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Journal ArticleDOI

L-Cysteine promotes the proliferation and differentiation of neural stem cells via the CBS/H₂S pathway.

TLDR
The present data suggest that L-cysteine can enhance proliferation and differentiation of NSCs via the CBS/H2S pathway, which may serve as a useful inference for elucidating its role in regulating the fate of N SCs in physiological and pathological settings.
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This article is published in Neuroscience.The article was published on 2013-05-01. It has received 51 citations till now. The article focuses on the topics: Neural stem cell & Neurogenesis.

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International Union of Basic and Clinical Pharmacology. CII: Pharmacological Modulation of H2S Levels: H2S Donors and H2S Biosynthesis Inhibitors.

TL;DR: The present article overviews the currently known H 2S donors and H2S biosynthesis inhibitors, delineates their mode of action, and offers examples for their biologic effects and potential therapeutic utility.
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H2S and its role in redox signaling

TL;DR: This review focuses on H2S metabolism and provides an overview of the recent literature that sheds some light on its mechanism of action in cellular redox signaling in health and disease.
Journal ArticleDOI

Hydrogen sulfide in signaling pathways.

TL;DR: This review focuses on the metabolism of hydrogen sulfide (including enzymatic pathways of H₂S synthesis from l- and d-cysteine) and its signaling pathways in the cardiovascular system and the nervous system and describes how hydrogen sulfides may be used as therapeutic agent, i.e. in theiovascular diseases.
Journal ArticleDOI

Regulation of mitochondrial bioenergetic function by hydrogen sulfide. Part II. Pathophysiological and therapeutic aspects

TL;DR: The field of H2S‐induced therapeutic ‘suspended animation’ is overview, a concept in which a temporary pharmacological reduction in cell metabolism is achieved, producing a decreased oxygen demand for the experimental therapy of critical illness and/or organ transplantation.
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H2S biosynthesis and catabolism: new insights from molecular studies.

TL;DR: Recently, a number of laboratories have reported the use of siRNA methodologies and genetic mouse models to mimic the loss of function of genes involved in the biosynthesis and degradation of H2S within tissues, revealing new insights into the biology of H20 within the cardiovascular system, inflammatory disease, and in cell signalling.
References
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Journal ArticleDOI

The possible role of hydrogen sulfide as an endogenous neuromodulator

TL;DR: It is shown that physiological concentrations of H2S selectively enhance NMDA receptor-mediated responses and facilitate the induction of hippocampal long-term potentiation, suggesting that endogenous H 2S functions as a neuromodulator in the brain.
Journal ArticleDOI

Stem cells in the central nervous system.

TL;DR: The development of therapies for the reconstruction of the diseased or injured brain will be guided by the understanding of the origin and stability of cell type in the central nervous system.
Journal ArticleDOI

Stem cell therapy for human neurodegenerative disorders-how to make it work.

TL;DR: Findings raise hope for the development of stem cell therapies in human neurodegenerative disorders and need to know much more about how to control stem cell proliferation and differentiation into specific phenotypes, induce their integration into existing neural and synaptic circuits, and optimize functional recovery in animal models closely resembling the human disease.
Journal ArticleDOI

Hydrogen sulfide protects neurons from oxidative stress.

Yuka Kimura, +1 more
- 01 Jul 2004 - 
TL;DR: It is found that H2S increases the glutathione levels, which normally decrease during the cell death cascade, by enhancing the activity of γ‐ glutamylcysteine synthetase and up‐regulating cystine transport.
Journal ArticleDOI

Basic Helix-Loop-Helix Factors in Cortical Development

TL;DR: In this article, bHLH factors have key roles in corticogenesis, affecting the timing of differentiation and the specification of cell fate, and the formation of oligodendrocytes is triggered by an increase in the activity of Olig1 and Olig2, coupled with a decrease in Id activity.
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