The Adaptor Protein p66Shc Inhibits mTOR-Dependent Anabolic Metabolism-Reference-Cited by-同舟云学术

The Adaptor Protein p66Shc Inhibits mTOR-Dependent Anabolic Metabolism

Published:2014-02-18 Issue:313 Volume:7 Page:
ISSN:1945-0877
Container-title:Science Signaling
language:en
Short-container-title:Sci. Signal.

Author:

Soliman Mohamed A.¹²³,Abdel Rahman Anas M.¹,Lamming Dudley W.⁴,Birsoy Kivanç⁴,Pawling Judy¹,Frigolet Maria E.¹⁵,Lu Huogen¹⁵,Fantus I. George¹⁵,Pasculescu Adrian¹,Zheng Yong¹,Sabatini David M.⁴⁶⁷⁸⁹,Dennis James W.¹²,Pawson Tony¹²

Affiliation:

1. Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario M5G 1X5, Canada.

2. Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S 1A8, Canada.

3. Department of Biochemistry, Faculty of Pharmacy, Cairo University, Cairo 11562, Egypt.

4. Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, MA 02142, USA.

5. Banting and Best Diabetes Centre, Toronto General Research Institute, Faculty of Medicine, University of Toronto, Toronto, Ontario M5G 1L6, Canada.

6. Department of Biology, Massachusetts Institute of Technology (MIT), Cambridge, MA 02139, USA.

7. David H. Koch Institute for Integrative Cancer Research at MIT, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.

8. Broad Institute, Seven Cambridge Center, Cambridge, MA 02142, USA.

9. Howard Hughes Medical Institute, MIT, Cambridge, MA 02139, USA.

Abstract

The adaptor protein p66Shc unexpectedly inhibits glucose metabolism, which could be a useful therapeutic target for diabetes or cancer.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Cell Biology,Molecular Biology,Biochemistry

Reference38 articles.

1. Cell Signaling in Space and Time: Where Proteins Come Together and When They’re Apart

2. The mTOR-Regulated Phosphoproteome Reveals a Mechanism of mTORC1-Mediated Inhibition of Growth Factor Signaling

3. Phosphoproteomic Analysis Identifies Grb10 as an mTORC1 Substrate That Negatively Regulates Insulin Signaling

4. Peripheral Disruption of the Grb10 Gene Enhances Insulin Signaling and Sensitivity In Vivo

5. Mice with a Disruption of the Imprinted Grb10 Gene Exhibit Altered Body Composition, Glucose Homeostasis, and Insulin Signaling during Postnatal Life

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