Linked Life Data

17654825

Source:http://linkedlifedata.com/resource/pubmed/id/17654825

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2007-7-27
pubmed:abstractText
Murine embryonic stem cells (mESC) are capable of unlimiting proliferation with maintenance of pluripotency during long-term cultivation. Signaling pathways regulating the cell cycle of mESC are of the great interest for further investigation. This review concerns to the cell cycle regulation of mESC through different signaling pathways (LIF-STAT3, PI3K-Akt, Wnt-beta-catenin) and to the mechanisms of unlimited proliferation of mESC and their inability to undergo long-term block of proliferation in response to DNA-damaging and stress factors. The functioning of negative cell cycle regulators (cyclin-kinase inhibitors and Rb) and positive cell cycle regulators (cyclin-kinase complexes and E2F factors) are also topics of this review. It is considered that, permanent mitogenic stimuli are needed to prevent induction of apoptosis. Therefore, the agents which cause prolonged halt of proliferation without ongoing onset of differentiation or induction of apoptosis are currently unknown. The main focus is given to the role of the Wnt signaling pathway in sustaining the pluripotent state of mESC. The cell cycle regulation by downstream targets of LIF-STAT3, PI3-kinase and Wnt-beta-catenin pathways is discussed in light of cooperative action of these pathways for maintenance of undifferentiated state of mESC.
pubmed:language
rus
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0041-3771
pubmed:author
pubmed:issnType
Print
pubmed:volume
49
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
370-84
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
[Signaling pathways regulating proliferation of murine embryonic stem cells].
pubmed:publicationType
Journal Article, English Abstract, Review, Research Support, Non-U.S. Gov't