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Human CDKN1A Protein expressed in HEK-293 Cells - ABIN2713874
Porter, Farmaki, Altilia, Schools, West, Chen, Chang, Puzyrev, Lim, Rokow-Kittell, Friedhoff, Papavassiliou, Kalurupalle, Hurteau, Shi, Baran, Gyorffy, Wentland, Broude, Kiaris, Roninson: Cyclin-dependent kinase 8 mediates chemotherapy-induced tumor-promoting paracrine activities. in Proceedings of the National Academy of Sciences of the United States of America 2012
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, wee1, p21, PCNA and cdk2, but only weakly influences cyclin B1, cyclin B2 and cyclin E1 expression.
The effects of HJURP silencing were reversed by p21 knockdown. Likewise, p21 overexpression inhibited cell growth ability mediated by HJURP elevation. Mechanistically, HJURP destabilized p21 via the MAPK/ERK1/2 and AKT/GSK3beta pathways, which regulated the nucleus-cytoplasm translocation and ubiquitin-mediated degradation of p21.
The authors have found that USP18 has the novel ability to inhibit the antiviral function of p21 in differentiated THP-1 cells. USP18 enhanced reverse transcription of HIV-1 by downregulating p21 expression and upregulating intracellular dNTP levels.
Results indicate that long non-coding RNA PVT1 (PVT1) affected the role of mature adipogenic medium in triple-negative breast cancer (TNBC) cells via modulating cyclin-dependent kinase inhibitor 1A protein (p21) expression.
Fluctuations in the oscillatory pattern of the tumor suppressor p53 upon gamma radiation trigger a sharp switch between p21 and CDK2, leading to escape from arrest.
PAX8 positively regulates the expression of TP53 in high grade serous ovarian carcinoma (HGSC) and the pro-proliferative role of PAX8 is mediated by the gain of function activity of mutant p53. Surprisingly, mutant p53 transcriptionally activates the expression of p21, which localizes to the cytoplasm of HGSC cells where it plays a non-canonical, pro-proliferative role.
p65 NFkappaB-mediated p21 activation controls DNA damage-induced myeloid differentiation.
Mechanistic analyses indicated that DUXAP8 regulates PC cell proliferation partly through downregulation of tumor suppressor CDKN1A and KLF2 expression.
P21 expression is regulated by ARHGAP17 in cervical cancer.ARHGAP17 elevated P21 expression level through inhibiting PI3K/AKT signaling pathway.
RBMS2 acts as a tumor suppressor in breast cancer and positively regulated the expression of P21 by stabilizing its mRNA.
Data show that miR-301a suppressed the expression of cyclin-dependent kinase inhibitor p21 (p21) and Smad4 protein, and subsequently promoted G1/S cell cycle transition and cell proliferation in vitro and xenograft growth in nude mice in vivo.
Study demonstrated that CDCA3 may target p21 to promote colorectal cancer (CRC) cell proliferation and tumorigenesis, at least partially in an E2F1-mediated manner, and that CDCA3 may serve as a potential prognostic and therapeutic target of CRC.
Sorting nexin 10 (SNX10) was remarkably down-regulated in colorectal cancer (CRC) tissues which showed the increased activity of chaperone-mediated autophagy (CMA) and decreased expression of cyclin-dependent kinase inhibitor p21(Cip1/WAF1).
Data show that cyclin-dependent kinase inhibitor 1A protein (p21) is a target of long noncoding RNA MAPKAPK5-AS1.
mechanism experiments revealed that SNHG16 could epigenetically silence the expression of p21. The facts above pointed out that lncRNA-SNHG16 might be quite vital for the diagnosis and development of bladder cancer, and could even become an important therapeutic target for bladder cancer.
Meta-analysis found that significant association between the MDM2 rs2279744 polymorphism and increased retinoblastoma (Rb) risk, while MDM2 rs937283 polymorphism was associated with significantly decreased RB risk. However, as to the P21 rs1801270 polymorphism, a statistically significant association was not identified for RB.
eIF2alpha-P is cytoprotective in response to UVB by a mechanism featuring translation of a specific splice variant of CDKN1A that facilitates G1 arrest and subsequent DNA repair.
No significant differences were found in the frequency of alleles of CDKN1A gene in the group of healthy children and children with Down syndrome and dental caries.
In vitro studies in human lung fibroblasts revealed increased levels of p21 (p = 0.0032) and pAkt (p = 0.12) following treatment with serotonin.
Data suggest that CRNDE may function as an oncogene by modulating p21, finally contributing to the radioresistant phenotype formation of LAD cells.
Cyclin dependent kinase inhibitor 1A (p21) expressions is upregulated in non-cycling HCT116 p53(+/+) cells and HIV-1 reverse transcription is subsequently inhibited. The restrictions of HIV by p21 is associated with the suppression of ribonucleotide reductase R2 subunit expression and phosphorylation of SAMHD1 protein. siRNA knockdown of p21 increased HIV-2 infection in human monocyte derived macrophages.
p21 expression reports on Bovine herpesvirus 4 replication and could represent a host cell defensive response to infection-associated cellular damage.
demonstrate that NKX2-3 is a target molecule of EDA and critical for expression of the cell cycle regulator p21 in the enamel knot
the CAR-Akt-Foxo1 signalling pathway has an essential role in controlling hepatocyte proliferation by repressing the cell cycle regulator Cdkn1a (p21)
High cyclin A is associated with tumourigenic transformation.
Downregulation p21 promotes dexamethasone-induced apoptosis of MC3T3-E1 cells by inhibiting the antioxidant Nrf2/HO-1 pathway
Gene expressions in lung tissues from systemic bleomycin-treated mice were examined, revealing significant increased expression of Cdkn1alpha (a gene coding for p21), particularly in distal regions of the lung.
The downregulation of Cdkn1a and the upregulation of Cdk6.
Study reveal that p16Ink4a and p21Waf1/Cip1 upregulate CX3CR1 expression by preventing CDK-mediated phosphorylation and inactivation of SMAD3 in monocytic myeloid-derived suppressor cells promoting tumor growth through chemotaxis.
while muCT analysis indicates that p21(-/-) mice have enhanced bone healing capabilities, differences observed may not be due to the function of osteoblasts or osteoclasts
the deletion of Cdkn1a in vivo results in an elevated level of cell proliferation but not cell death.
p21 plays a relevant role in fasting adaptation through the positive regulation of PPARalpha.
The results suggested that TAZ may suppress apoptosis and premature senescence in spermatogenic cells by inhibiting the p53-p21 signaling pathway, thus playing important roles in the maintenance and control of reproductive function.
Results identify endoplasmic reticulum stress as an age-dependent modifier of islet survival and function by mechanisms implicating enhancement of CHOP activity and inhibition of the protective activity of p21.
Specifically, the proteins p18INK4C, p21CIP1 and p27KIP1 seem to play an outstanding role in the maintenance of the differentiated state of adipocytes.
Collectively, our findings demonstrate that PCAT-1 is a new candidate for use in OS diagnosis, prognosis and therapy.
results indicated that p21-deficient DMM mice were susceptible to alterations in Osteoarthritis (OA) phenotype, including enhanced osteoclast expression, macrophage infiltration, and MMP expression through IL-1beta-induced NF-kappaB signaling, suggesting that p21 regulation may constitute a possible therapeutic strategy for OA treatment.
our genetic and biochemical data show an important function of p21 in the regulation of growth-related processes in the heart.
The Smad3 and Bmal1 regulate p21 and S100A4 expression in myocardial stromal fibroblasts through TNF-alpha.
Data suggest BAF180 protein as a critical regulator of cellular senescence and HSC homeostasis, which is at least partially regulated through BAF180-mediated suppression of cell cycle regulator p21 expression.
Histone methyltransferase Suv39h1 attenuates high glucose-induced fibronectin 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.
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