Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P21817 (
RyR1
)
1,154
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Since the discovery of nitric oxide (NO) as gaseous signaling molecule, two other gaseous mediators, carbon monoxide (CO) and hydrogen sulfide (H
2
S) have been found to be also involved in many physiological and pathophysiological functions. This review will briefly summarize our recent progress in the pathophysiology of NO and H
2
S. In the photoreceptor cells, the level of intracellular Ca
2+
is kept relatively low by H
2
S. Intraperitoneal injection of H
2
S donor to mice protected photoreceptor cells from light-induced retinal degeneration caused by oxidative stress and elevation of intracellular Ca
2+
. Another gaseous mediator NO induces Ca
2+
release from the endoplasmic reticulum via S-nitrosylated type 1 ryanodine receptor (
RyR1
) Ca
2+
release channel. NO-induced Ca
2+
release (NICR) was abolished in primary cultured neurons from the knock-in mice, in which the S-nitrosylation site Cys-3636 of
RyR1
was replaced by
Ala
(Ryr1
C3636A
). The neurons in hippocampal CA3 region of Ryr1
C3636A
mice were protected against seizure-induced neuronal cell death. The result indicates that NICR is critical for status epilepticus-induced neurodegeneration. The developments in the pathophysiology of gaseous mediators in the central nervous system will provide a better pharmacological advances for the treatment of neurodegenerative diseases.
...
PMID:[Pathophysiological functions of gas mediators in neurodegeneration]. 3039 55
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