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Drug-Target Interaction

Drug

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PubChem ID:2396
Structure:
Synonyms:
"gö 6850"
"insolution™ bisindolylmaleimide i"
133052-90-1
1H-Pyrrole-2,5-dione,
1H-Pyrrole-2,5-dione, 3-(1-(3-(dimethylamino)propyl)-1H-indol-3-yl)-4-(1H-indol-3-yl)-
1uu8
1zrz
2-(1-(3-Dimethylaminopropyl)indol-3-yl)-3-(indol-3-yl)maleimide
2-[1-(3-Dimethylaminopropyl)-1H-indol-3-yl]-3-(1H-indol-3-yl)-maleimide
3-(1-(3-(Dimethylamino)propyl)-1H-indol-3-yl)-4-(1H-indol-3-yl)-1H-pyrrole-2,5-dione
3-{1-[3-(DIMETHYLAMINO)PROPYL]-1H-INDOL-3-YL}-4-(1H-INDOL-3-YL)-1H-PYRROLE-2,5-DIONE
6850
BI1
BIM-1
Bio2_000420
Bio2_000900
BiomolKI2_000039
BiomolKI_000031
BIS-1 cpd
Bisindolylmaleimide I
bisindoylmaleimide I
BSPBio_001160
C070515
C11238
C25H24N4O2
Gö 6850
GF 109203X
GF-109203X
GF109203X
GFX 203290
Go 6850
Go-6850
HSCI1_000290
IDI1_002175
IN1033
IN1518
IN1521
InSolution™ Bisindolylmaleimide I
KBio2_000500
KBio2_003068
KBio2_005636
KBio3_000919
KBio3_000920
KBioGR_000500
KBioSS_000500
LS-172856
NCGC00024760-01
NCGC00024760-02
NCGC00024760-03
NCGC00024760-04
nchembio.154-comp5
RBT205 INHIBITOR
Tocris-0741

Target

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Uniprot ID:PK3C3_HUMAN
Synonyms:
Phosphatidylinositol 3-kinase catalytic subunit type 3
Phosphatidylinositol 3-kinase p100 subunit
Phosphoinositide-3-kinase class 3
PI3-kinase type 3
PI3K type 3
PtdIns-3-kinase type 3
EC-Numbers:2.7.1.137
Organism:Homo sapiens
Human
PDB IDs:-

Binding Affinities:

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

References:

10710511
Protein kinase C modulates insulin action in human skeletal muscle.. R N Cortright; J L AzevedoJr; Q Zhou; M Sinha; W J Pories; S I Itani; G L Dohm (2000) American journal of physiology. Endocrinology and metabolism display abstract
There is good evidence from cell lines and rodents that elevated protein kinase C (PKC) overexpression/activity causes insulin resistance. Therefore, the present study determined the effects of PKC activation/inhibition on insulin-mediated glucose transport in incubated human skeletal muscle and primary adipocytes to discern a potential role for PKC in insulin action. Rectus abdominus muscle strips or adipocytes from obese, insulin-resistant, and insulin-sensitive patients were incubated in vitro under basal and insulin (100 nM)-stimulated conditions in the presence of GF 109203X (GF), a PKC inhibitor, or 12-deoxyphorbol 13-phenylacetate 20-acetate (dPPA), a PKC activator. PKC inhibition had no effect on basal glucose transport. GF increased (P < 0.05) insulin-stimulated 2-deoxyglucose (2-DOG) transport approximately twofold above basal. GF plus insulin also increased (P < 0.05) insulin receptor tyrosine phosphorylation 48% and phosphatidylinositol 3-kinase (PI 3-kinase) activity approximately 50% (P < 0.05) vs. insulin treatment alone. Similar results for GF on glucose uptake were observed in human primary adipocytes. Further support for the hypothesis that elevated PKC activity is related to insulin resistance comes from the finding that PKC activation by dPPA was associated with a 40% decrease (P < 0.05) in insulin-stimulated 2-DOG transport. Incubation of insulin-sensitive muscles with GF also resulted in enhanced insulin action ( approximately 3-fold above basal). These data demonstrate that certain PKC inhibitors augment insulin-mediated glucose uptake and suggest that PKC may modulate insulin action in human skeletal muscle.