Keine Produkte auf Ihrer Vergleichsliste.
Ihr Warenkorb ist leer.
Weitere Synonyme anzeigen
Wählen Sie die gewünschte Spezies
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.
SPSB1 is essential for the survival of ovarian cancer cells and suppresses p21 expression through ubiquitin-mediated destabilization of p21 protein in ovarian cancer cells.
MiR-302d-3p promotes RPE dedifferentiation, migration, proliferation and cell-cycle progression, inhibits RPE phagocytosis, and induces abnormal EC behavior by targeting p21(Waf1/Cip1).
RXRalpha provokes tumor suppression through p53/p21/p16 and PI3K-AKT signaling pathways during stem cell differentiation and in cancer cells.
these findings not only demonstrate that KIF4A contributes to colorectal carcinoma proliferation via modulation of p21-mediated cell cycle progression but also suggest the potential value of KIF4A as a clinical prognostic marker and target for molecular treatments.
Loss-of-function assays demonstrated that silenced FAM83H-AS1 obviously suppressed cell proliferation via regulating the cell-cycle distribution and cell apoptosis rate, and mechanistic experiments revealed that FAM83H-AS1 could epidemically silence CDKN1A expression through recruiting EZH2 to the promoter of CDKN1A, thereby influencing the cell cycle and proliferation.
Hutchinson-Gilford progeria cells show impaired lamin A/C-HDAC2 interplay and accumulation of p21 upon stress recovery.
We found that silencing Myo7a by means of RNAi inhibited melanoma cell growth through upregulation of cell cycle regulator p21 (also known as CDKN1A) and suppressed melanoma cell migration and invasion through downregulation of RhoGDI2 (also known as ARHGDIB)
this study showed that CDKN1A overexpression inhibited the proliferation of invasion of human fibroblast-like synoviocytes in rheumatoid arthritis
Decreased expression of KHSRP, thus increasing CDKN1a (p21) expression.
These results demonstrated that JSK could trigger cell cycle arrest at the G2/M phase and apoptosis in A549 and H460 cells, which was likely mediated via the p53/p21WAF1/CIP1 and p27KIP1 pathways. Overall, the results indicated that JSK may be used as an anticancer agent for the treatment of nonsmall cell lung cancer (NSCLC)
miR-363-3p is induced by HIF-2alpha to promote the stemness of melanoma cells via inhibiting p21.
Study found that PSMD2 was markedly upregulated in breast cancer. High PSMD2 expression was significantly correlated with poor prognosis. PSMD2 knockdown inhibited cell proliferation and arrested cell cycle at G0/G1 phase in vitro, as well as suppressed tumor growth in vivo. Mechanically, PSMD2 physically interacted with p21 and p27 and mediated their ubiquitin-proteasome degradation with the cooperation of USP14.
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.
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.
PPM1K Regulates Hematopoiesis and Leukemogenesis through CDC20-Mediated Ubiquitination of MEIS1 and p21.
this study identified P21 and Sharp1 as HDAC4 target genes.
Plasma/urine p21 levels increase acute kidney injury and as a result of renal aging.
Results provide evidence that elevated p21 expression is due to downregulation of serum exosomal miR-370 contributing in aggravating liver cytotoxic effect of Fructus Meliae Toosendan.
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.
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