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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.
We conducted a case-control study to determine the association between p21 C98A and C70T polymorphisms and the risk of meningioma.
PANDAR controlled the transcription of the CDKN1A gene by competitively binding with p53 protein.
AFAP1-AS1 epigenetically silences p21 transcription by binding to EZH2 thus promoting non-small cell lung cancer cell growth.
study revealed that berberine not only up-regulates mRNA and protein levels of p21/cip1 and p27/kip1 but also increases their nuclear localization and post-translational protein stability. Further, Akt inhibition was found to mediate berberine-mediated up-regulation of p21/cip1 but not the p27/kip1.
Acral Spitz nevi were characterized by strong and diffuse P16 and P21 expression, differentiating them from lentiginous melanoma.
p21Waf1 strongly suppressed L1 retrotransposition. The N-terminal kinase inhibitory domain (KID) of p21 was required for this inhibitory effect. Vpr and p21 coimmunoprecipitated with L1 ORF2p and they suppressed the L1 reverse transcriptase activity in LEAP assay, suggesting that Vpr and p21 inhibit ORF2p-mediated reverse transcription.
Immunoprecipitation and immunofluorescence staining reveled that UHRF2 combined with p21 in the nucleus. In addition, UHRF2 degraded p21 through ubiquitination and shortened the half-life of p21.
Study revealed that NUP155 controls mRNA translation CDKN1A, a key mediator of the p53 response.
results suggest that COMMD1 regulates cell proliferation and cell cycle progression by modulating p21 Cip1 levels
Together these data reveal for the first time the role of TRF2 in REST- repressor complex mediated transcription repression of CDKN1A.
DMSO and the process of freezing did not significantly change the expression of p21 and cyclin D1 genes in human amniotic fluid stem cells
This study uncovered a new mechanism by which FBXO22 functions as an oncogene in hepatocellular carcinoma pathogenesis and progression by mediating the ubiquitination and degradation of p21
The paradoxical effect of CIP1 expression on human breast carcinogenesis and explaining how the subcellular localization (nuclear or cytoplasmic) of Cip1 has an impact on both determining its fate as either cell-growth inhibitor or antiapoptotic molecule.[review]
Down-regulated P21 was negatively correlated with SNHG3 in glioma tumorigenesis.SNHG3 epigenetically silences p21 through sponging with EZH2.
found significant over-expression of the double strand break-fidelity genes CDKN1A and ERCC1, independent of promoter methylation and associated with chemorefractoriness in chronic myelomonocytic leukaemia
TRIB2 suppresses cellular senescence through interaction with AP4 to down-regulate p21 expression.
These studies suggest that MSK1 acts through a direct interaction with p53 to function as a transcriptional coactivator and that MSK1 activation by upstream MAPK signaling is important for efficient p21 gene expression.
MLK7AS1 has potential as a biomarker and may promote proliferation in CRC partially through downregulating p21 expression.
the knockdown of CASC15 triggered the silencing of ZEB1 in cytoplasm, which was shown to be associated with the competitive binding of CASC15 to miR-33a-5p.
the mechanism of chemoresistance by chemotherapy-driven increases in the CDKN1A/PTN/PTPRZ1 axis depended on the NF-kappaB pathway
p21 expression reports on Bovine herpesvirus 4 replication and could represent a host cell defensive response to infection-associated cellular damage.
Study demonstrated that overexpression of DNMT3A promoted the expression of cell proliferation markers but significantly decreased the expression of p21 to repress cell proliferation by the methylation of p21 promoter. Moreover, overexpression of DNMT3A decreased lipid accumulation and significantly down-regulated the levels of adipogenic marker genes through the methylation of PPARg promoter.
p21 controlled cell cycle regulation plays an essential role in suppressing telomere dysfunction-related tumorigenesis.
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
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