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
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 ELISA Kits) 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 ELISA Kits)/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 ELISA Kits)-33b-3p, a critical regulator of G1/S checkpoint, which potentially mediated the protection effects of miR (show MLXIP ELISA Kits)-33b-3p against cisplatin.
Ectopic expression of the CDK (show CDK4 ELISA Kits) inhibitor p21(Cip1) enhanced deregulated E2F (show E2F1 ELISA Kits) activity and pro-apoptotic E2F (show E2F1 ELISA Kits) 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 ELISA Kits) activity.
We also showed that knockdown of urothelial carcinoma-associated 1 increased the p21 protein (show NRAS ELISA Kits) expression through regulating enhancer of zeste homolog 2 (show EZH2 ELISA Kits). In addition, bioinformatics analysis and dual-luciferase reporter assays confirmed that miR (show MLXIP ELISA Kits)-495 was a target of urothelial carcinoma-associated 1 in renal cell carcinoma, and urothelial carcinoma-associated 1 promoted cell proliferation by negatively regulating miR (show MLXIP ELISA Kits)-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 ELISA Kits) suppresses p21 translation without disturbing the function of p53 (show TP53 ELISA Kits) to directly induce p21 mRNA expression, this process indirectly requires p53 (show TP53 ELISA Kits), perhaps in the form of another p53 (show TP53 ELISA Kits) target gene or as a still undefined posttranscriptional function of p53 (show TP53 ELISA Kits).
the silencing of Cyclin-dependent kinase 5 (show CDK5 ELISA Kits) preventing memory dysfunction
Results show that p21 expression is regulated by OLA1 (show OLA1 ELISA Kits) to promote cell proliferation and organogenesis.
AS160 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 (show ARID1A ELISA Kits) 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 (show ARID1A ELISA Kits)-deficient human breast cancer subtypes that retain one intact copy of the gene and also maintain wild-type TRP53 (show TP53 ELISA Kits) activity
We discovered that FXR1P (show FXR1 ELISA Kits)-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 ELISA Kits).
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 ELISA Kits)-producing Th1 (show HAND1 ELISA Kits) cells, thereby revealing beneficial roles in treating a wide range of chronic inflammatory diseases mediated by inflammatory T cells.
increases the number of ALP-positive colonies after iPSC induction and decreases expression levels of Eomes (show EOMES ELISA Kits) and p21 mRNAs. Based on these observations, we propose that the CCR4 (show CCR4 ELISA Kits)-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