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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 (Montrer CDK1 Kits ELISA), wee1 (Montrer WEE1 Kits ELISA), p21, PCNA (Montrer PCNA Kits ELISA) and cdk2 (Montrer CDK2 Kits ELISA), but only weakly influences cyclin B1 (Montrer CCNB1 Kits ELISA), cyclin B2 (Montrer CCNB2 Kits ELISA) and cyclin E1 (Montrer CCNE1 Kits ELISA) expression.
Nurr1 (Montrer NR4A2 Kits ELISA) was induced during intestinal regeneration after I/R injury. Nurr1 (Montrer NR4A2 Kits ELISA) promoted proliferation of intestinal epithelial cells after H/R injury. Nurr1 (Montrer NR4A2 Kits ELISA) inhibited p21 expression in a p53 (Montrer TP53 Kits ELISA)-independent manner. Nurr1 (Montrer NR4A2 Kits ELISA) inhibited p21 gene transcription by binding to p21 promoter directly.
Germline mutations in TERT (Montrer TERT Kits ELISA) (rs2736100, n = 33) and CDKN1A (rs2395655, n = 27) associated with idiopathic pulmonary fibrosis risk were detected in most samples.
methylation at m6A (Montrer GPM6A Kits ELISA) by METTL3 (Montrer METTL3 Kits ELISA)/METTL14 (Montrer METTL14 Kits ELISA) facilitates the methylation of m5C by NSUN2 (Montrer NSUN2 Kits ELISA), and vice versa. NSUN2 (Montrer NSUN2 Kits ELISA)-mediated m5C and METTL3 (Montrer METTL3 Kits ELISA)/METTL14 (Montrer METTL14 Kits ELISA)-mediated m6A (Montrer GPM6A Kits ELISA) 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 (Montrer IL9 Kits ELISA) 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.
expression of p21 potentially can contribute to inhibition of HIV-1 replication in monocyte-derived dendritic cells through multiple mechanisms. p21 decreased size of the intracellular dNTP pool; p21 prevented SAMHD1 (Montrer SAMHD1 Kits ELISA) phosphorylation and promoted SAMHD1 (Montrer SAMHD1 Kits ELISA) dNTPase-independent antiviral activity
C5a/C5aR pathway promotes gastric cancer pathogenesis by suppressing p21/p-p21 expression via activation of PI3K (Montrer PIK3CA Kits ELISA)/AKT (Montrer AKT1 Kits ELISA) signaling.
p21 expression showed a significant positive correlation with tumoral FOXP3 (Montrer FOXP3 Kits ELISA) expression in gastric adenocarcinoma cells.
The PPARgamma (Montrer PPARG Kits ELISA)-SETD8 (Montrer SETD8 Kits ELISA) axis constitutes an epigenetic, p53 (Montrer TP53 Kits ELISA)-independent checkpoint on p21-mediated cellular senescence.
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 (Montrer SMAD3 Kits ELISA) and Bmal1 (Montrer ARNTL Kits ELISA) regulate p21 and S100A4 (Montrer S100A4 Kits ELISA) expression in myocardial stromal fibroblasts through TNF-alpha (Montrer TNF Kits ELISA).
Data suggest BAF180 (Montrer PBRM1 Kits ELISA) protein as a critical regulator of cellular senescence and HSC (Montrer FUT1 Kits ELISA) homeostasis, which is at least partially regulated through BAF180 (Montrer PBRM1 Kits ELISA)-mediated suppression of cell cycle regulator p21 expression.
Histone methyltransferase Suv39h1 (Montrer SUV39H1 Kits ELISA) attenuates high glucose-induced fibronectin (Montrer FN1 Kits ELISA) 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 (Montrer CDK2 Kits ELISA) activity.
The study demonstrates an essential role of Setd2 in myoblast proliferation and differentiation, and uncovers Setd2-mediated molecular mechanism through regulating MyoG (Montrer MYOG Kits ELISA) and p21.
Schistosoma japonicum egg antigen p40 (Montrer LANCL1 Kits ELISA) through action on the STAT3 (Montrer STAT3 Kits ELISA)/p53 (Montrer TP53 Kits ELISA)/p21 pathway triggered cellular senescence, while knockdown of p53 (Montrer TP53 Kits ELISA) or STAT3 (Montrer STAT3 Kits ELISA) partly restored cell senescence.
Data show that Emu-Myc (Montrer MYC Kits ELISA) mice lacking both p21 and PUMA (Montrer BBC3 Kits ELISA) developed lymphoma at a rate considerably longer latency than Emu-Myc (Montrer MYC Kits ELISA);p53 (Montrer TP53 Kits ELISA)(+/-)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