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Validated All-in-One™ qPCR Primer for CDKN1C(NM_000076.1) Search again
Product ID:
HQP000356
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
BWCR, BWS, KIP2, WBS, p57, p57Kip2
Gene Description:
cyclin dependent kinase inhibitor 1C
Target Gene Accession:
NM_000076.1(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
The protein encoded by this gene is a tight-binding, strong inhibitor of several G1 cyclin/Cdk complexes and a negative regulator of cell proliferation. Mutations in this gene are implicated in sporadic cancers and Beckwith-Wiedemann syndorome, suggesting that this gene is a tumor suppressor candidate. Three transcript variants encoding two different isoforms have been found for this gene. [provided by RefSeq].
Gene References into function
- Identification and functional characterization of an intragenic DNA binding site for the spumaretroviral trans-activator in the human p57Kip2 gene
- Induction of p57(KIP2) expression by p73beta
- Down-regulation of p57 may play a role in the dedifferentiation of thyroid carcinoma.
- DNA methylation and histone deacetylation of p57KIP2 promoter results in gene silencing of p57KIP2 in human tumors
- aberrant DNA methylation of the gene occurs in the promoter region in lymphoid malignancies of B-cell phenotype
- findings support the hypothesis that misexpression of p57 is involved in the abnormal development of androgenetic complete moles
- Expression of p57kip2, Rb protein and PCNA and their relationships with clinicopathology in human pancreatic cancer.
- P57/KIP2 is a determinant pro-survival factor for cell protection from green tea polyphenol-induced apoptosis.
- frequently methylated in adult patients with ALL, and that inactivation of a pathway composed of p73, p15, and p57KIP2 predicts for poor prognosis in Ph-negative patients
- identified a functional glucocorticoid response element, located 5 kilo bases upstream of the transcription start site in the human p57(Kip2) promoter
- SCFSkp2 complex plays an important role in cell-cycle progression by determining the abundance of p57Kip2 and that of the related CDK inhibitor p27Kip1.
- it is evident that B-Myb protein may promote cell proliferation by a non-transcriptional mechanism that involves release of active cyclin/cyclin dependent kinase 2 from cyclin-dependent inhibitor 1C p57(KIP2)
- p57KIP2 modulates stress-activated signaling by functioning as an endogenous inhibitor of JNK/SAPK
- p57 may act as a key regulator in embryogenesis by regulating cell cycle through binding to Cdks and the regulating actin dynamics through binding to LIMK-1
- loss of p57KIP2 expression appears associated with colorectal carcinogenesis
- An epimutation at KvDMR1, the absence of maternal methylation, causes the aberrant silencing of CDKN1C, some 180 kb away on the maternal chromosome.
- Diminished CDKN1C expression is associated with loss of methylation of CpG & H3K9 at DMR-LIT1, & is involved in esophageal cancer. DMR-LIT1 epigenetically regulates CDKN1C expression through histone modifications at DMR-LIT1 promoter.
- p57KIP2 was weakly expressed in 4/6 glioblastoma (GBM) specimens by western blot. p57KIP2 immunoreactivity was positive in 8/40 GBMs, and was primarily nuclear in location. The motility of glioma cells was significantly reduced after p57KIP2 induction.
- Aberrant methylation of p57KIP2 gene is associated with lung and breast cancers and malignant mesotheliomas
- p57 is up-regulated in the process of decidualization.
- Variants in CDKN1C may contribute to the inter-individual variation in birth weight.
- p57KIP2 is part of an imprinted gene network that may play a role in Beckwith-Wiedemann syndrome.
- endothelial cells of infantile hemangiomas not associated with Beckwith-Wiedemann syndrome normally express p57(KIP2) while chorioangiomas do not
- The Cyclin-Dependent Kinase Inhibitor p57 plays key roles in cell cycle regulation, and was methylation-negative in myeloid neoplasia.
- Transcripts of P57KIP2, imprinted genes related to BWS, were detected in human oocytes and at all stages of preimplantation embryos.
- The P57 was methylated in 2 (10%) pediatric patients , compared to 20 (37%)respectively in adult patients.
- identification of a novel p73-Kip2/p57 pathway that coordinates mitotic exit and transition to G1
- The absence of methylation and repressive chromatin structure at the CDKN1C promoter in Beckwith-Wiedemann Syndrome patients with loss of methylation at KvDMR1 suggests a direct role of this epimutation in silencing CDKN1C.
- The decreased expression of p57(kip2) and/or overexpression of cyclinE protein and PCNA may contribute to the occurrence and progression of pancreatic cancer.
- Methylation of p57(KIP2) may contribute to the malignant progression of gastric MALT lymphomas.
- Recent advances in epigenetic control of the CDKN1C/KCNQ1OT1 imprinted domain in both humans and mice, causing Beckwith-Wiedemann syndrome and cancer. (review)
- Global gene expression analysis in neuroblastoma cells engineered to acutely express the E protein E47 and Id2, showed that p57Kip2 is a target of E47.
- These results suggest that the tumor suppressive properties of p57KIP2 in leukemia may depend on the intrinsic promoter DNA methylation status of the gene.
- TGF-beta1 and/or TGF-beta2 inhibit proliferation of primary cultured human limbal epithelial cells, and p57 and p15 play roles in this process.
- CTIP2 associates with the NuRD complex on the promoter of p57KIP2, a newly identified CTIP2 target gene.
- findings suggest p57kip2 may play a role in the regulation of meiotic progression of early spermatocytes & cell cycle arrest & differentiation of spermatids
- These data demonstrate the role of BMP2 compared to BMP6 in the inhibition of growth and induction of differentiation of keratinocytes; p57(Kip2) and p21(Cip1) have a BMP2/6-induced expression.
- Genetic evidence links the association between DNA-variants in the CDKN1C gene with a risk of atherosclerosis and myocardial infarction.
- mechanism whereby p57(Kip2) influences the mitochondrial apoptotic cell death pathway in cancer cells
- In this study, P57kip2 immunostaining was absent in the trophoblastic layers of CHM and was positive in the trophoblast layer of nonmolar villi and MD.
- We did not find p16, p14, and p57 to be useful as prognostic markers in stage III ovarian cancer
- demonstrate that these myoblasts are unable to complete myogenic differentiation because of an inability to up-regulate p57Kip2 transcription
- The expression of CDKN1C decreases in the large majority of breast cancers and does not appear to be mediated by AI/LOH at the gene. CDKN1C may be a breast cancer tumor suppressor.
- cyclin-dependent kinase inhibitor p57(Kip2) and vascular endothelial growth factor mRNAs are selectively translated by an IRES-independent mechanism under hypoxic stress
- miR-221 has an oncogenic function in hepatocarcinogenesis by targeting CDKN1B/p27 and CDKN1C/p57, hence promoting proliferation by controlling cell-cycle inhibitors.
- p57(Kip2) down-regulation is a well-established feature of urothelial carcinoma. Probably, this down-regulation of cyclin-dependent kinase inhibitors supports the proliferation phase of oncogenesis.
- The loss of p57 expression in placental mesenchymal dysplasia could be of diagnostic value in helping to distinguish this rare placental lesion from its mimickers.