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Drug-Target Interaction

Drug

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PubChem ID:445154
Structure:
Synonyms:
"trans-3,4′,5-trihydroxystilbene"
(E)-5-(2-(4-hydroxyphenyl)ethenyl)-1,3-benzenediol
(E)-5-(p-Hydroxystyryl)resorcinol
(E)-5-[2-(4-hydroxyphenyl)ethenyl]-1,3-benzendiol
(E)-5-[2-(4-Hydroxyphenyl)ethenyl]-1,3-benzenediol
(E)-resveratrol
1,3-Benzenediol, 5-(2-(4-hydroxyphenyl)ethenyl)-, (E)-
1,3-Benzenediol, 5-(2-(4-hydroxyphenyl)ethenyl)-, (E)-;
3,4',5-Stilbenetriol
3,4',5-trihydroxy-stilbene
3,4',5-Trihydroxy-trans-stilbene
3,4',5-Trihydroxystilbene
3,5,4'-Trihydroxy-trans-stilbene
3,5,4'-Trihydroxystilbene
3,5-Dihydroxy-4'-methoxystilbene
31100-06-8
31100-06-8 (DELETED)
34092_FLUKA
34092_RIEDEL
5-((1E)-2-(4-Hydroxyphenyl)ethenyl)-1,3-benzenediol
5-[(1E)-2-(4-Hydroxyphenyl)ethenyl]-1,3-benzenediol
5-[(1E)-2-(4-hydroxyphenyl)ethenyl]benzene-1,3-diol
5-[(1E)-2-(4-hydroxyphenyl)vinyl]benzene-1,3-diol
5-[(E)-2-(4-hydroxyphenyl)ethenyl]benzene-1,3-diol
5-[(E)-2-(4-hydroxyphenyl)vinyl]benzene-1,3-diol
5-[2-(4-hydroxyphenyl)ethenyl]benzene-1,3-diol
501-36-0
533C1DA0-4104-42B5-9D32-9265F40857E4
AC-727
AC1L9HIC
AIDS-025474
AIDS025474
BB_NC-2570
BPBio1_000479
BRD-K25591257-001-01-2
BRD-K80738081-001-06-2
BRD-K80738081-001-10-4
BSPBio_000435
BSPBio_001114
BSPBio_003461
C03582
C059514
C14H12O3
CCG-38874
CCRIS 8952
CHEBI:27881
CHEBI:45713
CHEMBL165
CPD-83
CPD000058206
CU-01000001503-3
DB02709
EU-0101111
FT-0082623
HMS1362H15
HMS1569F17
HMS1792H15
HMS1921N04
HMS1990H15
HMS2052I09
HMS2096F17
HMS2232A18
HMS3263O04
HSDB 7571
I06-0437
IDI1_002152
KSC-10-164
KUC104385N
LMPK13090005
Lopac0_001111
LS-2146
LUKBXSAWLPMMSZ-OWOJBTEDSA-
MLS000069735
MLS001055357
MLS001076538
MLS002207121
MLS002222231
MolPort-002-499-801
NCGC00017352-05
NCGC00017352-06
NCGC00017352-07
NCGC00017352-08
NCGC00017352-09
NCGC00017352-10
NCGC00017352-11
NCGC00017352-12
NCGC00017352-13
NCGC00017352-14
NCGC00017352-15
NCGC00017352-16
NCGC00017352-17
NCGC00017352-18
NCGC00017352-19
NCGC00024003-00
NCGC00024003-04
NCGC00024003-05
NCGC00024003-06
NCGC00024003-07
NCGC00024003-08
NCGC00024003-09
NCGC00024003-10
NCGC00024003-11
NCGC00024003-12
NCGC00024003-13
NCGC00024003-14
nchembio.140-comp2
nchembio.281-comp10
NSC 327430
NSC327430
Prestwick2_000508
Prestwick3_000508
Prestwick_619
PREVENTION 8 (RESVERATROL)
R 5010
R0071
R5010_SIGMA
Resveratrol
Resveratrol, E-
resveratrol-3-sulfate
Resveratrol-Supplied by Selleck Chemicals
Resvida
RM-1812
RV
S1396_Selleck
SAM001246888
SDCCGMLS-0002998.P003
SGCUT00007
SMR000058206
SPECTRUM1502223
Spectrum5_000552
SRT 501
SRT-501
SRT501
ST057251
STL
TL8003323
to_000079
trans-1,2-(3,4',5-Trihydroxydiphenyl)ethylene
trans-3,4′,5-Trihydroxystilbene
trans-3,4',5-trihydroxystilbene
trans-Resveratrol
ZINC00006787

Target

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Uniprot ID:AKT1_MOUSE
Synonyms:
AKT1 kinase
C-AKT
PKB
Protein kinase B
RAC-alpha serine/threonine-protein kinase
RAC-PK-alpha
Thymoma viral proto-oncogene
EC-Numbers:2.7.11.1
Organism:Mouse
Mus musculus
PDB IDs:-

Binding Affinities:

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

References:

18562309
Resveratrol inhibits cardiac hypertrophy via AMP-activated protein kinase and Akt.. Anita Y M Chan; Vernon W Dolinsky; Carrie-Lynn M Soltys; Benoit Viollet; Shairaz Baksh; Peter E Light; Jason R B Dyck (2008) The Journal of biological chemistry display abstract
Whereas studies involving animal models of cardiovascular disease demonstrated that resveratrol is able to inhibit hypertrophic growth, the mechanisms involved have not been elucidated. Because studies in cells other than cardiomyocytes revealed that AMP-activated protein kinase (AMPK) and Akt are affected by resveratrol, we hypothesized that resveratrol prevents cardiac myocyte hypertrophy via these two kinase systems. Herein, we demonstrate that resveratrol reduces phenylephrine-induced protein synthesis and cell growth in rat cardiac myocytes via alterations of intracellular pathways involved in controlling protein synthesis (p70S6 kinase and eukaryotic elongation factor-2). Additionally, we demonstrate that resveratrol negatively regulates the calcineurin-nuclear factor of activated T cells pathway thus modifying a critical component of the transcriptional mechanism involved in pathological cardiac hypertrophy. Our data also indicate that these effects of resveratrol are mediated via AMPK activation and Akt inhibition, and in the case of AMPK, is dependent on the presence of the AMPK kinase, LKB1. Taken together, our data suggest that resveratrol exerts anti-hypertrophic effects by activating AMPK via LKB1 and inhibiting Akt, thus suppressing protein synthesis and gene transcription.