Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species
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 ELISA Kits), wee1 (show WEE1 ELISA Kits), p21, PCNA (show PCNA ELISA Kits) and cdk2 (show CDK2 ELISA Kits), but only weakly influences cyclin B1 (show CCNB1 ELISA Kits), cyclin B2 (show CCNB2 ELISA Kits) and cyclin E1 (show CCNE1 ELISA Kits) 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 (show TP53 ELISA Kits)-p21 signal pathway.
The BRG1 (show SMARCA4 ELISA Kits)/SIRT1 (show SIRT1 ELISA Kits)/p53 (show TP53 ELISA Kits) signal axis is a novel mechanism of cell senescence in CRC (show CALR ELISA Kits).
The p21's PCNA (show PCNA ELISA Kits) interacting region (PIR (show PIR ELISA Kits)), and not its cyclin-dependent kinase (show CDK1 ELISA Kits) binding domain, is needed to prevent the replication defects and the genomic instability caused by p21 depletion.
KDM6A (show KDM6A ELISA Kits) and p21CIP1 expression are essential to curb E7 induced replication stress to levels that do not markedly interfere with cell viability
HOXA11 (show HOXA11 ELISA Kits)-AS could simultaneously interact with enhancer of zeste homolog 2 (show EZH2 ELISA Kits) to suppress its target p21 protein (show NRAS ELISA Kits) expression
The intensity of p21 and Bcl-2 (show BCL2 ELISA Kits) expressions in different grades of OSCC indicates a key role in progression of oral neoplasia.
The findings identify that CHD4 (show CHD4 ELISA Kits) deficiency preferentially impairs cell survival via increasing the level of p21.
Glyoxalase 2 expression in prostate cancer was dependent on androgen receptor (show AR ELISA Kits) and was aimed at stimulating cell proliferation and eluding apoptosis through a mechanism involving the p53 (show TP53 ELISA Kits)-p21 axis
data suggest that PUMA (show BBC3 ELISA Kits) cooperates with p21 to regulate normal acinus (show ACIN1 ELISA Kits) 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 (show CDK2 ELISA Kits) 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 ELISA Kits) and p21.
Schistosoma japonicum egg antigen p40 (show LANCL1 ELISA Kits) through action on the STAT3 (show STAT3 ELISA Kits)/p53 (show TP53 ELISA Kits)/p21 pathway triggered cellular senescence, while knockdown of p53 (show TP53 ELISA Kits) or STAT3 (show STAT3 ELISA Kits) partly restored cell senescence.
Data show that Emu-Myc (show MYC ELISA Kits) mice lacking both p21 and PUMA (show BBC3 ELISA Kits) developed lymphoma at a rate considerably longer latency than Emu-Myc (show MYC ELISA Kits);p53 (show TP53 ELISA Kits)(+/-)mice.
Study reports that p27 (show CDKN1B ELISA Kits) normally exerts a negative feedback on p21 expression: p27 (show CDKN1B ELISA Kits) directly represses the expression of the transcription factor Pitx2 (show PITX2 ELISA Kits) which in turn maintains decreased p21 levels. Consequently, in cells lacking p27 (show CDKN1B ELISA Kits), de-repression of Pitx2 (show PITX2 ELISA Kits) causes the up-regulation of p21 showing a new mechanism by which p27 (show CDKN1B ELISA Kits) regulates cell cycle progression by transcriptionally regulating the expression of Pitx2 (show PITX2 ELISA Kits) 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 ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits) signalling in skin carcinogenesis.these data show that ROCK2 (show ROCK2 ELISA Kits) activation induces malignancy in ras(Ha)-initiated/promoted papillomas in the context of p53 (show TP53 ELISA Kits) loss and novel NF-kappaB (show NFKB1 ELISA Kits) expression
In this study, we found upregulation of several hemostasis-related genes, including the thrombin (show F2 ELISA Kits)-activatable receptor PAR-1 (protease-activated receptor-1 (show F2R ELISA Kits)), in Runx1 (show RUNX1 ELISA Kits)/Cbfb (show CBFB ELISA Kits)-deleted MLL (show MLL ELISA Kits)-AF9 (show MLLT3 ELISA Kits) cells. Similar to the effect of Runx1 (show RUNX1 ELISA Kits)/Cbfb (show CBFB ELISA Kits) deletion, PAR-1 (show MARK2 ELISA Kits) overexpression induced CDKN1A/p21 expression and attenuated proliferation in MLL (show MLL ELISA Kits)-AF9 (show MLLT3 ELISA Kits) 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 (show TP53 ELISA Kits)-p21 pathway participates in oncogene (show RAB1A ELISA Kits)-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