Dickey et al. mine / Howard Hughes Medical Institute / University of South Florida / Akt/PAR1/MARK2 complex / CHIP/ Hsp90 complex / University of Pennsylvania Medical School / CHIP/Hsp90 complex / University of South Florida College / Mayo Clinic / University of North Carolina / Hsp90/ CHIP complex / Hsp90 scaffold / Chapel Hill / Hsp90 complex / bridge PAR1/MARK2 / Hsp90/CHIP complex / /
IndustryTerm
reagents/analytic tools / cell culture systems / kinase/chaperone signaling network / stress recovery systems / /
Institute for Diabetes / Obesity and Metabolism / CurePSP / Alzheimer’s Association / Department of Molecular Pharmacology and Physiology / University of Pennsylvania Medical School / Philadelphia / National Academy of Sciences / Metabolism and Howard Hughes Medical Institute / Johns Hopkins University School of Medicine / Division of Cardiology / Florida College / University of North Carolina / Chapel Hill / Lee Moffitt Cancer Center / Department of Neuroscience / American Federation for Aging Research / and National Institutes of Health Grants R01-AG17216-08 / University of South Florida / Tampa / /
Person
Yong-Jie Zhang / Richard Voellemy / Peter Davies / Morris J. Birnbaum / Godfrey V / H. Lee Moffitt / Dave Morgan / Peter Seubert / Mei Sun / Judith Dunmore / Ben Wolozin / John Koren / Bing-Wei Lu / Leonard Petrucelli / Jin Q. Cheng / Carlos Leon / Ann Med / Bobby Monks / Chad A. Dickey / Solomon H. Snyder / Cam Patterson / Rachel M. Bailey / Lester Binder / /
Akt and CHIP coregulate tau degradation through coordinated interactions Chad A. Dickey*†, John Koren*, Yong-Jie Zhang‡, Ya-fei Xu‡, Umesh K. Jinwal*, Morris J. Birnbaum§, Bobby Monks§, Mei Sun¶, Jin Q. Cheng¶,