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STAT3, HIF-1, glucose addiction and Warburg effect
Author(s) -
James Darnell
Publication year - 2010
Publication title -
aging
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.473
H-Index - 90
ISSN - 1945-4589
DOI - 10.18632/aging.100239
Subject(s) - signal transduction , cancer research , jak stat signaling pathway , phosphorylation , stat3 , tyrosine phosphorylation , biology , kinase , tyrosine kinase , tyrosine kinase 2 , cancer , receptor tyrosine kinase , stat , socs3 , microbiology and biotechnology , receptor , biochemistry , genetics , growth factor , platelet derived growth factor receptor
Oncogenes as the center of cancer research focused attention 30 years ago on signal transduction especially tyrosine phosphorylation. Discovery that the Jun oncoprotein was a site-specific DNA binding protein demanded a connection of signaling abnormalities with transcriptional control [1]. The cytokine responsive Jak-STAT pathway, discovered through studying α-interferon activation of STATs 1 and 2 by the Jak tyrosine kinases (Tyk2, Jak1, Jak2) was soon broadened to include the other five STATs [2]. The first description of STAT3 in 1994 [3] raised suspicion in the direction of cancer because IL-6 and EGF, already recognized to have cancer connections, were the originally recognized ligands that activated the STAT3 homodimer.

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