Linked Life Data

19443606

Source:http://linkedlifedata.com/resource/pubmed/id/19443606

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2009-6-16
pubmed:abstractText
Fully grown mammalian oocytes are arrested at the first meiotic prophase until a surge of gonadotrophin at the mid-cycle. The actions of gonadotrophins, follicle stimulating hormone (FSH) and luteinizing hormone (LH), on oocyte meiotic resumption are believed to be mediated in large part through increasing the production of cyclic adenosine 3',5'-monophosphate and subsequent activation of mitogen-activated protein kinase (MAPK) in its surrounding cumulus granulosa cells. Recent findings indicate that gonadotrophins-induced epidermal growth factor-like growth factors, meiosis activating sterol and gonadal steroid hormones, possibly via protein kinase A II and protein kinase C pathways, are involved in the activation of MAPK. Another second messenger cyclic guanosine 3',5'-monophosphate induced by nitric oxide or natriuretic peptides system mediates the function of gonadotrophins during oocyte meiotic resumption. FSH and LH induced pathways may either directly overlap or each hormone may utilize redundant pathways in oocyte maturation. A detailed appreciation of different FSH and LH-activated signaling pathways in mammalian oocytes will be needed in understanding their actions in follicular development and oocyte maturation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
1460-2407
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
399-409
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
The signal pathway of gonadotrophins-induced mammalian oocyte meiotic resumption.
pubmed:affiliation
State Key Laboratory for Agrobiotechnology, College of Biological Sciences, China Agricultural University, Beijing, P.R. China.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't