HIGD1A Regulates Oxygen Consumption, ROS Production, and AMPK Activity during Glucose Deprivation to Modulate Cell Survival and Tumor Growth (Q28505980)

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English	HIGD1A Regulates Oxygen Consumption, ROS Production, and AMPK Activity during Glucose Deprivation to Modulate Cell Survival and Tumor Growth	scientific journal article

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scholarly article

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24 January 2017

HIGD1A Regulates Oxygen Consumption, ROS Production, and AMPK Activity during Glucose Deprivation to Modulate Cell Survival and Tumor Growth (English)

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24 January 2017

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HIG1 domain family, member 1A

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GOA release 2020-03-11

Michael P. Murphy

9

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Stefanie S Jeffrey

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Kurosh Ameri

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Arman Jahangiri

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Ravi Nagarajan

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Melike Pekmezci

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Vien Nguyen

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Yerem Yeghiazarians

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Emin Maltepe

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Anthony M Rajah

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Kathryn V Tormos

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Matthew L Wheeler

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Timothy A Sanders

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Paolo F Rinaudo

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Joseph F Costello

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Manish K Aghi

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12 February 2015

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24 January 2017

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2 June 2020

891-899

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2 June 2020

Recurrent epimutations activate gene body promoters in primary glioblastoma

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Nuclear localization of the mitochondrial factor HIGD1A during metabolic stress

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AMPK activators suppress cervical cancer cell growth through inhibition of DVL3 mediated Wnt/β-catenin signaling activity

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HIF-1 mediates adaptation to hypoxia by actively downregulating mitochondrial oxygen consumption

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HIF-1-mediated expression of pyruvate dehydrogenase kinase: a metabolic switch required for cellular adaptation to hypoxia

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The AMP-activated protein kinase alpha2 catalytic subunit controls whole-body insulin sensitivity

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Loss of expression of the DRR 1 gene at chromosomal segment 3p21.1 in renal cell carcinoma

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HIF-1 alpha is required for solid tumor formation and embryonic vascularization.

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Cellular and developmental control of O2 homeostasis by hypoxia-inducible factor 1 alpha

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AMPK: a nutrient and energy sensor that maintains energy homeostasis

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Physiological roles of mitochondrial reactive oxygen species

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Dormancy of cancer cells with suppression of AKT activity contributes to survival in chronic hypoxia

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AMPK is a negative regulator of the Warburg effect and suppresses tumor growth in vivo

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Mitochondrial reactive oxygen species enhance AMP-activated protein kinase activation in the endothelium of patients with coronary artery disease and diabetes

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Glucose deprivation activates a metabolic and signaling amplification loop leading to cell death

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Glycolytic phenotype and AMP kinase modify the pathologic response of tumor xenografts to VEGF neutralization

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Identifiers

10.1016/J.CELREP.2015.01.020

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24 January 2017

Europe PubMed Central

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:25683712%20AND%20SRC:MED&resulttype=core&format=json

2 June 2020

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