISA试剂盒) and p21.
Schistosoma japonicum egg antigen p40 (显示 LANCL1 ELISA试剂盒) through action on the STAT3 (显示 STAT3 ELISA试剂盒)/p53 (显示 TP53 ELISA试剂盒)/p21 pathway triggered cellular senescence, while knockdown of p53 (显示 TP53 ELISA试剂盒) or STAT3 (显示 STAT3 ELISA试剂盒) partly restored cell senescence.
Data show that Emu-Myc (显示 MYC ELISA试剂盒) mice lacking both p21 and PUMA (显示 BBC3 ELISA试剂盒) developed lymphoma at a rate considerably longer latency than Emu-Myc (显示 MYC ELISA试剂盒);p53 (显示 TP53 ELISA试剂盒)(+/-)mice.
Study reports that p27 (显示 CDKN1B ELISA试剂盒) normally exerts a negative feedback on p21 expression: p27 (显示 CDKN1B ELISA试剂盒) directly represses the expression of the transcription factor Pitx2 (显示 PITX2 ELISA试剂盒) which in turn maintains decreased p21 levels. Consequently, in cells lacking p27 (显示 CDKN1B ELISA试剂盒), de-repression of Pitx2 (显示 PITX2 ELISA试剂盒) causes the up-regulation of p21 showing a new mechanism by which p27 (显示 CDKN1B ELISA试剂盒) regulates cell cycle progression by transcriptionally regulating the expression of Pitx2 (显示 PITX2 ELISA试剂盒) 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 (显示 ROCK2 ELISA试剂盒)/NF-kappaB (显示 NFKB1 ELISA试剂盒) signalling in skin carcinogenesis.these data show that ROCK2 (显示 ROCK2 ELISA试剂盒) activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 (显示 TP53 ELISA试剂盒) loss and novel NF-kappaB (显示 NFKB1 ELISA试剂盒) expression
In this study, we found upregulation of several hemostasis-related genes, including the thrombin (显示 F2 ELISA试剂盒)-activatable receptor PAR-1 (protease-activated receptor-1 (显示 F2R ELISA试剂盒)), in Runx1 (显示 RUNX1 ELISA试剂盒)/Cbfb (显示 CBFB ELISA试剂盒)-deleted MLL (显示 MLL ELISA试剂盒)-AF9 (显示 MLLT3 ELISA试剂盒) cells. Similar to the effect of Runx1 (显示 RUNX1 ELISA试剂盒)/Cbfb (显示 CBFB ELISA试剂盒) deletion, PAR-1 (显示 MARK2 ELISA试剂盒) overexpression induced CDKN1A/p21 expression and attenuated proliferation in MLL (显示 MLL ELISA试剂盒)-AF9 (显示 MLLT3 ELISA试剂盒) cells
both in vitro and in vivo studies proved that CypD 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 on the p53 (显示 TP53 ELISA试剂盒)-p21 pathway participates in oncogene (显示 RAB1A ELISA试剂盒)-dependent transformation.
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