PTEN公司
张力素
癌症研究
蛋白质酪氨酸磷酸酶
生物
抑癌基因
转移
PTPN11型
基因产物
前列腺癌
癌症
基因
突变
癌变
激酶
PI3K/AKT/mTOR通路
信号转导
细胞生物学
遗传学
基因表达
克拉斯
作者
Jing Li,Clifford Yen,Danny Liaw,Katrina Podsypanina,Shikha Bose,Steven I. Wang,Janusz Puc,Christa Miliaresis,Linda Rodgers,W. Richard McCombie,Sandra H. Bigner,Beppino C. Giovanella,Michael Ittmann,Ben Tycko,Hanina Hibshoosh,Michael Wigler,Ramon Parsons
出处
期刊:Science
[American Association for the Advancement of Science]
日期:1997-03-28
卷期号:275 (5308): 1943-1947
被引量:4796
标识
DOI:10.1126/science.275.5308.1943
摘要
Mapping of homozygous deletions on human chromosome 10q23 has led to the isolation of a candidate tumor suppressor gene, PTEN , that appears to be mutated at considerable frequency in human cancers. In preliminary screens, mutations of PTEN were detected in 31% (13/42) of glioblastoma cell lines and xenografts, 100% (4/4) of prostate cancer cell lines, 6% (4/65) of breast cancer cell lines and xenografts, and 17% (3/18) of primary glioblastomas. The predicted PTEN product has a protein tyrosine phosphatase domain and extensive homology to tensin, a protein that interacts with actin filaments at focal adhesions. These homologies suggest that PTEN may suppress tumor cell growth by antagonizing protein tyrosine kinases and may regulate tumor cell invasion and metastasis through interactions at focal adhesions.
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