Recombinant Mouse Cyclin-dependent kinase 4 inhibitor B (Cdkn2b)

1. miR-541 contributes to microcystin-LR-induced testicular toxicity by regulating the expression of p15 and promoting apoptosis. PMID:27608041
2. Loss of CDKN2B may not only promote cardiovascular disease through the development of atherosclerosis but may also impair TGFbeta signaling and hypoxic neovessel maturation. PMID:26596284
3. Radiation-induced double strand breaks cooperate with loss of Ink4 and Arf tumor suppressors to generate high-grade gliomas that are commonly driven by Met amplification and activation. PMID:24632607
4. Data indicate that loss of cyclin-dependent kinase inhibitor p15 (p15Ink4b) collaborates with oncogene fusion protein Nup98-HoxD13 transgene in the development of predominantly myeloid neoplasms. PMID:24449168
5. Loss of CDKN2B promotes atherosclerosis by increasing the size and complexity of the lipid-laden necrotic core through impaired efferocytosis. PMID:24531546
6. Reduced CDKN2B expression and increased p53-dependent smooth muscle cell apoptosis may be one mechanism underlying the 9p21.3 association with aneurysmal disease. PMID:23162013
7. mRNA expression of p15 gene in mouse bone marrow cells decreases after exposure to 1,4-benzoquinone, but the CpG islands methylation status in promoter is not affected. PMID:21619792
8. p15Ink4b is an important modulator of cDC development and has a novel function for this tumor suppressor in the regulation of adaptive immune responses. PMID:22461492
9. findings indicate that in lymphoid tissue the inactivation of both p15 alleles is unlikely to be the first event in tumor development PMID:22227036
10. new animal model demonstrates experimentally that p15Ink4b is a tumor suppressor for myeloid leukemia, and its loss may play an active role in the establishment of preleukemic conditions PMID:20457873
11. is not consistently inactivated in murine myeloid cells transformed in vivo by deregulated c-Myc PMID:12642863
12. Ink4b is hypermethylated in murine myeloid leukemia PMID:14681685
13. review experiments and present examples of new models of myeloid leukemia where retroviruses have collaborated with a transgene [Cbfbeta-MYH111 from Inv(16)] and with loss of a tumor suppressor (Ink4b) mice to induce leukemia. PMID:14757439
14. regulation of the Ink4b promoter is apparently myeloid specific because both ICSBP and PU.1 are myeloid commitment factors. PMID:14976051
15. results strongly suggest that p15(Ink4b) loss must be accompanied by additional oncogenic changes for RUNX1-ETO-associated acute myeloid leukemia to develop PMID:18037485
16. Expression of exogenous p15AS in mouse embryonic stem cells caused p15 silencing and increased growth, through heterochromatin formation, as well as DNA methylation after differentiation of the embryonic stem cells PMID:18185590
17. Results indicate that Jhdm1b is an H3K36 demethylase that regulates cell proliferation and senescence through p15(Ink4b). PMID:18836456

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UNIGENE: Mm.423094

KEGG: mmu:12579

STRING: 10090.ENSMUSP00000095595