Autophagy is required for mitochondrial function, lipid metabolism, growth, and fate of KRASG12D-driven lung tumors

Autophagy

Volumn 9, Issue 10, 2013, Pages 1636-1638

  Guo, Jessie Yanxiang ^a,b   White, Eileen ^a,b  

^a RUTGERS CANCER INSTITUTE OF NEW JERSEY   (United States)

^b RUTGERS UNIVERSITY   (United States)

Author keywords

Autophagy; Fatty acid oxidation; KRAS; Metabolism; Mitochondria; NSCLC; Oncocytoma; P53

Indexed keywords

GLUTAMINE; K RAS PROTEIN; KRAS PROTEIN, HUMAN; ONCOPROTEIN; RAS PROTEIN;

ARTICLE; AUTOPHAGY; CANCER GROWTH; CANCER INHIBITION; CELL GROWTH; FATTY ACID OXIDATION; GENE DELETION; GENETIC ENGINEERING; HUMAN; LIPID METABOLISM; LUNG NON SMALL CELL CANCER; MITOCHONDRION; NONHUMAN; ONCOCYTOMA; ONCOGENE K RAS; ANIMAL; CELL PROLIFERATION; GENETICS; LUNG TUMOR; METABOLISM; PATHOLOGY; PHYSIOLOGY;

ANIMALS; AUTOPHAGY; CELL PROLIFERATION; HUMANS; LIPID METABOLISM; LUNG NEOPLASMS; MITOCHONDRIA; PROTO-ONCOGENE PROTEINS; RAS PROTEINS;

EID: 84885609770     PISSN: 15548627     EISSN: 15548635     Source Type: Journal    
DOI: 10.4161/auto.26123     Document Type: Article

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