Literature DB >> 2238087

Brittle bones--fragile molecules: disorders of collagen gene structure and expression.

P H Byers1.   

Abstract

Mutations in the genes that encode the chains of type I collagen, the major structural protein in most tissues, usually produce brittle bones. The consequences of even apparently minor mutations--single base substitutions--can range from lethal to mild, and the phenotypic consequences reflect the nature and position of the mutation. The manner in which phenotypes are produced depends on the effect of the mutation on the structural integrity of the molecule and on whether or how the abnormal molecules can be incorporated into an extracellular matrix.

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Year:  1990        PMID: 2238087     DOI: 10.1016/0168-9525(90)90235-x

Source DB:  PubMed          Journal:  Trends Genet        ISSN: 0168-9525            Impact factor:   11.639


  58 in total

Review 1.  A bit of give and take: the relationship between the extracellular matrix and the developing chondrocyte.

Authors:  Danielle J Behonick; Zena Werb
Journal:  Mech Dev       Date:  2003-11       Impact factor: 1.882

2.  A dominant mutation in the COL1A1 gene that substitutes glycine for valine causes recurrent lethal osteogenesis imperfecta.

Authors:  J Bonaventure; L Cohen-Solal; C Lasselin; P Maroteaux
Journal:  Hum Genet       Date:  1992-08       Impact factor: 4.132

3.  A single base mutation in type I procollagen (COL1A1) that converts glycine alpha 1-541 to aspartate in a lethal variant of osteogenesis imperfecta: detection of the mutation with a carbodiimide reaction of DNA heteroduplexes and direct sequencing of products of the PCR.

Authors:  J P Zhuang; C D Constantinou; A Ganguly; D J Prockop
Journal:  Am J Hum Genet       Date:  1991-06       Impact factor: 11.025

4.  Reflex sympathetic dystrophy syndrome with microtrabecular fracture in a patient with osteogenesis imperfecta.

Authors:  R Neri; A Martini; D Trippi; V Zampa; G Pasero
Journal:  Clin Rheumatol       Date:  1997-06       Impact factor: 2.980

5.  Osteogenesis imperfecta due to recurrent point mutations at CpG dinucleotides in the COL1A1 gene of type I collagen.

Authors:  C J Pruchno; D H Cohn; G A Wallis; M C Willing; B J Starman; X M Zhang; P H Byers
Journal:  Hum Genet       Date:  1991-05       Impact factor: 4.132

6.  The molecular defect in a family with mild atypical osteogenesis imperfecta and extreme joint hypermobility: exon skipping caused by an 11-bp deletion from an intron in one COL1A2 allele.

Authors:  A C Nicholls; J Oliver; D V Renouf; D A Heath; F M Pope
Journal:  Hum Genet       Date:  1992-03       Impact factor: 4.132

Review 7.  Perinatal lethal osteogenesis imperfecta.

Authors:  W G Cole; R Dalgleish
Journal:  J Med Genet       Date:  1995-04       Impact factor: 6.318

8.  Genotype-phenotype correlations in nonlethal osteogenesis imperfecta caused by mutations in the helical domain of collagen type I.

Authors:  Frank Rauch; Liljana Lalic; Peter Roughley; Francis H Glorieux
Journal:  Eur J Hum Genet       Date:  2010-01-20       Impact factor: 4.246

9.  Glycine substitutions in the triple-helical region of type VII collagen result in a spectrum of dystrophic epidermolysis bullosa phenotypes and patterns of inheritance.

Authors:  A M Christiano; J A McGrath; K C Tan; J Uitto
Journal:  Am J Hum Genet       Date:  1996-04       Impact factor: 11.025

10.  Defective splicing of mRNA from one COL1A1 allele of type I collagen in nondeforming (type I) osteogenesis imperfecta.

Authors:  M L Stover; D Primorac; S C Liu; M B McKinstry; D W Rowe
Journal:  J Clin Invest       Date:  1993-10       Impact factor: 14.808

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