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Growth Arrest-Specific Gene 6 (Gas6)/Adhesion Related Kinase (Ark) Signaling Promotes Gonadotropin-Releasing Hormone Neuronal Survival via Extracellular Signal-Regulated Kinase (ERK) and Akt
We identified Ark, the mouse homolog of the receptor tyrosine kinase Axl (Ufo, Tyro7), in a screen for novel factors involved in GnRH neuronal migration by using differential-display PCR on cell lines derived at two windows during GnRH neuronal development. Ark is expressed in Gn10 GnRH cells, devel...
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Published in: | Molecular endocrinology (Baltimore, Md.) Md.), 1999-02, Vol.13 (2), p.191-201 |
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container_title | Molecular endocrinology (Baltimore, Md.) |
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creator | Allen, Melissa P Zeng, Chan Schneider, Kristina Xiong, Xiaoyan Meintzer, Mary Kay Bellosta, Paola Basilico, Claudio Varnum, Brian Heidenreich, Kim A Wierman, Margaret E |
description | We identified Ark, the mouse homolog of the
receptor tyrosine kinase Axl (Ufo, Tyro7), in a screen for novel
factors involved in GnRH neuronal migration by using
differential-display PCR on cell lines derived at two windows during
GnRH neuronal development. Ark is expressed in Gn10 GnRH cells,
developed from a tumor in the olfactory area when GnRH neurons are
migrating, but not in GT1–7 cells, derived from a tumor in the
forebrain when GnRH neurons are postmigratory. Since Ark (Axl)
signaling protects from programmed cell death in fibroblasts, we
hypothesized that it may play an antiapoptotic role in GnRH neurons.
Gn10 (Ark positive) GnRH cells were more resistant to serum
withdrawal-induced apoptosis than GT1–7 (Ark negative) cells, and this
effect was augmented with the addition of Gas6, the Ark (Axl) ligand.
Gas6/Ark stimulated the extracellular signal-regulated kinase, ERK, and
the serine-threonine kinase, Akt, a downstream component of the
phosphoinositide 3-kinase (PI3-K) pathway. To determine whether ERK or
Akt activation is required for the antiapoptotic effects of Gas6/Ark in
GnRH neurons, cells were serum starved in the absence or presence of
Gas6, with or without inhibitors of ERK and PI3-K signaling cascades.
Gas6 rescued Gn10 cells from apoptosis, and this effect was blocked by
coincubation of the cells with the mitogen-activated protein/ERK kinase
(MEK) inhibitor, PD98059, or wortmannin (but not rapamycin).
These data support an important role for Gas6/Ark signaling via the ERK
and PI3-K (via Akt) pathways in the protection of GnRH neurons from
programmed cell death across neuronal migration. |
doi_str_mv | 10.1210/mend.13.2.0230 |
format | article |
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receptor tyrosine kinase Axl (Ufo, Tyro7), in a screen for novel
factors involved in GnRH neuronal migration by using
differential-display PCR on cell lines derived at two windows during
GnRH neuronal development. Ark is expressed in Gn10 GnRH cells,
developed from a tumor in the olfactory area when GnRH neurons are
migrating, but not in GT1–7 cells, derived from a tumor in the
forebrain when GnRH neurons are postmigratory. Since Ark (Axl)
signaling protects from programmed cell death in fibroblasts, we
hypothesized that it may play an antiapoptotic role in GnRH neurons.
Gn10 (Ark positive) GnRH cells were more resistant to serum
withdrawal-induced apoptosis than GT1–7 (Ark negative) cells, and this
effect was augmented with the addition of Gas6, the Ark (Axl) ligand.
Gas6/Ark stimulated the extracellular signal-regulated kinase, ERK, and
the serine-threonine kinase, Akt, a downstream component of the
phosphoinositide 3-kinase (PI3-K) pathway. To determine whether ERK or
Akt activation is required for the antiapoptotic effects of Gas6/Ark in
GnRH neurons, cells were serum starved in the absence or presence of
Gas6, with or without inhibitors of ERK and PI3-K signaling cascades.
Gas6 rescued Gn10 cells from apoptosis, and this effect was blocked by
coincubation of the cells with the mitogen-activated protein/ERK kinase
(MEK) inhibitor, PD98059, or wortmannin (but not rapamycin).
These data support an important role for Gas6/Ark signaling via the ERK
and PI3-K (via Akt) pathways in the protection of GnRH neurons from
programmed cell death across neuronal migration.</description><identifier>ISSN: 0888-8809</identifier><identifier>EISSN: 1944-9917</identifier><identifier>DOI: 10.1210/mend.13.2.0230</identifier><language>eng</language><publisher>Endocrine Society</publisher><ispartof>Molecular endocrinology (Baltimore, Md.), 1999-02, Vol.13 (2), p.191-201</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3040-1197ad433f63c5673598ea1e2f6d6ab094a8d85cfcb1b12dd1f339cab471d3f83</citedby><cites>FETCH-LOGICAL-c3040-1197ad433f63c5673598ea1e2f6d6ab094a8d85cfcb1b12dd1f339cab471d3f83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><creatorcontrib>Allen, Melissa P</creatorcontrib><creatorcontrib>Zeng, Chan</creatorcontrib><creatorcontrib>Schneider, Kristina</creatorcontrib><creatorcontrib>Xiong, Xiaoyan</creatorcontrib><creatorcontrib>Meintzer, Mary Kay</creatorcontrib><creatorcontrib>Bellosta, Paola</creatorcontrib><creatorcontrib>Basilico, Claudio</creatorcontrib><creatorcontrib>Varnum, Brian</creatorcontrib><creatorcontrib>Heidenreich, Kim A</creatorcontrib><creatorcontrib>Wierman, Margaret E</creatorcontrib><title>Growth Arrest-Specific Gene 6 (Gas6)/Adhesion Related Kinase (Ark) Signaling Promotes Gonadotropin-Releasing Hormone Neuronal Survival via Extracellular Signal-Regulated Kinase (ERK) and Akt</title><title>Molecular endocrinology (Baltimore, Md.)</title><description>We identified Ark, the mouse homolog of the
receptor tyrosine kinase Axl (Ufo, Tyro7), in a screen for novel
factors involved in GnRH neuronal migration by using
differential-display PCR on cell lines derived at two windows during
GnRH neuronal development. Ark is expressed in Gn10 GnRH cells,
developed from a tumor in the olfactory area when GnRH neurons are
migrating, but not in GT1–7 cells, derived from a tumor in the
forebrain when GnRH neurons are postmigratory. Since Ark (Axl)
signaling protects from programmed cell death in fibroblasts, we
hypothesized that it may play an antiapoptotic role in GnRH neurons.
Gn10 (Ark positive) GnRH cells were more resistant to serum
withdrawal-induced apoptosis than GT1–7 (Ark negative) cells, and this
effect was augmented with the addition of Gas6, the Ark (Axl) ligand.
Gas6/Ark stimulated the extracellular signal-regulated kinase, ERK, and
the serine-threonine kinase, Akt, a downstream component of the
phosphoinositide 3-kinase (PI3-K) pathway. To determine whether ERK or
Akt activation is required for the antiapoptotic effects of Gas6/Ark in
GnRH neurons, cells were serum starved in the absence or presence of
Gas6, with or without inhibitors of ERK and PI3-K signaling cascades.
Gas6 rescued Gn10 cells from apoptosis, and this effect was blocked by
coincubation of the cells with the mitogen-activated protein/ERK kinase
(MEK) inhibitor, PD98059, or wortmannin (but not rapamycin).
These data support an important role for Gas6/Ark signaling via the ERK
and PI3-K (via Akt) pathways in the protection of GnRH neurons from
programmed cell death across neuronal migration.</description><issn>0888-8809</issn><issn>1944-9917</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNp1kLFu2zAQhomiBeqmXTtzjAcpPFGSqVEIXKVI0BZxMgtn8uQwkUmDlNzm5fJspZEsHTrd4cjvP9zH2FcQORQgLvbkTA4yL3JRSPGOLaApy6xpYPWeLYRSKlNKNB_ZpxgfhYCyUrBgL13wv6cH3oZAcco2B9J2sJp35IjX_LzDWC8vWvNA0XrHb2nEiQy_tg4j8fM2PC35xu4cjtbt-K_g936iyDvv0Pgp-IN1WYII4-n9yoe9T8E_aA7px8g3czjaY2qOFvn6zxRQ0zjOI4a31ATv5n93rm-vlxyd4e3T9Jl9GHCM9OWtnrH7b-u7y6vs5mf3_bK9ybQUpcgAmhWaUsqhlrqqV7JqFCFQMdSmxq1oSlRGVXrQW9hCYQwMUjYat-UKjByUPGP5a64OPsZAQ38Ido_huQfRn-z3J_s9yL7oT_YTUL0Caex1sI4OSXDsH_0c0lnxf9xfTx-NTA</recordid><startdate>19990201</startdate><enddate>19990201</enddate><creator>Allen, Melissa P</creator><creator>Zeng, Chan</creator><creator>Schneider, Kristina</creator><creator>Xiong, Xiaoyan</creator><creator>Meintzer, Mary Kay</creator><creator>Bellosta, Paola</creator><creator>Basilico, Claudio</creator><creator>Varnum, Brian</creator><creator>Heidenreich, Kim A</creator><creator>Wierman, Margaret E</creator><general>Endocrine Society</general><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>19990201</creationdate><title>Growth Arrest-Specific Gene 6 (Gas6)/Adhesion Related Kinase (Ark) Signaling Promotes Gonadotropin-Releasing Hormone Neuronal Survival via Extracellular Signal-Regulated Kinase (ERK) and Akt</title><author>Allen, Melissa P ; Zeng, Chan ; Schneider, Kristina ; Xiong, Xiaoyan ; Meintzer, Mary Kay ; Bellosta, Paola ; Basilico, Claudio ; Varnum, Brian ; Heidenreich, Kim A ; Wierman, Margaret E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3040-1197ad433f63c5673598ea1e2f6d6ab094a8d85cfcb1b12dd1f339cab471d3f83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Allen, Melissa P</creatorcontrib><creatorcontrib>Zeng, Chan</creatorcontrib><creatorcontrib>Schneider, Kristina</creatorcontrib><creatorcontrib>Xiong, Xiaoyan</creatorcontrib><creatorcontrib>Meintzer, Mary Kay</creatorcontrib><creatorcontrib>Bellosta, Paola</creatorcontrib><creatorcontrib>Basilico, Claudio</creatorcontrib><creatorcontrib>Varnum, Brian</creatorcontrib><creatorcontrib>Heidenreich, Kim A</creatorcontrib><creatorcontrib>Wierman, Margaret E</creatorcontrib><collection>CrossRef</collection><jtitle>Molecular endocrinology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Allen, Melissa P</au><au>Zeng, Chan</au><au>Schneider, Kristina</au><au>Xiong, Xiaoyan</au><au>Meintzer, Mary Kay</au><au>Bellosta, Paola</au><au>Basilico, Claudio</au><au>Varnum, Brian</au><au>Heidenreich, Kim A</au><au>Wierman, Margaret E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Growth Arrest-Specific Gene 6 (Gas6)/Adhesion Related Kinase (Ark) Signaling Promotes Gonadotropin-Releasing Hormone Neuronal Survival via Extracellular Signal-Regulated Kinase (ERK) and Akt</atitle><jtitle>Molecular endocrinology (Baltimore, Md.)</jtitle><date>1999-02-01</date><risdate>1999</risdate><volume>13</volume><issue>2</issue><spage>191</spage><epage>201</epage><pages>191-201</pages><issn>0888-8809</issn><eissn>1944-9917</eissn><abstract>We identified Ark, the mouse homolog of the
receptor tyrosine kinase Axl (Ufo, Tyro7), in a screen for novel
factors involved in GnRH neuronal migration by using
differential-display PCR on cell lines derived at two windows during
GnRH neuronal development. Ark is expressed in Gn10 GnRH cells,
developed from a tumor in the olfactory area when GnRH neurons are
migrating, but not in GT1–7 cells, derived from a tumor in the
forebrain when GnRH neurons are postmigratory. Since Ark (Axl)
signaling protects from programmed cell death in fibroblasts, we
hypothesized that it may play an antiapoptotic role in GnRH neurons.
Gn10 (Ark positive) GnRH cells were more resistant to serum
withdrawal-induced apoptosis than GT1–7 (Ark negative) cells, and this
effect was augmented with the addition of Gas6, the Ark (Axl) ligand.
Gas6/Ark stimulated the extracellular signal-regulated kinase, ERK, and
the serine-threonine kinase, Akt, a downstream component of the
phosphoinositide 3-kinase (PI3-K) pathway. To determine whether ERK or
Akt activation is required for the antiapoptotic effects of Gas6/Ark in
GnRH neurons, cells were serum starved in the absence or presence of
Gas6, with or without inhibitors of ERK and PI3-K signaling cascades.
Gas6 rescued Gn10 cells from apoptosis, and this effect was blocked by
coincubation of the cells with the mitogen-activated protein/ERK kinase
(MEK) inhibitor, PD98059, or wortmannin (but not rapamycin).
These data support an important role for Gas6/Ark signaling via the ERK
and PI3-K (via Akt) pathways in the protection of GnRH neurons from
programmed cell death across neuronal migration.</abstract><pub>Endocrine Society</pub><doi>10.1210/mend.13.2.0230</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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source | Oxford Journals Online |
title | Growth Arrest-Specific Gene 6 (Gas6)/Adhesion Related Kinase (Ark) Signaling Promotes Gonadotropin-Releasing Hormone Neuronal Survival via Extracellular Signal-Regulated Kinase (ERK) and Akt |
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