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Journal ArticleDOI

Glyoxal and methylglyoxal trigger distinct signals for map family kinases and caspase activation in human endothelial cells.

TLDR
It is demonstrated that GO and MGO triggered two distinct signal cascades, one for PTK-dependent control of ERK and another forPTK-independent redox-linked activation of JNK/p38 MAPK and caspases in HUVECs, depending on the structure of the carbon skeleton of the chemicals.
About
This article is published in Free Radical Biology and Medicine.The article was published on 2001-07-01. It has received 134 citations till now. The article focuses on the topics: Staurosporine & MAPK/ERK pathway.

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Aldehyde sources, metabolism, molecular toxicity mechanisms, and possible effects on human health.

TL;DR: The human health risks from clinical and animal research studies are reviewed, including aldehydes as haptens in allergenic hypersensitivity diseases, respiratory allergies, and idiosyncratic drug toxicity; the potential carcinogenic risks of the carbonyl body burden.
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Intervention strategies to inhibit protein carbonylation by lipoxidation-derived reactive carbonyls.

TL;DR: This review focuses on fundamental studies on lipid‐derived RCS generation, their biological effects, and their reactivity with proteins, with particular emphasis to 4‐hydroxy‐trans‐2‐nonenal (HNE)‐, acrolein‐, malondialdehyde‐, and glyoxal (GO)‐modified proteins.
Journal ArticleDOI

The tandem of free radicals and methylglyoxal.

TL;DR: It is arrived at that a tight junction exists between methylglyoxal toxicity and free radical (particularly ROS) generation, though the toxicity of 1,2-dicarbonyl evolves even under anaerobic conditions, too.
Journal ArticleDOI

Reactive carbonyls and oxidative stress: potential for therapeutic intervention.

TL;DR: The metabolism of reactive carbonyls is described and the potential for manipulating levels of carbonyl-metabolizing enzymes through chemical intervention is discussed.
Journal ArticleDOI

Oxidative stress and aging: is methylglyoxal the hidden enemy?

TL;DR: The potential role of MG in the aging process through increasing oxidative stress besides causing AGEs formation is discussed and specific and effective scavengers and crosslink breakers of MG and A GEs are being developed and can become potential treatments to slow the Aging process and prevent many diseases.
References
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Journal ArticleDOI

Chemistry and biochemistry of 4-hydroxynonenal, malonaldehyde and related aldehydes.

TL;DR: This review provides a comprehensive summary on the chemical properties of 4-hydroxyalkenals and malonaldehyde, the mechanisms of their formation and their occurrence in biological systems and methods for their determination, as well as the many types of biological activities described so far.
Journal ArticleDOI

Opposing Effects of ERK and JNK-p38 MAP Kinases on Apoptosis

TL;DR: The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells.
Journal ArticleDOI

Specificity of receptor tyrosine kinase signaling: Transient versus sustained extracellular signal-regulated kinase activation

Christopher J. Marshall
- 27 Jan 1995 - 
TL;DR: Experiments with PC12 cells suggest that the duration of ERK activation is critical for cell signaling decisions, and the extracellular signal-regulated kinase (ERK-regulated) MAPK pathway may be sufficient for these cellular responses.
Journal ArticleDOI

The MAPK signaling cascade.

TL;DR: This review highlights primarily the first MAPK cascade to be discovered that uses the MEK and ERK isoforms and describes their involvement in different cellular processes, and it is now known that signaling pathways initiated by phorbol esters, iono‐phors, heat shock, and liganda for seven transmembrane receptors use distinct MAPK cascades with little or no cross‐reactivity between them.
Journal ArticleDOI

A protein kinase involved in the regulation of inflammatory cytokine biosynthesis.

TL;DR: Production of interleukin-1 and tumour necrosis factor from stimulated human monocytes is inhibited by a new series of pyridinyl-imidazole compounds, suggesting that the CSBPs are critical for cytokine production.
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