MISC

2003年7月

Loss of kindlin-1, a human homolog of the Caenorhabditis elegans actin-extracellular-matrix linker protein UNC-112, causes Kindler syndrome

AMERICAN JOURNAL OF HUMAN GENETICS
  • DH Siegel
  • GHS Ashton
  • HG Penagos
  • JV Lee
  • HS Feiler
  • KC Wilhelmsen
  • AP South
  • FJD Smith
  • AR Prescott
  • Wessagowit, V
  • N Oyama
  • M Akiyama
  • D Al Aboud
  • K Al Aboud
  • A Al Githami
  • K Al Hawsawi
  • A Al Ismaily
  • R Al-Suwaid
  • DJ Atherton
  • R Caputo
  • JD Fine
  • IJ Frieden
  • E Fuchs
  • RM Haber
  • T Harada
  • Y Kitajima
  • SB Mallory
  • H Ogawa
  • S Sahin
  • H Shimizu
  • Y Suga
  • G Tadini
  • K Tsuchiya
  • CB Wiebe
  • F Wojnarowska
  • AB Zaghloul
  • T Hamada
  • R Mallipeddi
  • RAJ Eady
  • WHI McLean
  • JA McGrath
  • EH Epstein
  • 全て表示

73
1
開始ページ
174
終了ページ
187
記述言語
英語
掲載種別
DOI
10.1086/376609
出版者・発行元
UNIV CHICAGO PRESS

Kindler syndrome is an autosomal recessive disorder characterized by neonatal blistering, sun sensitivity, atrophy, abnormal pigmentation, and fragility of the skin. Linkage and homozygosity analysis in an isolated Panamanian cohort and in additional inbred families mapped the gene to 20p12.3. Loss-of-function mutations were identified in the FLJ20116 gene ( renamed "KIND1" [ encoding kindlin-1]). Kindlin-1 is a human homolog of the Caenorhabditis elegans protein UNC-112, a membrane-associated structural/signaling protein that has been implicated in linking the actin cytoskeleton to the extracellular matrix (ECM). Thus, Kindler syndrome is, to our knowledge, the first skin fragility disorder caused by a defect in actin-ECM linkage, rather than keratin-ECM linkage.

リンク情報
DOI
https://doi.org/10.1086/376609
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000183904900015&DestApp=WOS_CPL
ID情報
  • DOI : 10.1086/376609
  • ISSN : 0002-9297
  • Web of Science ID : WOS:000183904900015

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