The Effect of Certain Conditions in the Regulation of Cystathionine γ-Lyase by Exogenous Hydrogen Sulfide in Mammalian Cells

@article{Wang2013TheEO,
  title={The Effect of Certain Conditions in the Regulation of Cystathionine $\gamma$-Lyase by Exogenous Hydrogen Sulfide in Mammalian Cells},
  author={Maoxian Wang and Zhanyun Guo and Shilong Wang},
  journal={Biochemical Genetics},
  year={2013},
  volume={51},
  pages={503-513}
}
Cystathionine γ-lyase (CSE), one of three enzymes in the trans-sulfuration pathway, is responsible for the production of endogenous hydrogen sulfide (H2S) using l-cysteine or l-homocysteine as a substrate. The regulatory mechanism of CSE by exogenous H2S remains unknown. The transcription and expression of the CSE gene regulated by exogenous H2S at approximately physiologic concentrations was investigated using luciferase assay, Western blotting, and quantitative RT-PCR. The results revealed… 

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References

SHOWING 1-10 OF 53 REFERENCES

Cystathionine γ-Lyase Overexpression Inhibits Cell Proliferation via a H2S-dependent Modulation of ERK1/2 Phosphorylation and p21Cip/WAK-1*

The hypothesis that endogenously produced H2S may play a fundamental role in cell proliferation and survival is supported.

Hydrogen sulfide is a novel mediator of lipopolysaccharide‐induced inflammation in the mouse

  • Ling-Xia LiM. Bhatia P. Moore
  • Medicine, Biology
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2005
It is suggested that H2S exhibits proinflammatory activity in endotoxic shock and a new approach to the development of novel drugs for this condition is suggested.

Hydrogen sulfide: its production and functions

It is demonstrated that a third H2S‐producing enzyme, 3‐mercaptopyruvate sulfurtransferase (3MST), is expressed in neurons and vascular endothelium, which reduces reactive oxygen species generated in these organelles and protects neurons from oxidative stress by reinstating the reduced glutathione levels.

3-Mercaptopyruvate sulfurtransferase produces hydrogen sulfide and bound sulfane sulfur in the brain.

3-mercaptopyruvate sulfurtransferase (3MST) in combination with Cysteine aminotransferase (CAT) produces H(2)S from cysteine, and the levels of bound sulfane sulfur are greatly increased in the cells expressing 3MST and CAT but not increased in cells expressing functionally defective mutant enzymes.

L-cysteine inhibits insulin release from the pancreatic beta-cell: possible involvement of metabolic production of hydrogen sulfide, a novel gasotransmitter.

It is suggested here that L-cysteine inhibits insulin release via multiple actions on the insulin secretory process through H(2)S production, which may participate in the deterioration of insulin release in this disease.

Pro‐apoptotic effect of endogenous H2S on human aorta smooth muscle cells

It is demonstrated that overexpression of CSE stimulates SMC apoptosis due to an increased endogenous production of H2S, which may provide a novel therapeutic approach in treating vascular diseases linked to abnormal cellular proliferation and vascular remodeling.

The possible role of hydrogen sulfide as an endogenous smooth muscle relaxant in synergy with nitric oxide.

Hydrogen sulfide (H2S), which is well known as a toxic gas, is produced endogenously in mammalian tissues from L-cysteine mainly by two pyridoxal-5'-phosphate-dependent enzymes, cystathionine

Hydrogen sulfide contributes to hypoxia-induced radioresistance on hepatoma cells.

It is demonstrated that H(2)S contributed to hypoxia-induced radioresistance probably via the opening of K(+)(ATP) channels, which suggests that the endogenous H( 2)S synthase could be a potential radiotherapeutic target for a hypoxic tumor.
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