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Drug-Target Interaction

Drug

show drug details
PubChem ID:289
Structure:
Synonyms:
1,2-benzenediol
1,2-dihydroxybenzene
1,3-dihydroxybenzene
120-80-9
12385-08-9
135011_SIAL
16474-89-8
16474-90-1
2-(5,8-Dihydroxy-1-methoxy-3-methyl(2-naphthyl))-5-methoxy-7-methylnaphthalene-1,4-diol
2-hydroxyphenol
20244-21-7
20244-21-7 (unspecified hydrochloride salt)
37349-32-9
4-06-00-05557 (Beilstein Handbook Reference)
430749_ALDRICH
430749_SIAL
AB-131/40235236
AB1002105
AC1L18WM
AC1Q78GA
AG-D-45381
AI3-03995
AIDS-108194
AIDS108194
AKOS000119002
alpha-hydroxyphenol
BBL002408
BB_NC-2239
Benzcatechin
Benzene, o-dihydroxy-
benzene-1,2-diol
benzenediol
BIDD:ER0327
bmse000385
Brenzcatechin
BRN 0471401
C 9510
C.I. 76500
C.I. Oxidation Base 26
C00090
c0097
C01785
C034221
C15571
C3561_SIAL
C9510_SIAL
C9593_SIGMA
CAQ
Catechin
Catechin (phenol)
CATECHOL
Catechol (phenol)
catechol dipotassium salt
catechol sodium salt
catechol, 14C-labeled cpd
Catechol-pyrocatechol
Catechol-UL-14C
CCG-204375
CCRIS 741
CHEBI:18135
CHEMBL280998
CI 76500
CI Oxidation Base 26
DB02232
Dihydroxybenzene
Durafur developer C
Durafur Developer CFouramine PCH
EINECS 204-427-5
EU-0100280
Fouramine PCH
Fourrine 68
HMS2233A17
HMS3260H22
HSDB 1436
I01-2906
Katechol
Katechol [Czech]
Lopac-C-9510
Lopac0_000280
LS-637
MLS002153385
MLS002303022
MolPort-000-871-939
NCGC00015283-01
NCGC00015283-02
NCGC00015283-03
NCGC00015283-04
NCGC00015283-05
NCGC00015283-06
NCGC00015283-07
NCGC00015283-08
NCGC00091262-01
NCGC00091262-02
NCGC00091262-03
nchembio801-comp10
NCI-C55856
NSC 1573
NSC1573
o Dihydroxybenzene
o-Benzenediol
o-Dihydroxybenzene
o-Dioxybenzene
o-Diphenol
o-Hydroquinone
o-Hydroxyphenol
o-Phenylenediol
ortho-Benzenediol
ortho-Dihydroxybenzene
ortho-Dioxybenzene
ortho-Hydroquinone
ortho-Hydroxyphenol
ortho-Phenylenediol
Oxyphenic acid
P0317
P0567
Pelagol Grey C
phenol derivative, 2
Phthalhydroquinone
pyrocatechin
Pyrocatechine
Pyrocatechinic acid
Pyrocatechinic acidPyrocatechol
pyrocatechol
pyrocatechol-ul-14C
Pyrocatechuic acid
Pyrokatechin
Pyrokatechin [Czech]
Pyrokatechol
Pyrokatechol [Czech]
SMR000326660
ST5214346
STK398651
WLN: QR BQ
ZINC13512214

Target

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Uniprot ID:JUN_MOUSE
Synonyms:
Activator protein 1
AH119
AP1
Jun A
Proto-oncogene c-jun
Transcription factor AP-1
V-jun avian sarcoma virus 17 oncogene homolog
EC-Numbers:-
Organism:Mouse
Mus musculus
PDB IDs:-

Binding Affinities:

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

References:

18095272
Fyn is a novel target of (-)-epigallocatechin gallate in the inhibition of JB6 Cl41 cell transformation.. Zhiwei He; Faqing Tang; Svetlana Ermakova; Ming Li; Qing Zhao; Yong-Yeon Cho; Wei-Ya Ma; Hong-Seok Choi; Ann M Bode; Chung S Yang; Zigang Dong (2008) Molecular carcinogenesis display abstract
The cancer preventive action of (-)-epigallocatechin gallate (EGCG), found in green tea, is strongly supported by epidemiology and laboratory research data. However, the mechanism by which EGCG inhibits carcinogenesis and cell transformation is not clear. In this study, we report that EGCG suppressed epidermal growth factor (EGF)-induced cell transformation in JB6 cells. We also found that EGCG inhibited EGF-induced Fyn kinase activity and phosphorylation in vitro and in vivo. Fyn was implicated in the process because EGF-induced JB6 cell transformation was inhibited by small interfering RNA (siRNA)-Fyn-JB6 cells. With an in vitro protein-binding assay, we found that EGCG directly bound with the GST-Fyn-SH2 domain but not the GST-Fyn-SH3 domain. The K(d) value for EGCG binding to the Fyn SH2 domain was 0.367 +/- 0.122 microM and B(max) was 1.35 +/- 0.128 nmol/mg. Compared with control JB6 Cl41 cells, EGF-induced phosphorylation of p38 MAP kinase (p38 MAPK) (Thr180/Tyr182), ATF-2 (Thr71) and signal transducer and activator of transcription 1 (STAT1) (Thr727) was decreased in siRNA-Fyn-JB6 cells. EGCG could inhibit the phosphorylation of p38 MAPK, ATF-2, and STAT1. The DNA binding ability of AP-1, STAT1, and ATF-2 was also decreased in siRNA-Fyn-JB6 cells. Overall, these results demonstrated that EGCG interacted with Fyn and inhibited Fyn kinase activity and thereby regulated EGF-induced cell transformation. Inhibition of Fyn kinase activity is a novel and important mechanism that may be involved in EGCG-induced inhibition of cell transformation.
9331105
Inhibition of tumor promoter-induced activator protein 1 activation and cell transformation by tea polyphenols, (-)-epigallocatechin gallate, and theaflavins.. Z Dong; W Ma; C Huang; C S Yang (1997) Cancer research display abstract
(-)-Epigallocatechin gallate (EGCG) and theaflavins are believed to be key active components in tea for the chemoprevention against cancer. However, the molecular mechanisms by which EGCG and theaflavins block carcinogenesis are not clear. We have used the JB6 mouse epidermal cell line, a system that has been used extensively as an in vitro model for tumor promotion studies, to examine the anti-tumor promotion effects of EGCG and theaflavins at the molecular level. EGCG and theaflavins inhibited epidermal growth factor- or 12-O-tetradecanoylphorbol-13-acetate-induced cell transformation in a dose-dependent manner. At the dose range (5-20 microM) that inhibited cell transformation, EGCG and theaflavins also inhibited AP-1-dependent transcriptional activity and DNA binding activity. The inhibition of AP-1 activation occurs through the inhibition of a c-Jun NH2-terminal kinase-dependent, but not an extracellular signal-regulated protein kinase (Erk) 1-dependent or Erk2-dependent, pathway. Because the transcription factor AP-1 is important for tumor promoter-induced neoplastic transformation, the inhibitory effects on AP-1 activation by EGCG and theaflavins may further explain the anti-tumor promotion action of these tea constituents.