◀ Back to HSP90AA1
HSP90AA1 — HSP90B1
Pathways - manually collected, often from reviews:
-
KEGG Pathways in cancer:
Complex of AR-HSP90AA1-HSP90AB1-HSP90B1
→
Complex of AR
(protein-protein, activation)
-
KEGG Prostate cancer:
Complex of AR-HSP90AA1-HSP90AB1-HSP90B1
→
Complex of AR
(protein-protein, activation)
-
KEGG Prostate cancer:
None
→
Complex of AR-HSP90AA1-HSP90AB1-HSP90B1
(protein-compound, activation)
-
KEGG Prostate cancer:
None
→
Complex of AR-HSP90AA1-HSP90AB1-HSP90B1
(protein-compound, activation)
-
KEGG Prostate cancer:
None
→
Complex of AR-HSP90AA1-HSP90AB1-HSP90B1
(protein-compound, activation)
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Tramentozzi et al., Mol Immunol 2008
:
However, the most striking alterations in the cell cytoskeleton, characterized by dramatic rearrangement of actin and increased formation of podosomes, were induced by
Grp94 with IgG, and were
mediated by the enhanced expression of
HSP90
Tramentozzi et al., Cell Stress Chaperones 2011
(MAP Kinase Signaling System) :
Effects of
Grp94 on PBMCs were
mediated by an intense activation of the MEK-ERK1/2 pathway and by an increased expression of
HSP90
Tramentozzi et al., J Cell Mol Med 2011
:
Functioning of the PI3K/Akt pathway was crucially dependent on functional heat-shock protein (HSP)90, and both
Grp94-IgG and CTT caused and
increased expression of
HSP90 , promoting its localization to podosomes ... By preventing the chaperoning capacity of HSP90 with the inhibitor purine-scaffold ( PU ) -H71 that blocked the ATP binding site on HSP90, it was possible to inhibit the expression of Akt and secretion of
HSP90 and MMP-9
induced by
Grp94-IgG , thus completely reversing the angiogenic pattern