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The mechanism of CSF arrest in vertebrate oocytes
A cytoplasmic activity in mature oocytes responsible for second meiotic metaphase arrest was identified over 30 years ago in amphibian oocytes. In Xenopus oocytes cytostatic factor (CSF) activity is initiated by the progesterone-dependent synthesis of Mos, a MAPK kinase kinase that activates the MAP...
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Published in: | Molecular and cellular endocrinology 2002-02, Vol.187 (1), p.173-178 |
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creator | Maller, James L Schwab, Markus S Gross, Stefan D Taieb, Frédéric E Roberts, B.Tibor Tunquist, Brian J |
description | A cytoplasmic activity in mature oocytes responsible for second meiotic metaphase arrest was identified over 30 years ago in amphibian oocytes. In
Xenopus oocytes cytostatic factor (CSF) activity is initiated by the progesterone-dependent synthesis of Mos, a MAPK kinase kinase that activates the MAPK pathway. CSF arrest is mediated by a sole MAPK target, the protein kinase p90
Rsk. Rsk phosphorylates and activates the Bub1 protein kinase, which may cause metaphase arrest due to inhibition of the anaphase-promoting complex (APC) by a conserved mechanism defined genetically in yeast and mammalian cells. CSF arrest in vertebrate oocytes by p90
Rsk provides a link between the MAPK pathway and the spindle assembly checkpoint in the cell cycle. |
doi_str_mv | 10.1016/S0303-7207(01)00695-5 |
format | article |
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Xenopus oocytes cytostatic factor (CSF) activity is initiated by the progesterone-dependent synthesis of Mos, a MAPK kinase kinase that activates the MAPK pathway. CSF arrest is mediated by a sole MAPK target, the protein kinase p90
Rsk. Rsk phosphorylates and activates the Bub1 protein kinase, which may cause metaphase arrest due to inhibition of the anaphase-promoting complex (APC) by a conserved mechanism defined genetically in yeast and mammalian cells. CSF arrest in vertebrate oocytes by p90
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Xenopus oocytes cytostatic factor (CSF) activity is initiated by the progesterone-dependent synthesis of Mos, a MAPK kinase kinase that activates the MAPK pathway. CSF arrest is mediated by a sole MAPK target, the protein kinase p90
Rsk. Rsk phosphorylates and activates the Bub1 protein kinase, which may cause metaphase arrest due to inhibition of the anaphase-promoting complex (APC) by a conserved mechanism defined genetically in yeast and mammalian cells. CSF arrest in vertebrate oocytes by p90
Rsk provides a link between the MAPK pathway and the spindle assembly checkpoint in the cell cycle.</description><subject>Animals</subject><subject>Bub1</subject><subject>Cell Cycle - physiology</subject><subject>Cytostatic factor</subject><subject>Female</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>MAP Kinase Signaling System - physiology</subject><subject>MAPK</subject><subject>Meiosis</subject><subject>Oocyte maturation</subject><subject>Oocytes - cytology</subject><subject>Oocytes - metabolism</subject><subject>Proto-Oncogene Proteins c-mos - physiology</subject><subject>Rsk</subject><subject>Spindle assembly checkpoint</subject><subject>Vertebrates - physiology</subject><issn>0303-7207</issn><issn>1872-8057</issn><issn>0303-7207</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNqFkE1LAzEQhoMotn78BGVPoofVmWSzSU8ixS8oeLD3kM1OaKTb1WRb8N-7dUs9ehoYnved4WHsAuEWAcu7dxAgcsVBXQPeAJQTmcsDNkateK5BqkM23iMjdpLSBwAoyfUxGyFOtBZcjhnOF5Q15BZ2FVKTtT6bvj9lNkZKXRZW2YZiR1W0HWVt6747SmfsyNtlovPdPGXzp8f59CWfvT2_Th9muStK7HKrK-dlLWoqnSisk2VFUEwqZUkit1jryleV5c47jcqhJ0DurKCCe3JenLKboXZhl-YzhsbGb9PaYF4eZma7A16qiRbFBnv2amA_Y_u17j83TUiOlku7onadjMJSqUKIHpQD6GKbUiS_b0YwW63mV6vZOjOA5lerkX3ucndgXTVU_6V2HnvgfgCoN7IJFE1ygVaO6hDJdaZuwz8nfgAtGoac</recordid><startdate>20020222</startdate><enddate>20020222</enddate><creator>Maller, James L</creator><creator>Schwab, Markus S</creator><creator>Gross, Stefan D</creator><creator>Taieb, Frédéric E</creator><creator>Roberts, B.Tibor</creator><creator>Tunquist, Brian J</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-9612-2069</orcidid></search><sort><creationdate>20020222</creationdate><title>The mechanism of CSF arrest in vertebrate oocytes</title><author>Maller, James L ; Schwab, Markus S ; Gross, Stefan D ; Taieb, Frédéric E ; Roberts, B.Tibor ; Tunquist, Brian J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-a8bcf5d3de6c34ac56be049b7ae512a1d8bfbba2cfc817c1fe012ca3e42fecf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Bub1</topic><topic>Cell Cycle - physiology</topic><topic>Cytostatic factor</topic><topic>Female</topic><topic>Humans</topic><topic>Life Sciences</topic><topic>MAP Kinase Signaling System - physiology</topic><topic>MAPK</topic><topic>Meiosis</topic><topic>Oocyte maturation</topic><topic>Oocytes - cytology</topic><topic>Oocytes - metabolism</topic><topic>Proto-Oncogene Proteins c-mos - physiology</topic><topic>Rsk</topic><topic>Spindle assembly checkpoint</topic><topic>Vertebrates - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maller, James L</creatorcontrib><creatorcontrib>Schwab, Markus S</creatorcontrib><creatorcontrib>Gross, Stefan D</creatorcontrib><creatorcontrib>Taieb, Frédéric E</creatorcontrib><creatorcontrib>Roberts, B.Tibor</creatorcontrib><creatorcontrib>Tunquist, Brian J</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Molecular and cellular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maller, James L</au><au>Schwab, Markus S</au><au>Gross, Stefan D</au><au>Taieb, Frédéric E</au><au>Roberts, B.Tibor</au><au>Tunquist, Brian J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The mechanism of CSF arrest in vertebrate oocytes</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2002-02-22</date><risdate>2002</risdate><volume>187</volume><issue>1</issue><spage>173</spage><epage>178</epage><pages>173-178</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><eissn>0303-7207</eissn><abstract>A cytoplasmic activity in mature oocytes responsible for second meiotic metaphase arrest was identified over 30 years ago in amphibian oocytes. In
Xenopus oocytes cytostatic factor (CSF) activity is initiated by the progesterone-dependent synthesis of Mos, a MAPK kinase kinase that activates the MAPK pathway. CSF arrest is mediated by a sole MAPK target, the protein kinase p90
Rsk. Rsk phosphorylates and activates the Bub1 protein kinase, which may cause metaphase arrest due to inhibition of the anaphase-promoting complex (APC) by a conserved mechanism defined genetically in yeast and mammalian cells. CSF arrest in vertebrate oocytes by p90
Rsk provides a link between the MAPK pathway and the spindle assembly checkpoint in the cell cycle.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>11988325</pmid><doi>10.1016/S0303-7207(01)00695-5</doi><tpages>6</tpages><orcidid>https://orcid.org/0000-0001-9612-2069</orcidid></addata></record> |
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subjects | Animals Bub1 Cell Cycle - physiology Cytostatic factor Female Humans Life Sciences MAP Kinase Signaling System - physiology MAPK Meiosis Oocyte maturation Oocytes - cytology Oocytes - metabolism Proto-Oncogene Proteins c-mos - physiology Rsk Spindle assembly checkpoint Vertebrates - physiology |
title | The mechanism of CSF arrest in vertebrate oocytes |
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