Title : VHL-deficient renal cancer cells gain resistance to mitochondria-activating apoptosis inducers by activating AKT through the IGF1R-PI3K pathway.

Pub. Date : 2016 Oct

PMID : 27460078






3 Functional Relationships(s)
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Protein Name
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1 In 2DG-ABT-sensitive cells, a 4-h 2DG treatment caused the dissociation of Mcl-1 from Bak, while ABT treatment alone caused the dissociation of Bcl-xL from Bak without substantially reducing Mcl-1 levels. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid MCL1 apoptosis regulator, BCL2 family member Homo sapiens
2 In 2DG-ABT-sensitive cells, a 4-h 2DG treatment caused the dissociation of Mcl-1 from Bak, while ABT treatment alone caused the dissociation of Bcl-xL from Bak without substantially reducing Mcl-1 levels. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid MCL1 apoptosis regulator, BCL2 family member Homo sapiens
3 In 2DG-ABT-resistant cells, Mcl-1 dissociated from Bak only when AKT activity was inhibited during the 4-h 2DG treatment. 2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid MCL1 apoptosis regulator, BCL2 family member Homo sapiens