Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The VSports app下载. gov means it’s official. Federal government websites often end in . gov or . mil. Before sharing sensitive information, make sure you’re on a federal government site. .

Https

The site is secure V体育官网. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely. .

. 1997 Nov 28;91(5):649-59.
doi: 10.1016/s0092-8674(00)80452-3.

Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF

T Kamijo  1 , F Zindy, M F Roussel, D E Quelle, J R Downing, R A Ashmun, G Grosveld, C J Sherr
Affiliations
Free article

Tumor suppression at the mouse INK4a locus mediated by the alternative reading frame product p19ARF

T Kamijo et al. Cell. .
Free article

Abstract (V体育官网入口)

The INK4a tumor suppressor locus encodes p16INK4a, an inhibitor of cyclin D-dependent kinases, and p19ARF, an alternative reading frame protein that also blocks cell proliferation. Surprisingly, mice lacking p19ARF but expressing functional p16INK4a develop tumors early in life. Their embryo fibroblasts (MEFs) do not senesce and are transformed by oncogenic Ha-ras alone VSports手机版. Conversion of ARF+/+ or ARF+/- MEF strains to continuously proliferating cell lines involves loss of either p19ARF or p53. p53-mediated checkpoint control is unperturbed in ARF-null fibroblast strains, whereas p53-negative cell lines are resistant to p19ARF-induced growth arrest. Therefore, INK4a encodes growth inhibitory proteins that act upstream of the retinoblastoma protein and p53. Mutations and deletions targeting this locus in cancer cells are unlikely to be functionally equivalent. .

PubMed Disclaimer

"V体育安卓版" Publication types

VSports - MeSH terms

VSports最新版本 - Substances

LinkOut - more resources (V体育平台登录)