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Drug-Target Interaction

Drug

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PubChem ID:3006531
Structure:
Synonyms:
(2Z,3Z)-2,3-bis[amino-(2-aminophenyl)sulfanylmethylidene]butanedinitrile
(2Z,3Z)-bis{amino[(2-aminophenyl)sulfanyl]methylidene}butanedinitrile
1,4-diamino-2,3-dicyano-1,4-bis(2-aminophenylthio)butadiene
1,4-Diamino-2,3-dicyano-1,4-bis(o-aminophenylmercapto)butadiene
109511-58-2
5BM
AC1MHKLF
AIDS-186610
AIDS186610
BiomolKI2_000012
BiomolKI_000002
BMK1-B2
BRD-K18787491-001-04-5
BSPBio_001224
Butanedinitrile, bis(amino((2-aminophenyl)thio)methylene)-
C113580
CCG-100606
CHEBI:257660
CHEMBL34704
HMS1362N05
HMS1792N05
HMS1990N05
IDI1_002207
LS-182537
MolPort-006-069-048
NCGC00025029-02
NCGC00025029-03
NCGC00025029-04
nchembio.282-comp1
nchembio.496-comp3
SMP2_000197
Succinonitrile, bis(amino(o-aminophenylthio)methylene)-
U 0126
U-0126
U0126
U0126 cpd
U126 cpd
UO 126
UO-126
UO126

Target

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Uniprot ID:MK03_HUMAN
Synonyms:
ERK-1
ERT2
Extracellular signal-regulated kinase 1
Insulin-stimulated MAP2 kinase
MAP kinase 1
MAPK 1
Microtubule-associated protein 2 kinase
Mitogen-activated protein kinase 3
p44-ERK1
p44-MAPK
EC-Numbers:2.7.11.24
Organism:Homo sapiens
Human
PDB IDs:2ZOQ
Structure:
2ZOQ

Binding Affinities:

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

References:

12446589
Progestin and G protein-coupled receptor 30 inhibit mitogen-activated protein kinase activity in MCF-7 breast cancer cells.. Tytti M Ahola; Niina Alkio; Tommi Manninen; Timo Ylikomi (2002) Endocrinology display abstract
We have previously shown that the G protein-coupled receptor (GPR)30 is critical for progestin-induced growth inhibition. In this study, we addressed signal transduction pathways involved in progestin-mediated signaling. Progestin could not provide any additional growth inhibitory effect to MCF-7 cells treated with specific MAPK kinase inhibitors, PD98059 and U0126. Medroxyprogesteroneacetate (MPA) induced a late (22-23 h) decrease in ERK-1 and -2 activities verified by immunoblotting and kinase assay. The inactivation was abrogated by antiprogestin. Transient expression of GPR30 decreased ERK-1 and -2 activity; and in the cells in which GPR30 expression was decreased by the antisense, ERK activities were increased. The antisense-expressing cells were able to significantly resist the growth-inhibitory effect of the MAPK kinase inhibitors PD98059 and U0126 but not that of other factors tested. Interestingly, the decrease of ERK activity induced by MPA was abrogated by GPR30 antisense. Collectively, these results show that MAPK activity is inhibited by progestin and GPR30 and suggest that progestin-induced ERK inactivation is mediated through GPR30. Coupled with our previous findings, the data imply that up-regulation of GPR30 by progestin leads to ERK-1 and -2 inactivation associated with MPA-induced growth inhibition.