Glucose-6-phosphate isomerase deficiency results in mTOR activation, failed translocation of lipin 1α to the nucleus and hypersensitivity to glucose: Implications for the inherited glycolytic disease-Reference-Cited by-同舟云学术

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Glucose-6-phosphate isomerase deficiency results in mTOR activation, failed translocation of lipin 1α to the nucleus and hypersensitivity to glucose: Implications for the inherited glycolytic disease

Published:2011-11 Issue:11 Volume:1812 Page:1393-1402
ISSN:0925-4439
Container-title:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
language:en
Short-container-title:Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Author:

Haller Jorge F.,Krawczyk Sarah A.,Gostilovitch Lubov,Corkey Barbara E.,Zoeller Raphael A.

Funder

Boston Obesity Nutrition Research Cente

Publisher

Elsevier BV

Subject

Molecular Biology,Molecular Medicine

Reference46 articles.

1. Glucose-6-phosphate isomerase deficiency;Kugler;Baillieres Best Pract. Res. Clin. Haematol.,2000

2. Molecular basis of neurological dysfunction coupled with haemolytic anaemia in human glucose-6-phosphate isomerase (GPI) deficiency;Kugler;Hum. Genet.,1998

3. Glucose phosphate isomerase deficiency with hereditary nonspherocytic hemolytic anemia;Hutton;J. Pediatr.,1974

4. Glucose-6-phosphate isomerase deficiency associated with nonspherocytic hemolytic anemia in the mouse: an animal model for the human disease;Merkle;Blood,1993

5. Isolation of novel animal cell lines defective in glycerolipid biosynthesis reveals mutations in glucose-6-phosphate isomerase;Haller;J. Biol. Chem.,2010

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