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The Role of TRP Channels in Oxidative Stress-induced Cell Death

Overview of attention for article published in Journal of Membrane Biology, April 2006
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  • Good Attention Score compared to outputs of the same age (65th percentile)
  • Good Attention Score compared to outputs of the same age and source (75th percentile)

Mentioned by

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1 Wikipedia page

Citations

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127 Dimensions

Readers on

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89 Mendeley
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Title
The Role of TRP Channels in Oxidative Stress-induced Cell Death
Published in
Journal of Membrane Biology, April 2006
DOI 10.1007/s00232-005-0839-3
Pubmed ID
Authors

B.A. Miller

Abstract

The transient receptor potential (TRP) protein superfamily is a diverse group of voltage-independent calcium-permeable cation channels expressed in mammalian cells. These channels have been divided into six subfamilies, and two of them, TRPC and TRPM, have members that are widely expressed and activated by oxidative stress. TRPC3 and TRPC4 are activated by oxidants, which induce Na(+) and Ca(2+) entry into cells through mechanisms that are dependent on phospholipase C. TRPM2 is activated by oxidative stress or TNFalpha, and the mechanism involves production of ADP-ribose, which binds to an ADP-ribose binding cleft in the TRPM2 C-terminus. Treatment of HEK 293T cells expressing TRPM2 with H(2)O(2) resulted in Ca(2+) influx and increased susceptibility to cell death, whereas coexpression of the dominant negative isoform TRPM2-S suppressed H(2)O(2)-induced Ca(2+) influx, the increase in [Ca(2+)](i), and onset of apoptosis. U937-ecoR monocytic cells expressing increased levels of TRPM2 also exhibited significantly increased [Ca(2+)](i) and increased apoptosis after treatment with H(2)O(2) or TNFalpha. A dramatic increase in caspase 8, 9, 3, 7, and PARP cleavage was observed in TRPM2-expressing cells, demonstrating a downstream mechanism through which cell death is mediated. Inhibition of endogenous TRPM2 function through three approaches, depletion of TRPM2 by RNA interference, blockade of the increase in [Ca(2+)](i) through TRPM2 by calcium chelation, or expression of the dominant negative splice variant TRPM2-S protected cell viability. H(2)O(2) and amyloid beta-peptide also induced cell death in primary cultures of rat striatal cells, which endogenously express TRPM2. TRPM7 is activated by reactive oxygen species/nitrogen species, resulting in cation conductance and anoxic neuronal cell death, which is rescued by suppression of TRPM7 expression. TRPM2 and TRPM7 channels are physiologically important in oxidative stress-induced cell death.

Mendeley readers

The data shown below were compiled from readership statistics for 89 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Chile 1 1%
United Kingdom 1 1%
Belgium 1 1%
Spain 1 1%
United States 1 1%
Unknown 84 94%

Demographic breakdown

Readers by professional status Count As %
Researcher 24 27%
Student > Ph. D. Student 22 25%
Student > Bachelor 13 15%
Student > Master 11 12%
Professor 9 10%
Other 6 7%
Unknown 4 4%
Readers by discipline Count As %
Agricultural and Biological Sciences 38 43%
Medicine and Dentistry 14 16%
Biochemistry, Genetics and Molecular Biology 9 10%
Neuroscience 9 10%
Immunology and Microbiology 3 3%
Other 9 10%
Unknown 7 8%

Attention Score in Context

This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 29 April 2009.
All research outputs
#3,498,504
of 12,219,721 outputs
Outputs from Journal of Membrane Biology
#99
of 606 outputs
Outputs of similar age
#81,890
of 273,974 outputs
Outputs of similar age from Journal of Membrane Biology
#2
of 8 outputs
Altmetric has tracked 12,219,721 research outputs across all sources so far. This one is in the 49th percentile – i.e., 49% of other outputs scored the same or lower than it.
So far Altmetric has tracked 606 research outputs from this source. They receive a mean Attention Score of 3.2. This one is in the 24th percentile – i.e., 24% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 273,974 tracked outputs that were published within six weeks on either side of this one in any source. This one has gotten more attention than average, scoring higher than 65% of its contemporaries.
We're also able to compare this research output to 8 others from the same source and published within six weeks on either side of this one. This one has scored higher than 6 of them.