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anti-Human CDKN2C Antikörper:
anti-Mouse (Murine) CDKN2C Antikörper:
anti-Rat (Rattus) CDKN2C Antikörper:
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Human Monoclonal CDKN2C Primary Antibody für IF, IHC - ABIN267060
Gagrica, Brookes, Anderton, Rowe, Peters: Contrasting behavior of the p18INK4c and p16INK4a tumor suppressors in both replicative and oncogene-induced senescence. in Cancer research 2012
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genetic association studies in population in Houston TX: Data suggest that CDKN2C copy number variations are associated with sporadic medullary thyroid carcinoma; these associations include presence of distant metastasis at presentation and decreased overall survival.
CDKN2C gene deletion is associated with plasma cell post-transplantation lymphoproliferative disorders.
The differences in p18(INK4c)and p57(Kip2 (zeige CDKN1C Antikörper))activities in chronic myeloid leukemia (zeige BCL11A Antikörper) and normal stem cells suggest a different cell cycle regulation.
Our study suggests that p18 is a limiting factor for the noncanonical HSC (zeige FUT1 Antikörper) differentiation path in lymphoid lineages.
CDKN2C inactivation contributes to the leukemogenesis in acute promyelocytic leukemia (zeige PML Antikörper).
DNA methyltransferase 3A (zeige DNMT3A Antikörper) promotes cell proliferation by silencing CDK (zeige CDK4 Antikörper) inhibitor p18INK4C in gastric carcinogenesis
Data suggest that cell cycle-dependent kinase inhibitors CDKN2C/p18 and CDKN1A/p21 (zeige CDKN1A Antikörper) facilitate cell cycle entry/cell proliferation of quiescent adult human pancreatic beta cells in primary culture (from tissues obtained from organ donors).
this studydemonstrated abundant levels of the critical negative cell-cycle regulators, p27(Kip1 (zeige CDKN1B Antikörper)), its phosphorylated form, p-p27 (zeige PAK2 Antikörper)(S10 (zeige L1CAM Antikörper)), p18Ink4c, and GSK-3 (zeige GSK3b Antikörper), in beta-cells of both adult human and mouse pancreatic islets, which contribute to maintenance of beta-cell quiescence.
in 85 sporadic parathyroid adenomas, study identified alterations in 5 adenomas: 2 contained heterozygous changes in CDKN1A, 1 germline and 1 of undetermined germline status; 1 had a CDKN2B (zeige CDKN2B Antikörper) germline alteration, accompanied by loss of the normal allele in the tumor (LOH); 2 had variants of CDKN2C, 1 somatic and 1 germline with LOH
Mutations in CDKN2C is associated with sporadic parathyroid adenoma.
CD4 (zeige CD4 Antikörper)+ T cells from mice genetically deficient for p18ink4c divide more rapidly than wild-type cells in response to antigenic, costimulatory and growth factor signals.
p18 represents a potent and specific target for enhancing the self-renewal property of HSC (zeige FUT1 Antikörper), as demonstrated the effect of inhibitors
p18 may play protective roles and may be associated with or partially account for the cytoprotective effects of HO-1 (zeige HMOX1 Antikörper) in cisplatin-induced acute kidney injury.
Cdk4 (zeige CDK4 Antikörper) and Cdk6 (zeige CDK6 Antikörper) cooperate in hematopoietic tumor development and suggest a role for Cdk6 (zeige CDK6 Antikörper) in sequestering INK4 (zeige CDKN2A Antikörper) proteins away from Cdk4 (zeige CDK4 Antikörper).
Gata3 (zeige GATA3 Antikörper)/Ruvbl2 (zeige RUVBL2 Antikörper) complex regulates T helper 2 cell proliferation via repression of Cdkn2c expression.
deletion of P18 results in a deacreased proliferation of hematopoietic progenitor cells (HPCs) suggesting a positive role for P18 on HPCs in vivo
A p18 -74 C/T mutation is the leading causal variant for the cell expansion that characterizes NZB and NZM2410 lupus-prone mouse strains.
This study demonstrated the predominant expression MEN1-related genes, particularly MLL (zeige MLL Antikörper) and p27 (zeige CDKN1B Antikörper), in the endocrine organs, and a tissue-specific haploinsuffiency of MLL (zeige MLL Antikörper) may lead to a decrease in levels of p27 (zeige CDKN1B Antikörper) and p18 mRNAs in endocrine organs.
Cdkn2c plays a critical role in B1a cell self-renewal and its impaired expression leads to an accumulation of these cells with high autoreactive potential.
define the first physiologic function for Noxa (zeige PMAIP1 Antikörper) and suggest that by repressing Noxa (zeige PMAIP1 Antikörper), induction of G arrest by p18INK4c bypasses a homeostatic cell-cycle checkpoint in intermediate plasma cells (iPCs) for PC differentiation
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. Studies in the knockout mice suggested the roles of this gene in regulating spermatogenesis, as well as in suppressing tumorigenesis. Two alternatively spliced transcript variants of this gene, which encode an identical protein, have been reported.
cyclin-dependent kinase inhibitor 2C (p18, inhibits CDK4)
, cyclin-dependent kinase 4 inhibitor C
, CDK6 inhibitor p18
, cyclin-dependent inhibitor
, cyclin-dependent kinase 6 inhibitor p18
, cyclin-dependent kinase 6 inhibitor