The novel Akt inhibitor API-1 induces c-FLIP degradation and synergizes with TRAIL to augment apoptosis independent of Akt inhibition.
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Akt inhibitors in cancer treatment: The long journey from drug discovery to clinical use (Review)hnRNPK inhibits GSK3β Ser9 phosphorylation, thereby stabilizing c-FLIP and contributes to TRAIL resistance in H1299 lung adenocarcinoma cells.Effect of API-1 and FR180204 on cell proliferation and apoptosis in human DLD-1 and LoVo colorectal cancer cells.The E3 ubiquitin ligases β-TrCP and FBXW7 cooperatively mediates GSK3-dependent Mcl-1 degradation induced by the Akt inhibitor API-1, resulting in apoptosis.mTOR complex 2 is involved in regulation of Cbl-dependent c-FLIP degradation and sensitivity of TRAIL-induced apoptosis.The proteasome deubiquitinase inhibitor b-AP15 enhances DR5 activation-induced apoptosis through stabilizing DR5.
P2860
The novel Akt inhibitor API-1 induces c-FLIP degradation and synergizes with TRAIL to augment apoptosis independent of Akt inhibition.
description
2012 nî lūn-bûn
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2012年の論文
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2012年論文
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2012年論文
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2012年論文
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2012年論文
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2012年論文
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2012年论文
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2012年论文
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2012年论文
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name
The novel Akt inhibitor API-1 ...... independent of Akt inhibition.
@ast
The novel Akt inhibitor API-1 ...... independent of Akt inhibition.
@en
type
label
The novel Akt inhibitor API-1 ...... independent of Akt inhibition.
@ast
The novel Akt inhibitor API-1 ...... independent of Akt inhibition.
@en
prefLabel
The novel Akt inhibitor API-1 ...... independent of Akt inhibition.
@ast
The novel Akt inhibitor API-1 ...... independent of Akt inhibition.
@en
P2093
P2860
P1476
The novel Akt inhibitor API-1 ...... independent of Akt inhibition.
@en
P2093
P2860
P304
P356
10.1158/1940-6207.CAPR-11-0548
P577
2012-02-16T00:00:00Z