PTEN modulates GDNF/RET mediated chemotaxis and branching morphogenesis in the developing kidney
The RET receptor tyrosine kinase is activated by GDNF and controls outgrowth and invasion of the ureteric bud epithelia in the developing kidney. In renal epithelial cells and in enteric neuronal precursor cells, activation of RET results in chemotaxis as Ret expressing cells invade the surrounding...
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| Veröffentlicht in: | Developmental biology 2007-07, Vol.307 (2), p.290-299 |
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| creator | Kim, Doyeob Dressler, Gregory R. |
| description | The RET receptor tyrosine kinase is activated by GDNF and controls outgrowth and invasion of the ureteric bud epithelia in the developing kidney. In renal epithelial cells and in enteric neuronal precursor cells, activation of RET results in chemotaxis as Ret expressing cells invade the surrounding GDNF expressing tissue. One potential downstream signaling pathway governing RET mediated chemotaxis may require phosphatidylinositol 3-kinase (PI3K), which generates PI(3,4,5) triphosphate. The
PTEN tumor suppressor gene encodes a protein and lipid phosphatase that regulates cell growth, apoptosis and many other cellular processes. PTEN helps regulate cellular chemotaxis by antagonizing the PI3K signaling pathway through dephosphorylation of phosphotidylinositol triphosphates. In this report, we show that PTEN suppresses RET mediated cell migration and chemotaxis in cell culture assays, that RET activation results in asymmetric localization of inositol triphosphates and that loss of PTEN affects the pattern of branching morphogenesis in developing mouse kidneys. These data suggest a critical role for the PI3K/PTEN axis in shaping the pattern of epithelial branches in response to RET activation. |
| doi_str_mv | 10.1016/j.ydbio.2007.04.051 |
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PTEN tumor suppressor gene encodes a protein and lipid phosphatase that regulates cell growth, apoptosis and many other cellular processes. PTEN helps regulate cellular chemotaxis by antagonizing the PI3K signaling pathway through dephosphorylation of phosphotidylinositol triphosphates. In this report, we show that PTEN suppresses RET mediated cell migration and chemotaxis in cell culture assays, that RET activation results in asymmetric localization of inositol triphosphates and that loss of PTEN affects the pattern of branching morphogenesis in developing mouse kidneys. These data suggest a critical role for the PI3K/PTEN axis in shaping the pattern of epithelial branches in response to RET activation.</description><identifier>ISSN: 0012-1606</identifier><identifier>EISSN: 1095-564X</identifier><identifier>DOI: 10.1016/j.ydbio.2007.04.051</identifier><identifier>PMID: 17540362</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Branching morphogenesis ; Cell Line ; Cell Movement ; Chemotaxis ; Dogs ; GDNF ; Glial Cell Line-Derived Neurotrophic Factor - genetics ; Glial Cell Line-Derived Neurotrophic Factor - metabolism ; Green Fluorescent Proteins - metabolism ; Kidney - cytology ; Kidney - embryology ; Kidney - metabolism ; Mice ; Mice, Transgenic ; Morphogenesis ; Mutation ; Phosphatidylinositol 3-Kinases - metabolism ; Phosphatidylinositol Phosphates - metabolism ; Proto-Oncogene Proteins c-ret - genetics ; Proto-Oncogene Proteins c-ret - metabolism ; PTEN ; PTEN Phosphohydrolase - genetics ; PTEN Phosphohydrolase - metabolism ; Recombinant Proteins - metabolism ; RET ; Signal Transduction</subject><ispartof>Developmental biology, 2007-07, Vol.307 (2), p.290-299</ispartof><rights>2007 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-1ce5df4412404604ecfd332e2a74501b25754bf711aae3a20d3608e438ecfc953</citedby><cites>FETCH-LOGICAL-c488t-1ce5df4412404604ecfd332e2a74501b25754bf711aae3a20d3608e438ecfc953</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S001216060700872X$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,3537,27903,27904,65309</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17540362$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Doyeob</creatorcontrib><creatorcontrib>Dressler, Gregory R.</creatorcontrib><title>PTEN modulates GDNF/RET mediated chemotaxis and branching morphogenesis in the developing kidney</title><title>Developmental biology</title><addtitle>Dev Biol</addtitle><description>The RET receptor tyrosine kinase is activated by GDNF and controls outgrowth and invasion of the ureteric bud epithelia in the developing kidney. In renal epithelial cells and in enteric neuronal precursor cells, activation of RET results in chemotaxis as Ret expressing cells invade the surrounding GDNF expressing tissue. One potential downstream signaling pathway governing RET mediated chemotaxis may require phosphatidylinositol 3-kinase (PI3K), which generates PI(3,4,5) triphosphate. The
PTEN tumor suppressor gene encodes a protein and lipid phosphatase that regulates cell growth, apoptosis and many other cellular processes. PTEN helps regulate cellular chemotaxis by antagonizing the PI3K signaling pathway through dephosphorylation of phosphotidylinositol triphosphates. In this report, we show that PTEN suppresses RET mediated cell migration and chemotaxis in cell culture assays, that RET activation results in asymmetric localization of inositol triphosphates and that loss of PTEN affects the pattern of branching morphogenesis in developing mouse kidneys. These data suggest a critical role for the PI3K/PTEN axis in shaping the pattern of epithelial branches in response to RET activation.</description><subject>Animals</subject><subject>Branching morphogenesis</subject><subject>Cell Line</subject><subject>Cell Movement</subject><subject>Chemotaxis</subject><subject>Dogs</subject><subject>GDNF</subject><subject>Glial Cell Line-Derived Neurotrophic Factor - genetics</subject><subject>Glial Cell Line-Derived Neurotrophic Factor - metabolism</subject><subject>Green Fluorescent Proteins - metabolism</subject><subject>Kidney - cytology</subject><subject>Kidney - embryology</subject><subject>Kidney - metabolism</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Morphogenesis</subject><subject>Mutation</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>Phosphatidylinositol Phosphates - metabolism</subject><subject>Proto-Oncogene Proteins c-ret - genetics</subject><subject>Proto-Oncogene Proteins c-ret - metabolism</subject><subject>PTEN</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>PTEN Phosphohydrolase - metabolism</subject><subject>Recombinant Proteins - metabolism</subject><subject>RET</subject><subject>Signal Transduction</subject><issn>0012-1606</issn><issn>1095-564X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtvEzEUhS0EoqHwC5DQrNjN9PoxrwVIqKQtUlUQChI747HvZBwmdmpPIvLvcZqIxwZWlny_c-6xDyEvKRQUaHWxKvams75gAHUBooCSPiIzCm2Zl5X4-pjMACjLaQXVGXkW4woAeNPwp-SM1qUAXrEZ-fZpMb_L1t5sRzVhzK7f311dfJ4vsjUam25Mpgdc-0n9sDFTzmRdUE4P1i2TKGwGv0SHMc2sy6YBM4M7HP3mMP9ujcP9c_KkV2PEF6fznHy5mi8ub_Lbj9cfLt_d5lo0zZRTjaXphaBMgKhAoO4N5wyZqkUJtGNlitz1NaVKIVcMDK-gQcGbROq25Ofk7dF3s-1Sdo1uCmqUm2DXKuylV1b-PXF2kEu_k4yyNm1NBq9PBsHfbzFOcm2jxnFUDv02yhqqVpRN_V-QtnUFddsmkB9BHXyMAftfaSjIQ4VyJR8qlIcKJQiZKkyqV38-5Lfm1FkC3hwBTN-5sxhk1BadToUF1JM03v5zwU_F5K9X</recordid><startdate>20070715</startdate><enddate>20070715</enddate><creator>Kim, Doyeob</creator><creator>Dressler, Gregory R.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><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>7QR</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20070715</creationdate><title>PTEN modulates GDNF/RET mediated chemotaxis and branching morphogenesis in the developing kidney</title><author>Kim, Doyeob ; Dressler, Gregory R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c488t-1ce5df4412404604ecfd332e2a74501b25754bf711aae3a20d3608e438ecfc953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Branching morphogenesis</topic><topic>Cell Line</topic><topic>Cell Movement</topic><topic>Chemotaxis</topic><topic>Dogs</topic><topic>GDNF</topic><topic>Glial Cell Line-Derived Neurotrophic Factor - genetics</topic><topic>Glial Cell Line-Derived Neurotrophic Factor - metabolism</topic><topic>Green Fluorescent Proteins - metabolism</topic><topic>Kidney - cytology</topic><topic>Kidney - embryology</topic><topic>Kidney - metabolism</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Morphogenesis</topic><topic>Mutation</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>Phosphatidylinositol Phosphates - metabolism</topic><topic>Proto-Oncogene Proteins c-ret - genetics</topic><topic>Proto-Oncogene Proteins c-ret - metabolism</topic><topic>PTEN</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>PTEN Phosphohydrolase - metabolism</topic><topic>Recombinant Proteins - metabolism</topic><topic>RET</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Doyeob</creatorcontrib><creatorcontrib>Dressler, Gregory R.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Developmental biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Doyeob</au><au>Dressler, Gregory R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PTEN modulates GDNF/RET mediated chemotaxis and branching morphogenesis in the developing kidney</atitle><jtitle>Developmental biology</jtitle><addtitle>Dev Biol</addtitle><date>2007-07-15</date><risdate>2007</risdate><volume>307</volume><issue>2</issue><spage>290</spage><epage>299</epage><pages>290-299</pages><issn>0012-1606</issn><eissn>1095-564X</eissn><abstract>The RET receptor tyrosine kinase is activated by GDNF and controls outgrowth and invasion of the ureteric bud epithelia in the developing kidney. In renal epithelial cells and in enteric neuronal precursor cells, activation of RET results in chemotaxis as Ret expressing cells invade the surrounding GDNF expressing tissue. One potential downstream signaling pathway governing RET mediated chemotaxis may require phosphatidylinositol 3-kinase (PI3K), which generates PI(3,4,5) triphosphate. The
PTEN tumor suppressor gene encodes a protein and lipid phosphatase that regulates cell growth, apoptosis and many other cellular processes. PTEN helps regulate cellular chemotaxis by antagonizing the PI3K signaling pathway through dephosphorylation of phosphotidylinositol triphosphates. In this report, we show that PTEN suppresses RET mediated cell migration and chemotaxis in cell culture assays, that RET activation results in asymmetric localization of inositol triphosphates and that loss of PTEN affects the pattern of branching morphogenesis in developing mouse kidneys. These data suggest a critical role for the PI3K/PTEN axis in shaping the pattern of epithelial branches in response to RET activation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17540362</pmid><doi>10.1016/j.ydbio.2007.04.051</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Branching morphogenesis Cell Line Cell Movement Chemotaxis Dogs GDNF Glial Cell Line-Derived Neurotrophic Factor - genetics Glial Cell Line-Derived Neurotrophic Factor - metabolism Green Fluorescent Proteins - metabolism Kidney - cytology Kidney - embryology Kidney - metabolism Mice Mice, Transgenic Morphogenesis Mutation Phosphatidylinositol 3-Kinases - metabolism Phosphatidylinositol Phosphates - metabolism Proto-Oncogene Proteins c-ret - genetics Proto-Oncogene Proteins c-ret - metabolism PTEN PTEN Phosphohydrolase - genetics PTEN Phosphohydrolase - metabolism Recombinant Proteins - metabolism RET Signal Transduction |
| title | PTEN modulates GDNF/RET mediated chemotaxis and branching morphogenesis in the developing kidney |
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