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将猿猴病毒40大T抗原的转化功能和起始点结合功能与阻断分化的能力分离。

Separation of simian virus 40 large-T-antigen-transforming and origin-binding functions from the ability to block differentiation.

作者信息

Cherington V, Brown M, Paucha E, St Louis J, Spiegelman B M, Roberts T M

机构信息

Department of Pathology, Tufts University School of Medicine, Boston, Massachusetts 02111.

出版信息

Mol Cell Biol. 1988 Mar;8(3):1380-4. doi: 10.1128/mcb.8.3.1380-1384.1988.

DOI:10.1128/mcb.8.3.1380-1384.1988
PMID:2835674
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC363287/
Abstract

Wild-type simian virus 40 large T antigen is very effective at blocking adipocyte differentiation in 3T3-F442A cells as assayed by triglyceride accumulation, induction of glycerophosphate dehydrogenase activity, and expression of mRNAs for glycerophosphate dehydrogenase, the adipocyte serine protease adipsin, and the putative lipid-binding protein adipocyte P2. Point mutants defective for either origin-specific DNA binding or transformation blocked differentiation as completely as wild type.

摘要

野生型猿猴病毒40大T抗原在阻断3T3 - F442A细胞中的脂肪细胞分化方面非常有效，这通过甘油三酯积累、甘油磷酸脱氢酶活性的诱导以及甘油磷酸脱氢酶、脂肪细胞丝氨酸蛋白酶脂肪酶和假定的脂质结合蛋白脂肪细胞P2的mRNA表达来测定。对起始点特异性DNA结合或转化有缺陷的点突变体与野生型一样完全阻断分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47e6/363287/4b60abffd9de/molcellb00063-0382-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47e6/363287/4b60abffd9de/molcellb00063-0382-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/47e6/363287/4b60abffd9de/molcellb00063-0382-a.jpg

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