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A Novel Mutation in FGFR3 Causes Camptodactyly, Tall Stature, and Hearing Loss (CATSHL) Syndrome
Activating mutations of FGFR3, a negative regulator of bone growth, are well known to cause a variety of short-limbed bone dysplasias and craniosynostosis syndromes. We mapped the locus causing a novel disorder characterized by camptodactyly, tall stature, scoliosis, and hearing loss (CATSHL syndrom...
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| Published in: | American journal of human genetics 2006-11, Vol.79 (5), p.935-941 |
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| container_end_page | 941 |
| container_issue | 5 |
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| container_title | American journal of human genetics |
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| creator | Toydemir, Reha M. Brassington, Anna E. Bayrak-Toydemir, Pınar Krakowiak, Patrycja A. Jorde, Lynn B. Whitby, Frank G. Longo, Nicola Viskochil, David H. Carey, John C. Bamshad, Michael J. |
| description | Activating mutations of FGFR3, a negative regulator of bone growth, are well known to cause a variety of short-limbed bone dysplasias and craniosynostosis syndromes. We mapped the locus causing a novel disorder characterized by
camptodactyly,
tall
stature,
scoliosis, and
hearing
loss (CATSHL syndrome) to chromosome 4p. Because this syndrome recapitulated the phenotype of the
Fgfr3 knockout mouse, we screened
FGFR3 and subsequently identified a heterozygous missense mutation that is predicted to cause a p.R621H substitution in the tyrosine kinase domain and partial loss of FGFR3 function. These findings indicate that abnormal FGFR3 signaling can cause human anomalies by promoting as well as inhibiting endochondral bone growth. |
| doi_str_mv | 10.1086/508433 |
| format | article |
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camptodactyly,
tall
stature,
scoliosis, and
hearing
loss (CATSHL syndrome) to chromosome 4p. Because this syndrome recapitulated the phenotype of the
Fgfr3 knockout mouse, we screened
FGFR3 and subsequently identified a heterozygous missense mutation that is predicted to cause a p.R621H substitution in the tyrosine kinase domain and partial loss of FGFR3 function. These findings indicate that abnormal FGFR3 signaling can cause human anomalies by promoting as well as inhibiting endochondral bone growth.</description><identifier>ISSN: 0002-9297</identifier><identifier>EISSN: 1537-6605</identifier><identifier>DOI: 10.1086/508433</identifier><identifier>PMID: 17033969</identifier><identifier>CODEN: AJHGAG</identifier><language>eng</language><publisher>Chicago, IL: Elsevier Inc</publisher><subject>Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Base Sequence ; Biological and medical sciences ; Bone Diseases, Developmental - genetics ; Bones ; Diseases of the osteoarticular system ; DNA - genetics ; Female ; Fingers - abnormalities ; Fundamental and applied biological sciences. Psychology ; General aspects. Genetic counseling ; Genetics of eukaryotes. Biological and molecular evolution ; Genotype & phenotype ; Hearing loss ; Hearing Loss, Bilateral - genetics ; Hearing Loss, Sensorineural - genetics ; Heterozygote ; Humans ; Male ; Malformations and congenital and or hereditary diseases involving bones. Joint deformations ; Medical genetics ; Medical sciences ; Mice ; Mice, Knockout ; Models, Molecular ; Molecular and cellular biology ; Molecular Sequence Data ; Mutation ; Mutation, Missense ; Pedigree ; Phenotype ; Protein Structure, Tertiary ; Receptor, Fibroblast Growth Factor, Type 3 - chemistry ; Receptor, Fibroblast Growth Factor, Type 3 - deficiency ; Receptor, Fibroblast Growth Factor, Type 3 - genetics ; Sequence Homology, Amino Acid ; Syndrome ; Toes - abnormalities</subject><ispartof>American journal of human genetics, 2006-11, Vol.79 (5), p.935-941</ispartof><rights>2006 The American Society of Human Genetics</rights><rights>2006 INIST-CNRS</rights><rights>Copyright University of Chicago, acting through its Press Nov 2006</rights><rights>2006 by The American Society of Human Genetics. All rights reserved. 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-26dac8de5c59bc410511ac8eb89c11852ac65cbec7c7b984c3778aab254783053</citedby><cites>FETCH-LOGICAL-c559t-26dac8de5c59bc410511ac8eb89c11852ac65cbec7c7b984c3778aab254783053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1698566/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1698566/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18232524$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17033969$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Toydemir, Reha M.</creatorcontrib><creatorcontrib>Brassington, Anna E.</creatorcontrib><creatorcontrib>Bayrak-Toydemir, Pınar</creatorcontrib><creatorcontrib>Krakowiak, Patrycja A.</creatorcontrib><creatorcontrib>Jorde, Lynn B.</creatorcontrib><creatorcontrib>Whitby, Frank G.</creatorcontrib><creatorcontrib>Longo, Nicola</creatorcontrib><creatorcontrib>Viskochil, David H.</creatorcontrib><creatorcontrib>Carey, John C.</creatorcontrib><creatorcontrib>Bamshad, Michael J.</creatorcontrib><title>A Novel Mutation in FGFR3 Causes Camptodactyly, Tall Stature, and Hearing Loss (CATSHL) Syndrome</title><title>American journal of human genetics</title><addtitle>Am J Hum Genet</addtitle><description>Activating mutations of FGFR3, a negative regulator of bone growth, are well known to cause a variety of short-limbed bone dysplasias and craniosynostosis syndromes. We mapped the locus causing a novel disorder characterized by
camptodactyly,
tall
stature,
scoliosis, and
hearing
loss (CATSHL syndrome) to chromosome 4p. Because this syndrome recapitulated the phenotype of the
Fgfr3 knockout mouse, we screened
FGFR3 and subsequently identified a heterozygous missense mutation that is predicted to cause a p.R621H substitution in the tyrosine kinase domain and partial loss of FGFR3 function. These findings indicate that abnormal FGFR3 signaling can cause human anomalies by promoting as well as inhibiting endochondral bone growth.</description><subject>Amino Acid Sequence</subject><subject>Amino Acid Substitution</subject><subject>Animals</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Bone Diseases, Developmental - genetics</subject><subject>Bones</subject><subject>Diseases of the osteoarticular system</subject><subject>DNA - genetics</subject><subject>Female</subject><subject>Fingers - abnormalities</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>General aspects. Genetic counseling</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Genotype & phenotype</subject><subject>Hearing loss</subject><subject>Hearing Loss, Bilateral - genetics</subject><subject>Hearing Loss, Sensorineural - genetics</subject><subject>Heterozygote</subject><subject>Humans</subject><subject>Male</subject><subject>Malformations and congenital and or hereditary diseases involving bones. Joint deformations</subject><subject>Medical genetics</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Models, Molecular</subject><subject>Molecular and cellular biology</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Mutation, Missense</subject><subject>Pedigree</subject><subject>Phenotype</subject><subject>Protein Structure, Tertiary</subject><subject>Receptor, Fibroblast Growth Factor, Type 3 - chemistry</subject><subject>Receptor, Fibroblast Growth Factor, Type 3 - deficiency</subject><subject>Receptor, Fibroblast Growth Factor, Type 3 - genetics</subject><subject>Sequence Homology, Amino Acid</subject><subject>Syndrome</subject><subject>Toes - abnormalities</subject><issn>0002-9297</issn><issn>1537-6605</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNqFkdGLEzEQxoMoXj31T5AgKAq3mmw22eRFKOV6FaqCrc8xm52eOXaTXrJb6H9_KS3eeS8-Dcz8-L6Z-RB6TcknSqT4zImsGHuCJpSzuhCC8KdoQggpC1Wq-gy9SOmGEEolYc_RGa0JY0qoCfo9xd_DDjr8bRzM4ILHzuP51fwnwzMzJki59NshtMYO-25_gdem6_Aqs2OEC2x8ixdgovPXeBlSwh9m0_VqsfyIV3vfxtDDS_RsY7oEr071HP2aX65ni2L54-rrbLosLOdqKEqRHWQL3HLV2IoSTmluQCOVzVvz0ljBbQO2tnWjZGVZXUtjmpJXtWSEs3P05ai7HZseWgt-iKbT2-h6E_c6GKf_nXj3R1-HnaZCSS5EFnh_EojhdoQ06N4lC11nPIQxaSFVxQmp_gtSxSTj6gC-fQTehDH6_AVdUsWVEvKBmo35fxE2f1emRB-i1cdoM_jm4YH32CnLDLw7ASZZ022i8dale06WrOTlwZEcOchx7BxEnawDb6F1Eeyg2-Aee98B_ua4yw</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>Toydemir, Reha M.</creator><creator>Brassington, Anna E.</creator><creator>Bayrak-Toydemir, Pınar</creator><creator>Krakowiak, Patrycja A.</creator><creator>Jorde, Lynn B.</creator><creator>Whitby, Frank G.</creator><creator>Longo, Nicola</creator><creator>Viskochil, David H.</creator><creator>Carey, John C.</creator><creator>Bamshad, Michael J.</creator><general>Elsevier Inc</general><general>University of Chicago Press</general><general>Cell Press</general><general>The American Society of Human Genetics</general><scope>6I.</scope><scope>AAFTH</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>7TM</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20061101</creationdate><title>A Novel Mutation in FGFR3 Causes Camptodactyly, Tall Stature, and Hearing Loss (CATSHL) Syndrome</title><author>Toydemir, Reha M. ; Brassington, Anna E. ; Bayrak-Toydemir, Pınar ; Krakowiak, Patrycja A. ; Jorde, Lynn B. ; Whitby, Frank G. ; Longo, Nicola ; Viskochil, David H. ; Carey, John C. ; Bamshad, Michael J.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559t-26dac8de5c59bc410511ac8eb89c11852ac65cbec7c7b984c3778aab254783053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Amino Acid Sequence</topic><topic>Amino Acid Substitution</topic><topic>Animals</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Bone Diseases, Developmental - genetics</topic><topic>Bones</topic><topic>Diseases of the osteoarticular system</topic><topic>DNA - genetics</topic><topic>Female</topic><topic>Fingers - abnormalities</topic><topic>Fundamental and applied biological sciences. 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Joint deformations</topic><topic>Medical genetics</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Models, Molecular</topic><topic>Molecular and cellular biology</topic><topic>Molecular Sequence Data</topic><topic>Mutation</topic><topic>Mutation, Missense</topic><topic>Pedigree</topic><topic>Phenotype</topic><topic>Protein Structure, Tertiary</topic><topic>Receptor, Fibroblast Growth Factor, Type 3 - chemistry</topic><topic>Receptor, Fibroblast Growth Factor, Type 3 - deficiency</topic><topic>Receptor, Fibroblast Growth Factor, Type 3 - genetics</topic><topic>Sequence Homology, Amino Acid</topic><topic>Syndrome</topic><topic>Toes - abnormalities</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Toydemir, Reha M.</creatorcontrib><creatorcontrib>Brassington, Anna E.</creatorcontrib><creatorcontrib>Bayrak-Toydemir, Pınar</creatorcontrib><creatorcontrib>Krakowiak, Patrycja A.</creatorcontrib><creatorcontrib>Jorde, Lynn B.</creatorcontrib><creatorcontrib>Whitby, Frank G.</creatorcontrib><creatorcontrib>Longo, Nicola</creatorcontrib><creatorcontrib>Viskochil, David H.</creatorcontrib><creatorcontrib>Carey, John C.</creatorcontrib><creatorcontrib>Bamshad, Michael J.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</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>Nucleic Acids Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of human genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Toydemir, Reha M.</au><au>Brassington, Anna E.</au><au>Bayrak-Toydemir, Pınar</au><au>Krakowiak, Patrycja A.</au><au>Jorde, Lynn B.</au><au>Whitby, Frank G.</au><au>Longo, Nicola</au><au>Viskochil, David H.</au><au>Carey, John C.</au><au>Bamshad, Michael J.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Novel Mutation in FGFR3 Causes Camptodactyly, Tall Stature, and Hearing Loss (CATSHL) Syndrome</atitle><jtitle>American journal of human genetics</jtitle><addtitle>Am J Hum Genet</addtitle><date>2006-11-01</date><risdate>2006</risdate><volume>79</volume><issue>5</issue><spage>935</spage><epage>941</epage><pages>935-941</pages><issn>0002-9297</issn><eissn>1537-6605</eissn><coden>AJHGAG</coden><abstract>Activating mutations of FGFR3, a negative regulator of bone growth, are well known to cause a variety of short-limbed bone dysplasias and craniosynostosis syndromes. We mapped the locus causing a novel disorder characterized by
camptodactyly,
tall
stature,
scoliosis, and
hearing
loss (CATSHL syndrome) to chromosome 4p. Because this syndrome recapitulated the phenotype of the
Fgfr3 knockout mouse, we screened
FGFR3 and subsequently identified a heterozygous missense mutation that is predicted to cause a p.R621H substitution in the tyrosine kinase domain and partial loss of FGFR3 function. These findings indicate that abnormal FGFR3 signaling can cause human anomalies by promoting as well as inhibiting endochondral bone growth.</abstract><cop>Chicago, IL</cop><pub>Elsevier Inc</pub><pmid>17033969</pmid><doi>10.1086/508433</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | American journal of human genetics, 2006-11, Vol.79 (5), p.935-941 |
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| source | BACON - Elsevier - GLOBAL_SCIENCEDIRECT-OPENACCESS; Open Access: PubMed Central |
| subjects | Amino Acid Sequence Amino Acid Substitution Animals Base Sequence Biological and medical sciences Bone Diseases, Developmental - genetics Bones Diseases of the osteoarticular system DNA - genetics Female Fingers - abnormalities Fundamental and applied biological sciences. Psychology General aspects. Genetic counseling Genetics of eukaryotes. Biological and molecular evolution Genotype & phenotype Hearing loss Hearing Loss, Bilateral - genetics Hearing Loss, Sensorineural - genetics Heterozygote Humans Male Malformations and congenital and or hereditary diseases involving bones. Joint deformations Medical genetics Medical sciences Mice Mice, Knockout Models, Molecular Molecular and cellular biology Molecular Sequence Data Mutation Mutation, Missense Pedigree Phenotype Protein Structure, Tertiary Receptor, Fibroblast Growth Factor, Type 3 - chemistry Receptor, Fibroblast Growth Factor, Type 3 - deficiency Receptor, Fibroblast Growth Factor, Type 3 - genetics Sequence Homology, Amino Acid Syndrome Toes - abnormalities |
| title | A Novel Mutation in FGFR3 Causes Camptodactyly, Tall Stature, and Hearing Loss (CATSHL) Syndrome |
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