Inhibition of RhoA pathway rescues the endocytosis defects in Oligophrenin1 mouse model of mental retardation
The patho-physiological hypothesis of mental retardation caused by the deficiency of the RhoGAP Oligophrenin1 (OPHN1), relies on the well-known functions of Rho GTPases on neuronal morphology, i.e. dendritic spine structure. Here, we describe a new function of this Bin/Amphiphysin/Rvs domain contain...
Gespeichert in:
| Veröffentlicht in: | Human molecular genetics 2009-07, Vol.18 (14), p.2575-2583 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 2583 |
|---|---|
| container_issue | 14 |
| container_start_page | 2575 |
| container_title | Human molecular genetics |
| container_volume | 18 |
| creator | Khelfaoui, Malik Pavlowsky, Alice Powell, Andrew D. Valnegri, Pamela Cheong, Kenneth W. Blandin, Yann Passafaro, Maria Jefferys, John G.R. Chelly, Jamel Billuart, Pierre |
| description | The patho-physiological hypothesis of mental retardation caused by the deficiency of the RhoGAP Oligophrenin1 (OPHN1), relies on the well-known functions of Rho GTPases on neuronal morphology, i.e. dendritic spine structure. Here, we describe a new function of this Bin/Amphiphysin/Rvs domain containing protein in the control of clathrin-mediated endocytosis (CME). Through interactions with Src homology 3 domain containing proteins involved in CME, OPHN1 is concentrated to endocytic sites where it down-regulates the RhoA/ROCK signaling pathway and represses the inhibitory function of ROCK on endocytosis. Indeed disruption of Ophn1 in mice reduces the endocytosis of synaptic vesicles and the post-synaptic α-amino-3-hydroxy-5-methylisoazol-4-propionate (AMPA) receptor internalization, resulting in almost a complete loss of long-term depression in the hippocampus. Finally, pharmacological inhibition of this pathway by ROCK inhibitors fully rescued not only the CME deficit in OPHN1 null cells but also synaptic plasticity in the hippocampus from Ophn1 null model. Altogether, we uncovered a new patho-physiological mechanism for intellectual disabilities associated to mutations in RhoGTPases linked genes and also opened new directions for therapeutic approaches of congenital mental retardation. |
| doi_str_mv | 10.1093/hmg/ddp189 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2701329</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><oup_id>10.1093/hmg/ddp189</oup_id><sourcerecordid>1760787391</sourcerecordid><originalsourceid>FETCH-LOGICAL-c635t-70cd2b4e3fb26d2d7fef7638519aae4cff95c33a69d27a17c13b4fdcbb5e72c03</originalsourceid><addsrcrecordid>eNqFkl1rFDEYhQdR7LZ64w-QQdALcWy-JpncCEupbnWhIEqLNyGTj53UmWRMZqv7782yy1Z7oTfJRZ6c876HUxTPIHgLAcen3bA61XqEDX9QzCChoEKgwQ-LGeCUVJQDelQcp3QDAKQEs8fFEeQEQMSbWTFc-M61bnLBl8GWn7swL0c5dT_lpowmqbVJ5dSZ0ngd1GYKyaVSG2vUlErny8vercLYReOdh-UQ1snkU5t-KzYYP8k-y0wyarm1eFI8srJP5un-Pim-vj__craolpcfLs7my0pRXE8VA0qjlhhsW0Q10swayyhuasilNERZy2uFsaRcIyYhUxC3xGrVtrVhSAF8Urzb6Y7rdjBa5UGi7MUY3SDjRgTpxN8v3nViFW4FYgBixLPAm51Ad-_bYr4UzicTBwEAQTlGcgsz_mrvF8OPHNkkBpeU6XvpTc5EUEYgQQ39L4gAYIQ0LIMv7oE3YR19Dk0gCBEElGzXfL2DVAwpRWMPo0IgttUQuRpiV40MP_8zkzt034UMvNwDMinZ2yi9cunAoVwegCi_48J6_LdhteNcmsyvAynj95wHZrVYXH8T7NPVxxpeMXGNfwNysuAr</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>211210640</pqid></control><display><type>article</type><title>Inhibition of RhoA pathway rescues the endocytosis defects in Oligophrenin1 mouse model of mental retardation</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Khelfaoui, Malik ; Pavlowsky, Alice ; Powell, Andrew D. ; Valnegri, Pamela ; Cheong, Kenneth W. ; Blandin, Yann ; Passafaro, Maria ; Jefferys, John G.R. ; Chelly, Jamel ; Billuart, Pierre</creator><creatorcontrib>Khelfaoui, Malik ; Pavlowsky, Alice ; Powell, Andrew D. ; Valnegri, Pamela ; Cheong, Kenneth W. ; Blandin, Yann ; Passafaro, Maria ; Jefferys, John G.R. ; Chelly, Jamel ; Billuart, Pierre</creatorcontrib><description>The patho-physiological hypothesis of mental retardation caused by the deficiency of the RhoGAP Oligophrenin1 (OPHN1), relies on the well-known functions of Rho GTPases on neuronal morphology, i.e. dendritic spine structure. Here, we describe a new function of this Bin/Amphiphysin/Rvs domain containing protein in the control of clathrin-mediated endocytosis (CME). Through interactions with Src homology 3 domain containing proteins involved in CME, OPHN1 is concentrated to endocytic sites where it down-regulates the RhoA/ROCK signaling pathway and represses the inhibitory function of ROCK on endocytosis. Indeed disruption of Ophn1 in mice reduces the endocytosis of synaptic vesicles and the post-synaptic α-amino-3-hydroxy-5-methylisoazol-4-propionate (AMPA) receptor internalization, resulting in almost a complete loss of long-term depression in the hippocampus. Finally, pharmacological inhibition of this pathway by ROCK inhibitors fully rescued not only the CME deficit in OPHN1 null cells but also synaptic plasticity in the hippocampus from Ophn1 null model. Altogether, we uncovered a new patho-physiological mechanism for intellectual disabilities associated to mutations in RhoGTPases linked genes and also opened new directions for therapeutic approaches of congenital mental retardation.</description><identifier>ISSN: 0964-6906</identifier><identifier>EISSN: 1460-2083</identifier><identifier>DOI: 10.1093/hmg/ddp189</identifier><identifier>PMID: 19401298</identifier><identifier>CODEN: HNGEE5</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Adult and adolescent clinical studies ; Animals ; Biological and medical sciences ; Cell physiology ; Cytoskeletal Proteins ; Cytoskeletal Proteins - chemistry ; Cytoskeletal Proteins - genetics ; Cytoskeletal Proteins - metabolism ; Disease Models, Animal ; Down-Regulation ; Endocytosis ; Fundamental and applied biological sciences. Psychology ; Genetics of eukaryotes. Biological and molecular evolution ; GTPase-Activating Proteins ; GTPase-Activating Proteins - chemistry ; GTPase-Activating Proteins - genetics ; GTPase-Activating Proteins - metabolism ; Humans ; Intellectual deficiency ; Intellectual Disability - genetics ; Intellectual Disability - metabolism ; Intellectual Disability - physiopathology ; Life Sciences ; Medical sciences ; Mental Retardation ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Molecular and cellular biology ; Neurons and Cognition ; Nuclear Proteins ; Nuclear Proteins - chemistry ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; Protein Binding ; Protein Structure, Tertiary ; Psychology. Psychoanalysis. Psychiatry ; Psychopathology. Psychiatry ; rho GTP-Binding Proteins ; rho GTP-Binding Proteins - genetics ; rho GTP-Binding Proteins - metabolism ; Signal Transduction</subject><ispartof>Human molecular genetics, 2009-07, Vol.18 (14), p.2575-2583</ispartof><rights>2009 The Author(s) 2009</rights><rights>2009 INIST-CNRS</rights><rights>2009 The Author(s)</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c635t-70cd2b4e3fb26d2d7fef7638519aae4cff95c33a69d27a17c13b4fdcbb5e72c03</citedby><cites>FETCH-LOGICAL-c635t-70cd2b4e3fb26d2d7fef7638519aae4cff95c33a69d27a17c13b4fdcbb5e72c03</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,1578,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21640269$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19401298$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://inserm.hal.science/inserm-00424014$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Khelfaoui, Malik</creatorcontrib><creatorcontrib>Pavlowsky, Alice</creatorcontrib><creatorcontrib>Powell, Andrew D.</creatorcontrib><creatorcontrib>Valnegri, Pamela</creatorcontrib><creatorcontrib>Cheong, Kenneth W.</creatorcontrib><creatorcontrib>Blandin, Yann</creatorcontrib><creatorcontrib>Passafaro, Maria</creatorcontrib><creatorcontrib>Jefferys, John G.R.</creatorcontrib><creatorcontrib>Chelly, Jamel</creatorcontrib><creatorcontrib>Billuart, Pierre</creatorcontrib><title>Inhibition of RhoA pathway rescues the endocytosis defects in Oligophrenin1 mouse model of mental retardation</title><title>Human molecular genetics</title><addtitle>Hum Mol Genet</addtitle><description>The patho-physiological hypothesis of mental retardation caused by the deficiency of the RhoGAP Oligophrenin1 (OPHN1), relies on the well-known functions of Rho GTPases on neuronal morphology, i.e. dendritic spine structure. Here, we describe a new function of this Bin/Amphiphysin/Rvs domain containing protein in the control of clathrin-mediated endocytosis (CME). Through interactions with Src homology 3 domain containing proteins involved in CME, OPHN1 is concentrated to endocytic sites where it down-regulates the RhoA/ROCK signaling pathway and represses the inhibitory function of ROCK on endocytosis. Indeed disruption of Ophn1 in mice reduces the endocytosis of synaptic vesicles and the post-synaptic α-amino-3-hydroxy-5-methylisoazol-4-propionate (AMPA) receptor internalization, resulting in almost a complete loss of long-term depression in the hippocampus. Finally, pharmacological inhibition of this pathway by ROCK inhibitors fully rescued not only the CME deficit in OPHN1 null cells but also synaptic plasticity in the hippocampus from Ophn1 null model. Altogether, we uncovered a new patho-physiological mechanism for intellectual disabilities associated to mutations in RhoGTPases linked genes and also opened new directions for therapeutic approaches of congenital mental retardation.</description><subject>Adult and adolescent clinical studies</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell physiology</subject><subject>Cytoskeletal Proteins</subject><subject>Cytoskeletal Proteins - chemistry</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Disease Models, Animal</subject><subject>Down-Regulation</subject><subject>Endocytosis</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>GTPase-Activating Proteins</subject><subject>GTPase-Activating Proteins - chemistry</subject><subject>GTPase-Activating Proteins - genetics</subject><subject>GTPase-Activating Proteins - metabolism</subject><subject>Humans</subject><subject>Intellectual deficiency</subject><subject>Intellectual Disability - genetics</subject><subject>Intellectual Disability - metabolism</subject><subject>Intellectual Disability - physiopathology</subject><subject>Life Sciences</subject><subject>Medical sciences</subject><subject>Mental Retardation</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Molecular and cellular biology</subject><subject>Neurons and Cognition</subject><subject>Nuclear Proteins</subject><subject>Nuclear Proteins - chemistry</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>Protein Binding</subject><subject>Protein Structure, Tertiary</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychopathology. Psychiatry</subject><subject>rho GTP-Binding Proteins</subject><subject>rho GTP-Binding Proteins - genetics</subject><subject>rho GTP-Binding Proteins - metabolism</subject><subject>Signal Transduction</subject><issn>0964-6906</issn><issn>1460-2083</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkl1rFDEYhQdR7LZ64w-QQdALcWy-JpncCEupbnWhIEqLNyGTj53UmWRMZqv7782yy1Z7oTfJRZ6c876HUxTPIHgLAcen3bA61XqEDX9QzCChoEKgwQ-LGeCUVJQDelQcp3QDAKQEs8fFEeQEQMSbWTFc-M61bnLBl8GWn7swL0c5dT_lpowmqbVJ5dSZ0ngd1GYKyaVSG2vUlErny8vercLYReOdh-UQ1snkU5t-KzYYP8k-y0wyarm1eFI8srJP5un-Pim-vj__craolpcfLs7my0pRXE8VA0qjlhhsW0Q10swayyhuasilNERZy2uFsaRcIyYhUxC3xGrVtrVhSAF8Urzb6Y7rdjBa5UGi7MUY3SDjRgTpxN8v3nViFW4FYgBixLPAm51Ad-_bYr4UzicTBwEAQTlGcgsz_mrvF8OPHNkkBpeU6XvpTc5EUEYgQQ39L4gAYIQ0LIMv7oE3YR19Dk0gCBEElGzXfL2DVAwpRWMPo0IgttUQuRpiV40MP_8zkzt034UMvNwDMinZ2yi9cunAoVwegCi_48J6_LdhteNcmsyvAynj95wHZrVYXH8T7NPVxxpeMXGNfwNysuAr</recordid><startdate>20090715</startdate><enddate>20090715</enddate><creator>Khelfaoui, Malik</creator><creator>Pavlowsky, Alice</creator><creator>Powell, Andrew D.</creator><creator>Valnegri, Pamela</creator><creator>Cheong, Kenneth W.</creator><creator>Blandin, Yann</creator><creator>Passafaro, Maria</creator><creator>Jefferys, John G.R.</creator><creator>Chelly, Jamel</creator><creator>Billuart, Pierre</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><general>Oxford University Press (OUP)</general><scope>BSCLL</scope><scope>IQODW</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>7QP</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope></search><sort><creationdate>20090715</creationdate><title>Inhibition of RhoA pathway rescues the endocytosis defects in Oligophrenin1 mouse model of mental retardation</title><author>Khelfaoui, Malik ; Pavlowsky, Alice ; Powell, Andrew D. ; Valnegri, Pamela ; Cheong, Kenneth W. ; Blandin, Yann ; Passafaro, Maria ; Jefferys, John G.R. ; Chelly, Jamel ; Billuart, Pierre</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c635t-70cd2b4e3fb26d2d7fef7638519aae4cff95c33a69d27a17c13b4fdcbb5e72c03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Adult and adolescent clinical studies</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell physiology</topic><topic>Cytoskeletal Proteins</topic><topic>Cytoskeletal Proteins - chemistry</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Cytoskeletal Proteins - metabolism</topic><topic>Disease Models, Animal</topic><topic>Down-Regulation</topic><topic>Endocytosis</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetics of eukaryotes. Biological and molecular evolution</topic><topic>GTPase-Activating Proteins</topic><topic>GTPase-Activating Proteins - chemistry</topic><topic>GTPase-Activating Proteins - genetics</topic><topic>GTPase-Activating Proteins - metabolism</topic><topic>Humans</topic><topic>Intellectual deficiency</topic><topic>Intellectual Disability - genetics</topic><topic>Intellectual Disability - metabolism</topic><topic>Intellectual Disability - physiopathology</topic><topic>Life Sciences</topic><topic>Medical sciences</topic><topic>Mental Retardation</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Molecular and cellular biology</topic><topic>Neurons and Cognition</topic><topic>Nuclear Proteins</topic><topic>Nuclear Proteins - chemistry</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>Protein Binding</topic><topic>Protein Structure, Tertiary</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychopathology. Psychiatry</topic><topic>rho GTP-Binding Proteins</topic><topic>rho GTP-Binding Proteins - genetics</topic><topic>rho GTP-Binding Proteins - metabolism</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Khelfaoui, Malik</creatorcontrib><creatorcontrib>Pavlowsky, Alice</creatorcontrib><creatorcontrib>Powell, Andrew D.</creatorcontrib><creatorcontrib>Valnegri, Pamela</creatorcontrib><creatorcontrib>Cheong, Kenneth W.</creatorcontrib><creatorcontrib>Blandin, Yann</creatorcontrib><creatorcontrib>Passafaro, Maria</creatorcontrib><creatorcontrib>Jefferys, John G.R.</creatorcontrib><creatorcontrib>Chelly, Jamel</creatorcontrib><creatorcontrib>Billuart, Pierre</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Human molecular genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Khelfaoui, Malik</au><au>Pavlowsky, Alice</au><au>Powell, Andrew D.</au><au>Valnegri, Pamela</au><au>Cheong, Kenneth W.</au><au>Blandin, Yann</au><au>Passafaro, Maria</au><au>Jefferys, John G.R.</au><au>Chelly, Jamel</au><au>Billuart, Pierre</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of RhoA pathway rescues the endocytosis defects in Oligophrenin1 mouse model of mental retardation</atitle><jtitle>Human molecular genetics</jtitle><addtitle>Hum Mol Genet</addtitle><date>2009-07-15</date><risdate>2009</risdate><volume>18</volume><issue>14</issue><spage>2575</spage><epage>2583</epage><pages>2575-2583</pages><issn>0964-6906</issn><eissn>1460-2083</eissn><coden>HNGEE5</coden><abstract>The patho-physiological hypothesis of mental retardation caused by the deficiency of the RhoGAP Oligophrenin1 (OPHN1), relies on the well-known functions of Rho GTPases on neuronal morphology, i.e. dendritic spine structure. Here, we describe a new function of this Bin/Amphiphysin/Rvs domain containing protein in the control of clathrin-mediated endocytosis (CME). Through interactions with Src homology 3 domain containing proteins involved in CME, OPHN1 is concentrated to endocytic sites where it down-regulates the RhoA/ROCK signaling pathway and represses the inhibitory function of ROCK on endocytosis. Indeed disruption of Ophn1 in mice reduces the endocytosis of synaptic vesicles and the post-synaptic α-amino-3-hydroxy-5-methylisoazol-4-propionate (AMPA) receptor internalization, resulting in almost a complete loss of long-term depression in the hippocampus. Finally, pharmacological inhibition of this pathway by ROCK inhibitors fully rescued not only the CME deficit in OPHN1 null cells but also synaptic plasticity in the hippocampus from Ophn1 null model. Altogether, we uncovered a new patho-physiological mechanism for intellectual disabilities associated to mutations in RhoGTPases linked genes and also opened new directions for therapeutic approaches of congenital mental retardation.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>19401298</pmid><doi>10.1093/hmg/ddp189</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0964-6906 |
| ispartof | Human molecular genetics, 2009-07, Vol.18 (14), p.2575-2583 |
| issn | 0964-6906 1460-2083 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2701329 |
| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Adult and adolescent clinical studies Animals Biological and medical sciences Cell physiology Cytoskeletal Proteins Cytoskeletal Proteins - chemistry Cytoskeletal Proteins - genetics Cytoskeletal Proteins - metabolism Disease Models, Animal Down-Regulation Endocytosis Fundamental and applied biological sciences. Psychology Genetics of eukaryotes. Biological and molecular evolution GTPase-Activating Proteins GTPase-Activating Proteins - chemistry GTPase-Activating Proteins - genetics GTPase-Activating Proteins - metabolism Humans Intellectual deficiency Intellectual Disability - genetics Intellectual Disability - metabolism Intellectual Disability - physiopathology Life Sciences Medical sciences Mental Retardation Mice Mice, Inbred C57BL Mice, Knockout Molecular and cellular biology Neurons and Cognition Nuclear Proteins Nuclear Proteins - chemistry Nuclear Proteins - genetics Nuclear Proteins - metabolism Protein Binding Protein Structure, Tertiary Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry rho GTP-Binding Proteins rho GTP-Binding Proteins - genetics rho GTP-Binding Proteins - metabolism Signal Transduction |
| title | Inhibition of RhoA pathway rescues the endocytosis defects in Oligophrenin1 mouse model of mental retardation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-29T01%3A49%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Inhibition%20of%20RhoA%20pathway%20rescues%20the%20endocytosis%20defects%20in%20Oligophrenin1%20mouse%20model%20of%20mental%20retardation&rft.jtitle=Human%20molecular%20genetics&rft.au=Khelfaoui,%20Malik&rft.date=2009-07-15&rft.volume=18&rft.issue=14&rft.spage=2575&rft.epage=2583&rft.pages=2575-2583&rft.issn=0964-6906&rft.eissn=1460-2083&rft.coden=HNGEE5&rft_id=info:doi/10.1093/hmg/ddp189&rft_dat=%3Cproquest_pubme%3E1760787391%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=211210640&rft_id=info:pmid/19401298&rft_oup_id=10.1093/hmg/ddp189&rfr_iscdi=true |