Browse our CDKN2C Proteins (CDKN2C)

Human Cyclin-Dependent Kinase Inhibitor 2C (p18, Inhibits CDK4) (CDKN2C) interaction partners

1. Low P18 expression is associated with multiple endocrine neoplasia type 1-related pancreatic neuroendocrine tumors.

2. Cycling hypoxia could induce significant changes in CLDN1 and CLDN7 expression in nasopharyngeal cancer cells, indirectly regulation P18 expression and affecting cell invasion/proliferation.

3. 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.

4. CDKN2C gene deletion is associated with plasma cell post-transplantation lymphoproliferative disorders.

5. The differences in p18(INK4c)and p57(Kip2)activities in chronic myeloid leukemia and normal stem cells suggest a different cell cycle regulation.

6. Our study suggests that p18 is a limiting factor for the noncanonical HSC differentiation path in lymphoid lineages.

7. CDKN2C inactivation contributes to the leukemogenesis in acute promyelocytic leukemia.

8. DNA methyltransferase 3A promotes cell proliferation by silencing CDK inhibitor p18INK4C in gastric carcinogenesis

9. Data suggest that cell cycle-dependent kinase inhibitors CDKN2C/p18 and CDKN1A/p21 facilitate cell cycle entry/cell proliferation of quiescent adult human pancreatic beta cells in primary culture (from tissues obtained from organ donors).

10. this studydemonstrated abundant levels of the critical negative cell-cycle regulators, p27(Kip1), its phosphorylated form, p-p27(S10), p18Ink4c, and GSK-3, in beta-cells of both adult human and mouse pancreatic islets, which contribute to maintenance of beta-cell quiescence.

11. 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 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

12. Mutations in CDKN2C is associated with sporadic parathyroid adenoma.

13. Analysis of B1a lymphocyte phenotypes of p18-deficient C57BL/6 mice finds that p18 is a key regulator of the size of the B1a cell pool.

14. up-regulated HULC promotes proliferation of hepatoma cells through suppressing p18

15. Data indicate that the role of CDKN2C in the adverse outcome of cases with hemizygous deletion was less certain.

16. Expression of p15, p18 and p27 was not generally related to the MEN1 gene mutational status of the investigated 18 pancreatic endocrine tumours.

17. propose that the contrasting behavior of the two very similar INK4 proteins could reflect their respective roles in senescence versus differentiation

18. results demonstrate for the first time that N-Myc is a downstream target of RET2A signaling, and propose that induction of N-Myc by RET2A is a key step leading to lower p18 levels during MEN2A tumorigenesis

19. review presents the recent advances in MEN-4 and other multiple endocrine neoplasias and summarises the current knowledge of how P27KIP1 and p18-INK4C may be implicated in endocrine neoplasia [review]

20. conclude that E2F proteins and Sp1 play an important role in the control of p18 expression

Mouse (Murine) Cyclin-Dependent Kinase Inhibitor 2C (p18, Inhibits CDK4) (CDKN2C) interaction partners

1. Gata3 deficiency promotes B cell differentiation and proliferation, and cooperates with p18 loss to induce B cell lymphomas

2. These results indicate that p18 blocks reprogramming by targeting Cdk4/6-mediated cell cycle regulation.

3. Host Tumor Suppressor p18(INK4c) Functions as a Potent Cell-Intrinsic Inhibitor of Murine Gammaherpesvirus 68 Reactivation and Pathogenesis.

4. Specifically, the proteins p18INK4C, p21CIP1 and p27KIP1 seem to play an outstanding role in the maintenance of the differentiated state of adipocytes.

5. CD4+ T cells from mice genetically deficient for p18ink4c divide more rapidly than wild-type cells in response to antigenic, costimulatory and growth factor signals.

6. p18 represents a potent and specific target for enhancing the self-renewal property of HSC, as demonstrated the effect of inhibitors

7. p18 may play protective roles and may be associated with or partially account for the cytoprotective effects of HO-1 in cisplatin-induced acute kidney injury.

8. Cdk4 and Cdk6 cooperate in hematopoietic tumor development and suggest a role for Cdk6 in sequestering INK4 proteins away from Cdk4.

9. Gata3/Ruvbl2 complex regulates T helper 2 cell proliferation via repression of Cdkn2c expression.

10. deletion of P18 results in a deacreased proliferation of hematopoietic progenitor cells (HPCs) suggesting a positive role for P18 on HPCs in vivo

11. A p18 -74 C/T mutation is the leading causal variant for the cell expansion that characterizes NZB and NZM2410 lupus-prone mouse strains.

12. This study demonstrated the predominant expression MEN1-related genes, particularly MLL and p27, in the endocrine organs, and a tissue-specific haploinsuffiency of MLL may lead to a decrease in levels of p27 and p18 mRNAs in endocrine organs.

13. 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.

14. define the first physiologic function for Noxa and suggest that by repressing Noxa, induction of G arrest by p18INK4c bypasses a homeostatic cell-cycle checkpoint in intermediate plasma cells (iPCs) for PC differentiation

15. p18 and p27 are involved in B lymphopoiesis, and knockdown of p18 and p27 blocks the differentiation from hematopoietic stem cells to B lymphocytes.

16. CDK inhibitor p18(INK4c) is required for the generation of functional plasma cells

17. Here we show that treatment of p18 null and heterozygous mice with a chemical carcinogen resulted in tumor development at an accelerated rate.Hence, p18 is a haploinsufficient tumor suppressor in mice.

18. p18 is involved in cell cycle progression after partial hepatectomy.

19. Ink4 proteins might function in governing neuronal cell cycle exit as well as in a non-cell-autonomous manner in controlling the production of diffusible mitogens and chemokines that influence postnatal development of the cerebellar EGL.

20. p19(INK4d) in addition to p21(WAF1/Cip1) is an important molecular target of HDAC inhibitors inducing growth arrest