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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:DNAS1_HUMAN
Synonyms:
Deoxyribonuclease I
Deoxyribonuclease-1
DNase I
Dornase alfa
EC-Numbers:3.1.21.1
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

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

References:

14734806
Histone deacetylase (HDAC) inhibitor activation of p21WAF1 involves changes in promoter-associated proteins, including HDAC1.. C-Y Gui; L Ngo; W S Xu; V M Richon; P A Marks (2004) Proceedings of the National Academy of Sciences of the United States of America display abstract
Histone deacetylase (HDAC) inhibitors (HDACi) cause cancer cell growth arrest and/or apoptosis in vivo and in vitro. The HDACi suberoylanilide hydroxamic acid (SAHA) is in phase I/II clinical trials showing significant anticancer activity. Despite wide distribution of HDACs in chromatin, SAHA alters the expression of few genes in transformed cells. p21(WAF1) is one of the most commonly induced. SAHA does not alter the expression of p27(KIPI), an actively transcribed gene, or globin, a silent gene, in ARP-1 cells. Here we studied SAHA-induced changes in the p21(WAF1) promoter of ARP-1 cells to better understand the mechanism of HDACi gene activation. Within 1 h, SAHA caused modifications in acetylation and methylation of core histones and increased DNase I sensitivity and restriction enzyme accessibility in the p21(WAF1) promoter. These changes did not occur in the p27(KIPI) or epsilon-globin gene-related histones. The HDACi caused a marked decrease in HDAC1 and Myc and an increase in RNA polymerase II in proteins bound to the p21(WAF1) promoter. Thus, this study identifies effects of SAHA on p21(WAF1)-associated proteins that explain, at least in part, the selective effect of HDACi in altering gene expression.