Evidence map›Paper›PMID 16892082›Full record

ReviewOncogene2006

Mitochondrial hexokinases, novel mediators of the antiapoptotic effects of growth factors and Akt.

R B Robey, N Hay

Abstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 286 papers.

0numbers the graph read from it
0cells of the map it votes in
286citing papers in PubMed
12.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

286 citing papers in PubMed, 531 citations in OpenAlex.

  1. Trial
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  5. The moonlighting functions of glycolytic enzymes in tumorigenesis.Cellular oncology (Dordrecht, Netherlands) · 2026
    Review
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  8. Frontiers in immunology · 2026
    Article
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226 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 1 country.

R B RobeyResearch and Development Service, White River Junction VA Medical Center, White River Junction, VT 05009-0001, USA.
N Hay
University of Illinois Chicago · USWhite River Junction VA Medical Center · US

Funding

PI3K/PTEN/Akt signaling and the genesis of cancerR01CA090764 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI Nissim Hay · 2001 to 2026
$9.4M
The Role of Akt in Cell Survival and Cell GrowthR01AG016927 · NIA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI HAY, NISSIM · 1998 to 2023
$9.0M
NCI NIH HHS CA090764NIA NIH HHS AG016927
6 · The paper itself

Abstract

Cell survival has been closely linked to both trophic growth factor signaling and cellular metabolism. Such couplings have obvious physiologic and pathophysiologic implications, but their underlying molecular bases remain incompletely defined. As a common mediator of both the metabolic and anti-apoptotic effects of growth factors, the serine/threonine kinase Akt - also known as protein kinase B or PKB - is capable of regulating and coordinating these inter-related processes. The glucose dependence of the antiapoptotic effects of growth factors and Akt plus a strong correlation between Akt-regulated mitochondrial hexokinase association and apoptotic susceptibility suggest a major role for hexokinases in these effects. Mitochondrial hexokinases catalyse the first obligatory step of glucose metabolism and directly couple extramitochondrial glycolysis to intramitochondrial oxidative phosphorylation, and are thus well suited to play this role. The ability of Akt to regulate energy metabolism appears to have evolutionarily preceded the capacity to control cell survival. This suggests that Akt-dependent metabolic regulatory functions may have given rise to glucose-dependent antiapoptotic effects that evolved as an adaptive sensing system involving hexokinases and serve to ensure mitochondrial homeostasis, thereby coupling metabolism to cell survival. We hypothesize that the enlistment of Akt and hexokinase in the control of mammalian cell apoptosis evolved as a response to the recruitment of mitochondria to the apoptotic cascade. The central importance of mitochondrial hexokinases in cell survival also suggests that they may represent viable therapeutic targets in cancer.

Indexed as

ApoptosisCell SurvivalGrowth SubstancesHexokinaseHumansMitochondriaNeoplasmsOncogene Protein v-aktGrowth SubstancesHexokinaseOncogene Protein v-akt

Identifiers

PMID16892082
OpenAlexW2026555011

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.