Browse our CDKN2C Proteins (CDKN2C)

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

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

2. 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.

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

4. The differences in p18(INK4c)and p57(Kip2 (show CDKN1C Proteins))activities in chronic myeloid leukemia (show BCL11A Proteins) and normal stem cells suggest a different cell cycle regulation.

5. Our study suggests that p18 is a limiting factor for the noncanonical HSC (show FUT1 Proteins) differentiation path in lymphoid lineages.

6. CDKN2C inactivation contributes to the leukemogenesis in acute promyelocytic leukemia (show PML Proteins).

7. DNA methyltransferase 3A (show DNMT3A Proteins) promotes cell proliferation by silencing CDK (show CDK4 Proteins) inhibitor p18INK4C in gastric carcinogenesis

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

9. this studydemonstrated abundant levels of the critical negative cell-cycle regulators, p27(Kip1 (show CDKN1B Proteins)), its phosphorylated form, p-p27 (show PAK2 Proteins)(S10 (show L1CAM Proteins)), p18Ink4c, and GSK-3, in beta-cells of both adult human and mouse pancreatic islets, which contribute to maintenance of beta-cell quiescence.

10. 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 (show CDKN2B Proteins) 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

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

1. Gata3 (show GATA3 Proteins) 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 (show CDK4 Proteins)-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 (show CDKN1A Proteins) and p27KIP1 (show CDKN1B Proteins) seem to play an outstanding role in the maintenance of the differentiated state of adipocytes.

5. CD4 (show CD4 Proteins)+ 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 (show FUT1 Proteins), 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 (show HMOX1 Proteins) in cisplatin-induced acute kidney injury.

8. Cdk4 (show CDK4 Proteins) and Cdk6 (show CDK6 Proteins) cooperate in hematopoietic tumor development and suggest a role for Cdk6 (show CDK6 Proteins) in sequestering INK4 proteins away from Cdk4 (show CDK4 Proteins).

9. Gata3 (show GATA3 Proteins)/Ruvbl2 (show RUVBL2 Proteins) 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