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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.
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.
Data indicate how cyclin dependent kinase inhibitor 1A (p21) regulates the proliferation-quiescence decision to maintain genomic stability.
The first evidence for non-repair functions of MGMT in cell cycle and highlight the involvement of PCNA in MGMT downregulation, with p21 attenuating the process.
Scriptaid was also able to dose dependently and significantly induce MM cell cycle arrest at the G2/M phase.
High CDKN1A expression is associated with migration, invasion, and progression of bladder cancer.
CDKN1A role in DANCR-mediated tumor cell growth.
CDKN1A expression was seen only in five cases and that too focally in the cytoplasm, thereby warranting removal of analysis of CDKN1A positivity from the study
Results show that knockdown of GABPB1 in clear cell renal cell carcinoma cell lines significantly decreased the ability to form colonies by inducing the expression of p21Waf/Cip1.
Authors demonstrate that HMGB2 transcription is repressed by p21 during radiation-induced senescence through the ATM-p53-p21 DNA damage signaling cascade. The loss of p21 abolished the downregulation of HMGB2 caused by ionizing radiation, and the conditional induction of p21 was sufficient to repress the transcription of HMGB2.
p21 expression reports on Bovine herpesvirus 4 replication and could represent a host cell defensive response to infection-associated cellular damage.
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.
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 activity.
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