PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 2650818

Cellular oxygen utilization during multiple organ failure.

G Gutierrez·N Lund·C W Bryan-Brown
View original source ↗Export metadata ↓

Abstract

Organ survival depends on adequate tissue oxygenation and normal metabolic function. In MSOF there are changes in O2 transport and cellular bioenergetics. These metabolic alterations may set in motion mechanisms of cellular damage that will affect microcirculatory control and the ability of the cell to maintain both function and homeostasis.

Explore related subjects

Adenosine TriphosphateHumansMicrocirculationMultiple Organ FailureOxygen ConsumptionOxyhemoglobinsShock, SepticJournal ArticleResearch Support, U.S. Gov't, P.H.S.Review

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G Gutierrez, N Lund, C W Bryan-Brown. 1989. Cellular oxygen utilization during multiple organ failure.. https://pubmed.ncbi.nlm.nih.gov/2650818/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2022

The human mitochondrial genome contains a second light strand promoter.

The human mitochondrial genome must be replicated and expressed in a timely manner to maintain energy metabolism and supply cells with adequate levels of adenosine triphosphate. Central to this process is the idea that replication primers and gene products both arise via transcription from a single light strand promoter (LSP) such that primer formation can influence gene expression, with no consensus as to how this is regulated. Here, we report the discovery of a second light strand promoter (LSP2) in humans, with features characteristic of a bona fide mitochondrial promoter. We propose that the position of LSP2 on the mitochondrial genome allows replication and gene expression to be orchestrated from two distinct sites, which expands our long-held understanding of mitochondrial gene expression in humans.

Adenosine Triphosphate↗
PubMed2021

GCN2 kinase activation by ATP-competitive kinase inhibitors.

Small-molecule kinase inhibitors represent a major group of cancer therapeutics, but tumor responses are often incomplete. To identify pathways that modulate kinase inhibitor response, we conducted a genome-wide knockout (KO) screen in glioblastoma cells treated with the pan-ErbB inhibitor neratinib. Loss of general control nonderepressible 2 (GCN2) kinase rendered cells resistant to neratinib, whereas depletion of the GADD34 phosphatase increased neratinib sensitivity. Loss of GCN2 conferred neratinib resistance by preventing binding and activation of GCN2 by neratinib. Several other Food and Drug Administration (FDA)-approved inhibitors, such erlotinib and sunitinib, also bound and activated GCN2. Our results highlight the utility of genome-wide functional screens to uncover novel mechanisms of drug action and document the role of the integrated stress response (ISR) in modulating the response to inhibitors of oncogenic kinases.

Adenosine Triphosphate↗
PubMed1992

31P NMR studies of the ATP/alpha-crystallin complex: functional implications.

Evidence is presented for the binding of ATP to alpha-crystallin in the lens by 31P NMR spectroscopic measurements. The chemical shift data as well as the T1 and T2 values indicate that P beta and P gamma of ATP are of prime importance in binding. In addition, it is demonstrated that the association of alpha-crystallin with purified fiber cell membranes is significantly enhanced by the addition of ATP. These results suggest that ATP modulates the functional behavior of alpha-crystallin.

Adenosine Triphosphate↗