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Drug-Target Interaction

Drug

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PubChem ID:5280445
Structure:
Synonyms:
"3′,4′,5,7-tetrahydroxyflavone"
2-(3,4-Dihydroxyphenyl)-5,7-dihydroxy-4-benzopyrone
2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4H-1-benzopyran-4-one
2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4H-chromen-4-one
2-(3,4-dihydroxyphenyl)-5,7-dihydroxychromen-4-one
23A002A4-B47B-46CD-848C-65042EACF3FF
3′,4′,5,7-Tetrahydroxyflavone
3',4',5,7-Tetrahydroxy-Flavone
3',4',5,7-Tetrahydroxyflavone
491-70-3
4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-
4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5,7-dihydroxy- (9CI)
4H-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-
4H-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-;
5,7,3',4'-Tetrahydroxyflavone
5-18-05-00296 (Beilstein Handbook Reference)
AC-1125
AC1NQX1A
ACon1_000223
AIDS-001406
AIDS001406
AKOS002140588
BB_NC-1244
BIDD:ER0122
BIDD:PXR0059
BPBio1_001011
BRD-K05236810-001-05-9
BRN 0292084
BSPBio_000919
C.I. 75590
C.I. Natural Yellow 2
C01514
C15H10O6
CAS-491-70-3
CCRIS 3790
CHEBI:15864
CHEMBL151
Cyanidenon 1470
D047311
Digitoflavone
EINECS 207-741-0
Flacitran
FLAVONE, 3',4',5,7-TETRAHYDROXY-
HMS1570N21
HMS2097N21
HMS2220C06
I06-0436
IN1269
L 9283
L9283_SIGMA
LMPK12110006
Lopac0_000660
LS-69039
Luteolin
Luteolin, 3',4',5,7-Tetrahydroxyflavone, Luteoline, Luteolol
Luteolin-Supplied by Selleck Chemicals
Luteoline
Luteolol
MEGxp0_000143
MLS000697655
MLS000860038
MLS002154043
MolPort-000-706-683
NCGC00016467-01
NCGC00016467-02
NCGC00016467-03
NCGC00016467-04
NCGC00016467-05
NCGC00016467-06
NCGC00016467-07
NCGC00142375-01
NCGC00142375-02
NCGC00142375-03
NCGC00179375-01
NCGC00179375-02
Oprea1_849964
Prestwick0_000870
Prestwick1_000870
Prestwick2_000870
Prestwick3_000870
Prestwick_122
S00110
S2320_Selleck
Salifazide
SMP2_000042
SMR000326896
SPBio_002840
ST024703
STK801923
TNP00073
Weld Lake
Yama kariyasu
ZINC18185774

Target

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Uniprot ID:AKT1_HUMAN
Synonyms:
C-AKT
PKB
Protein kinase B
RAC-alpha serine/threonine-protein kinase
RAC-PK-alpha
EC-Numbers:2.7.11.1
Organism:Homo sapiens
Human
PDB IDs:1H10 1UNP 1UNQ 1UNR 2UVM 2UZR 2UZS 3CQU 3CQW
Structure:
3CQW

Binding Affinities:

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

References:

16762341
Luteolin inhibits lipopolysaccharide actions on human gingival fibroblasts.. Gloria Gutiérrez-Venegas; Perla Kawasaki-Cárdenas; Santa Rita Arroyo-Cruz; Silvia Maldonado-Frías (2006) European journal of pharmacology display abstract
Periodontal disease comprises a group of infections that lead to inflammation of the gingiva, periodontal tissue destruction, and in severe cases is accompanied by alveolar bone loss with tooth exfoliation. Actinobacillus actinomycetemcomitans is a Gram-negative microorganism, which possesses and produces lipopolysaccharide (LPS) molecules that play a key role in disease development. Human gingival fibroblasts are the major constituents of gingival connective tissue and may interact directly with bacteria and bacterial products including LPS. Flavonoids possess antioxidant and anti-inflammatory properties that reduce inflammatory molecule expression in macrophages and monocytes. In this study, we evaluated the ability of diverse flavonoids to regulate nitric oxide production of LPS-stimulated human gingival fibroblasts, and studied the effect of luteolin on diminish phosphorylation in mitogen-activated protein kinase (MAPK) family members as well as in protein kinase B (Akt), nuclear factor kappa B (NF-kappaB) activation, inducible nitric oxide synthase (NOS) expression, and nitric oxide (NO) synthesis. We also found that pretreatment with three flavonoids, including quercetin, genistein, and luteolin, blocked nitric oxide synthesis in a dose-dependent fashion. Luteolin exerted the strongest blocking action on expression of this inflammatory mediator. Luteolin pretreatment attenuated LPS-induced extracellular signal-regulated kinase, p38, and Akt phosphorylation. LPS treatment of human gingival fibroblasts resulted in NF-kappaB translocation. Cell pretreatment with luteolin abolished LPS effects on NF-kappaB translocation. In addition, luteolin treatment blocked LPS-induced cellular proliferation inhibition without affecting genetic material integrity. We concluded that luteolin interferes with LPS signaling pathways, reducing activation of several mitogen-activated protein kinase family members, and inhibits inflammatory mediator expression.