Hypoxia signals autophagy in tumor cells via AMPK activity, independent of HIF-1, BNIP3, and BNIP3L. (Q39972651)

16 September 2017

title

Hypoxia signals autophagy in tumor cells via AMPK activity, independent of HIF-1, BNIP3, and BNIP3L. (English)

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16 September 2017

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I Papandreou

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16 September 2017

A L Lim

series ordinal

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16 September 2017

K Laderoute

series ordinal

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16 September 2017

N C Denko

series ordinal

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16 September 2017

publication date

13 June 2008

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Cell Death & Differentiation

16 September 2017

published in

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16 September 2017

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16 September 2017

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16 September 2017

page(s)

1572-1581

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Hypoxia in cancer: significance and impact on clinical outcome

16 September 2017

cites work

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Anoxia-induced apoptosis occurs through a mitochondria-dependent pathway in lung epithelial cells

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BNIP3 is an RB/E2F target gene required for hypoxia-induced autophagy

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The energy sensing LKB1-AMPK pathway regulates p27(kip1) phosphorylation mediating the decision to enter autophagy or apoptosis

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Beclin 1, an autophagy gene essential for early embryonic development, is a haploinsufficient tumor suppressor

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Transcription factor HIF-1 is a necessary mediator of the pasteur effect in mammalian cells.

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Hypoxia induces autophagic cell death in apoptosis-competent cells through a mechanism involving BNIP3.

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Mitochondrial autophagy is an HIF-1-dependent adaptive metabolic response to hypoxia

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The response of c-jun/AP-1 to chronic hypoxia is hypoxia-inducible factor 1 alpha dependent.

21 January 2018

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Anoxia is necessary for tumor cell toxicity caused by a low-oxygen environment

21 January 2018

1 reference

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inferred from DOI database lookup

7 January 2021

based on heuristic

Identifiers

DOI

10.1038/CDD.2008.84

1 reference

16 September 2017

1 reference