TOR Deficiency in C. elegans Causes Developmental Arrest and Intestinal Atrophy by Inhibition of mRNA Translation-Reference-Cited by-同舟云学术

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TOR Deficiency in C. elegans Causes Developmental Arrest and Intestinal Atrophy by Inhibition of mRNA Translation

Published:2002-09 Issue:17 Volume:12 Page:1448-1461
ISSN:0960-9822
Container-title:Current Biology
language:en
Short-container-title:Current Biology

Author:

Long Xiaomeng,Spycher Carmen,Han Z.Stanley,Rose Ann M.,Müller Fritz,Avruch Joseph

Publisher

Elsevier BV

Subject

General Agricultural and Biological Sciences,General Biochemistry, Genetics and Molecular Biology

Reference65 articles.

1. Targets for cell cycle arrest by the immunosuppressant rapamycin in yeast;Heitman;Science,1991

2. TOR controls translation initiation and early G1 progression in yeast;Barbet;Mol. Biol. Cell,1996

3. Target of rapamycin proteins and their kinase activities are required for meiosis;Zheng;Proc. Natl. Acad. Sci. USA,1997

4. Tor, a phosphatidylinositol kinase homologue, controls autophagy in yeast;Noda;J. Biol. Chem.,1998

5. Rapamycin induces the G0 program of transcriptional repression in yeast by interfering with the TOR signaling pathway;Zaragoza;Mol. Cell. Biol.,1998

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