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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.
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.
Low CDKN1A expression is associated with cervical cancer.
p21 was involved in glioma cell proliferation after SNHG6 was downregulated.
overexpressed PKM2 led to increased CCND1 and decreased CDKN1A expression, whereas underexpressed PKM2 led to decreased CCND1 and increased CDKN1A expression in ovarian cancer cells.
the CDK inhibitor p21 begins rising in G2 in mother cells whose daughters exit mitosis into the pre-Restriction Point, CDK2(low) state. Furthermore, degradation of p21 coincides with escape from the CDK2(low) state and passage through the Restriction Point.
SAC decreased the levels of 5-methylcytosine, DNMT activity, messenger RNA (mRNA) and protein levels of DNMT1. Additionally, SAC treatment resulted in re-expression of the mRNA and proteins of silenced tumor suppressor gene CDKN1A accompany with reduced cell division control 2 expression.
Down-regulation of HOTAIR elicits an inhibitory effect on proliferation, invasion, and migration, while promoting the apoptosis of colorectal cancer cells through the up-regulation of p21.
Glutaredoxin-1 silencing induces cell senescence via p53/p21/p16 signaling axis.
p16, p21, and p53 proteins play an important role in the deregulation of the cell cycle and participate in the development of pancreatic intraepithelial neoplasia.
p21 expression reports on Bovine herpesvirus 4 replication and could represent a host cell defensive response to infection-associated cellular damage.
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.
The study demonstrates an essential role of Setd2 in myoblast proliferation and differentiation, and uncovers Setd2-mediated molecular mechanism through regulating MyoG and p21.
Schistosoma japonicum egg antigen p40 through action on the STAT3/p53/p21 pathway triggered cellular senescence, while knockdown of p53 or STAT3 partly restored cell senescence.
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