Gene interactions and pathways from curated databases and text-mining

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HDAC6 — HSP90AA1

Pathways - manually collected, often from reviews:

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Takakura et al., Nucleic Acids Res 2001 : Telomerase activation by histone deacetylase inhibitor in normal cells
Bali et al., J Biol Chem 2005 (Leukemia) : Depletion of HDAC6 levels also inhibited the binding of HSP90 to ATP, reduced the chaperone association of HSP90 with its client proteins, e.g. Bcr-Abl, and induced polyubiquitylation and partial depletion of Bcr-Abl
Regan et al., Int J Oncol 2011 (Neuroblastoma) : In addition, Hsp90 inhibition reduced HDAC6 expression and enhanced tubulin acetylation
Li et al., Cell Death Differ 2011 : The underlying mechanism is SAHA 's inhibition of HDAC6 , an essential positive regulator of HSP90
Espallergues et al., J Neurosci 2012 (Disease Models, Animal) : We provide pharmacological and genetic evidence indicating that the cytoplasmic lysine deacetylase HDAC6 controls Hsp90 acetylation in the brain, and thereby modulates Hsp90-GR protein-protein interactions, as well as hormone- and stress induced GR translocation, with a critical impact on GR downstream signaling and behavior