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Drug-Target Interaction

Drug

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PubChem ID:5311
Structure:
Synonyms:
149647-78-9
1zz1
4-Dimethylamino-N-(6-hydroxycarbamoylhexyl)benzamide
AC-1923
AC1L1K2K
AIDS-186714
AIDS186714
BRD-K81418486-001-10-3
C111237
CCRIS 8456
CHEBI:45716
CHEMBL98
D06320
DB02546
EC-000.2057
FT-0082592
HMS2219L20
HMS3264D20
LS-186548
LS-186997
LS-187780
M344
M344 compound
MK-0683
MK0683
MLS001065855
N'-hydroxy-N-phenyloctanediamide
N-Hydroxy-7-(4-dimethylaminobenzoyl)aminoheptanamide
N-Hydroxy-N'-phenyl octanediamide
N-hydroxy-N'-phenyl-octane-1,8-diotic acid diamide
N-hydroxy-N'-phenyloctanediamide
N-Hyrdroxy-N'-phenyloctanediamide
N1-hydroxy-N8-phenyloctanediamide
NCGC00168085-01
NCGC00168085-02
NCGC00168085-03
NCGC00168085-04
nchembio.275-comp2
nchembio.313-comp1
nchembio815-comp18
NHNPODA
NSC-701852
NSC701852
Octanediamide, N-hydroxy-N'-phenyl-
OCTANEDIOIC ACID HYDROXYAMIDE PHENYLAMIDE
P111011
S1047_Selleck
SAHA
SAHA cpd
SAHA, Suberoylanilide hydroxamic acid
SHH
SKI390
SMR000486344
Suberanilohydroxamic acid
Suberoylanilide hydroxamic acid
Suberoylanilide hydroxamic acid (SAHA)
SW-064652
UNII-58IFB293JI
Vorinostat
Vorinostat (JAN/USAN)
Vorinostat (USAN)
Vorinostat MSD
Vorinostat [USAN]
Vorinostat-Supplied by Selleck Chemicals
WIN64652
ZINC01543873
Zolinza
Zolinza (TN)
Zolinza, MK-0683, SAHA
ATC-Codes:

Target

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Uniprot ID:Q9H2M2_HUMAN
Synonyms:
Estrogen receptor alpha
EC-Numbers:-
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

18342836
Histone deacetylase inhibitor SAHA induces ERalpha degradation in breast cancer MCF-7 cells by CHIP-mediated ubiquitin pathway and inhibits survival signaling.. Xin Yi; Wei Wei; Sheng-Yu Wang; Zhi-Yan Du; Yuan-Ji Xu; Xiao-Dan Yu (2008) Biochemical pharmacology display abstract
Estrogen receptor alpha (ERalpha) plays an important role in the development and progression of breast cancer, and recent studies showed that ERalpha expression is associated with resistance to hormonal therapy. Therefore, a number of studies have explored ways to deplete ERalpha from breast cancer cells as a new therapy especially for hormone-refractory breast cancer. We reported here that suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, effectively depletes ERalpha in breast cancer MCF-7 cells. However, the intrinsic mechanisms by which SAHA decreases ERalpha levels are not clear. Our present data demonstrated that both inhibition of ERalpha mRNA level and promotion of ERalpha degradation by the proteasome contribute to SAHA-induced ERalpha depletion, indicating that SAHA may exert its effects through transcriptional and posttranslational mechanisms. Furthermore, the decrease of ERalpha protein level in MCF-7 cells after SAHA treatment is mainly the result of its rapid degradation by the ubiquitin-proteasome pathway rather than transcriptional inhibition. In addition, we showed that inactivation of the heat shock protein-90 (Hsp90) is involved in SAHA-induced ERalpha degradation, and ubiquitin ligase CHIP (C-terminal Hsc70 interacting protein) enhances SAHA-induced ERalpha degradation. SAHA-induced ERalpha depletion is paralleled with reduction of transcriptional activity of ERalpha and SAHA is able to effectively inhibit cell proliferation and induce apoptosis of MCF-7 cells. Taken together, our results revealed a mechanism for SAHA-induced ERalpha degradation and indicated that SAHA is a suitable pharmacological agent for depletion of ERalpha and a potential choice for breast cancer expressing high ERalpha.