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These data reveal a novel role for p21/waf1 in the resolution of inflammation via its ability to control neutrophil apoptosis.
role of SRSF7 (show SFRS7 Proteins) in cell proliferation through regulating p21 levels.
Data indicate that UBE2S and APC3 co-regulate the expression level of P21 at G2/M check point via the ubiquitin-proteasome system.
p53 (show TP53 Proteins)/p21 signaling pathway role in melanoma cells
The expression of p53 fulllength transcript and Delta133p53 isoforms alpha, beta and gamma transcripts, MDM2 and p21 transcripts were determined by reverse transcriptionquantitative polymerase chain reaction, in total RNA isolated from 17 lung carcinoma specimens and 17 corresponding adjacent noncancerous tissues.
CDKN1A (p21) was identified as a functional target of miR (show MLXIP Proteins)-33b-3p, a critical regulator of G1/S checkpoint, which potentially mediated the protection effects of miR (show MLXIP Proteins)-33b-3p against cisplatin.
Ectopic expression of the CDK (show CDK4 Proteins) inhibitor p21(Cip1) enhanced deregulated E2F (show E2F1 Proteins) activity and pro-apoptotic E2F (show E2F1 Proteins) target gene expression in cancer cells. Moreover, ectopic expression of p21(Cip1) augmented cancer specific cytotoxicity of Ad-ARF-TK, and apoptosis induced by p21(Cip1) was dependent on deregulated E2F (show E2F1 Proteins) activity.
We also showed that knockdown of urothelial carcinoma-associated 1 increased the p21 protein (show NRAS Proteins) expression through regulating enhancer of zeste homolog 2 (show EZH2 Proteins). In addition, bioinformatics analysis and dual-luciferase reporter assays confirmed that miR (show MLXIP Proteins)-495 was a target of urothelial carcinoma-associated 1 in renal cell carcinoma (show MOK Proteins), and urothelial carcinoma-associated 1 promoted cell proliferation by negatively regulating miR (show MLXIP Proteins)-495
reveal the tumour-promoting ability of p21 through deregulation of DNA replication licensing machinery-an unorthodox role to be considered in cancer treatment
data demonstrate that DDX41 (show DDX41 Proteins) suppresses p21 translation without disturbing the function of p53 (show TP53 Proteins) to directly induce p21 mRNA expression, this process indirectly requires p53 (show TP53 Proteins), perhaps in the form of another p53 (show TP53 Proteins) target gene or as a still undefined posttranscriptional function of p53 (show TP53 Proteins).
the silencing of Cyclin-dependent kinase 5 (show CDK5 Proteins) preventing memory dysfunction
Results show that p21 expression is regulated by OLA1 (show OLA1 Proteins) to promote cell proliferation and organogenesis.
AS160 (show TBC1D4 Proteins) regulates glucose-independent eukaryotic cell proliferation through p21-dependent control of the cell cycle.
telomerase activity and cardiomyocyte telomere length decrease sharply in wild-type mouse hearts after birth, resulting in cardiomyocytes with dysfunctional telomeres and anaphase bridges and positive for the cell-cycle arrest protein p21.
Consistent with the latter, Arid1a reexpression in tumor cells led to increased p21 (Cdkn1a) expression and dramatic accumulation of cells in G2 phase of the cell cycle. These results also indicate a potential opportunity for therapeutic intervention in ARID1A-deficient human breast cancer subtypes that retain one intact copy of the gene and also maintain wild-type TRP53 (show TP53 Proteins) activity
We discovered that FXR1P (show FXR1 Proteins)-deficient aNSCs have altered expression of a select number of cell-cycle genes, and we identified the mRNA of cyclin-dependent kinase inhibitor 1A (Cdkn1a, p21) as a direct target of FXR1P (show FXR1 Proteins).
These results demonstrate that CQ and AQ increase the expression level of p21 and inhibit T cell proliferation and the development of IFN-gamma (show IFNG Proteins)-producing Th1 (show HAND1 Proteins) cells, thereby revealing beneficial roles in treating a wide range of chronic inflammatory diseases mediated by inflammatory T cells.
increases the number of ALP (show CCL21A Proteins)-positive colonies after iPSC induction and decreases expression levels of Eomes (show EOMES Proteins) and p21 mRNAs. Based on these observations, we propose that the CCR4 (show CCR4 Proteins)-NOT deadenylase activity contributes to iPSC induction.
this study shows that p21 is upregulated in T effector cells but not natural regulatory T cells after treatment with azacitidine, which protects from graft-versus-host Disease
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.
CDK-interacting protein 1
, CDK-interaction protein 1
, DNA synthesis inhibitor
, cyclin-dependent kinase inhibitor 1
, melanoma differentiation associated protein 6
, wild-type p53-activated fragment 1
, melanoma differentiation-associated protein