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Validated All-in-One™ qPCR Primer for CDKN2C(NM_078626.2) Search again
Powered by BiozBy 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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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 member of the INK4 family of cyclin-dependent kinase inhibitors. This protein has been shown to interact with CDK4 or CDK6, and prevent the activation of the CDK kinases, thus function as a cell growth regulator that controls cell cycle G1 progression. Ectopic expression of this gene was shown to suppress the growth of human cells in a manner that appears to correlate with the presence of a wild-type RB1 function.
Gene References into function
- conclude that E2F proteins and Sp1 play an important role in the control of p18 expression
- Deletions in the CDKN2C locus and hypermethylation in the CDKN2C promoter region play a role in ovarian granulosa cell tumorogenesis.
- Inhibitor shows antitumor effect on glioma cells.
- p18INK4c may function as a tumor suppressor in Hodgkin lymphoma, and inactivation may contribute to cell cycle deregulation and defective terminal differentiation of the Reed-Sternberg cells.
- protein kinase C promotes human cancer cell growth through downregulation of p18(INK4c)
- p18(INK4C) loss may contribute to medulloblastoma formation in children
- Transfer of the p16(INK4a) and p18(INK4c) genes and CDK4I suppressed the production of MMP-3 and MCP-1.
- data suggest that p27 and p18 are unlikely to present classic tumor-suppressor genes in sporadic pancreatic endocrine tumors
- oncogenic RET and loss of p18 cooperate in the multistep tumorigenesis of medullary thyroid carcinoma
- These findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate tumor suppressor role for p18(INK4C) in human glioblastoma wherein it functions cooperatively with other INK4 family.
- deletions of CDKN2C are important in the progression and clinical outcome of myeloma
- P18 is a tumor suppressor gene involved in human medullary thyroid carcinoma and pheochromocytoma