Histone H2AX-dependent GABAA receptor regulation of stem cell proliferation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2008-01-09

AUTHORS

Michael Andäng, Jens Hjerling-Leffler, Annalena Moliner, T. Kalle Lundgren, Gonçalo Castelo-Branco, Evanthia Nanou, Ester Pozas, Vitezslav Bryja, Sophie Halliez, Hiroshi Nishimaru, Johannes Wilbertz, Ernest Arenas, Martin Koltzenburg, Patrick Charnay, Abdeljabbar El Manira, Carlos F. Ibañez, Patrik Ernfors

ABSTRACT

Stem cell renewalStem cell self-renewal involves the maintenance of pluripotency under continued proliferation. Proliferation of embryonic stem cells was thought to be constitutive and not to be regulated, because the normal cell cycle regulatory mechanism is not active in these cells. Now Andäng et al. present evidence for a fundamentally new mechanism of cell cycle regulation operating in embryonic stem cells and in other tissue-specific stem cell types. In it, endogenous GABA receptor signalling controls cell proliferation via a mechanism that involves cell cycle proteins previously associated with the cellular DNA damage checkpoint pathway. More... »

PAGES

460-464

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature06488

DOI

http://dx.doi.org/10.1038/nature06488

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1007182941

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18185516


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34 schema:description Stem cell renewalStem cell self-renewal involves the maintenance of pluripotency under continued proliferation. Proliferation of embryonic stem cells was thought to be constitutive and not to be regulated, because the normal cell cycle regulatory mechanism is not active in these cells. Now Andäng et al. present evidence for a fundamentally new mechanism of cell cycle regulation operating in embryonic stem cells and in other tissue-specific stem cell types. In it, endogenous GABA receptor signalling controls cell proliferation via a mechanism that involves cell cycle proteins previously associated with the cellular DNA damage checkpoint pathway.
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