Search results for "Extracellular matrix component"

showing 2 items of 2 documents

The fibronectin synergy site re-enforces cell adhesion and mediates a crosstalk between integrin classes

2017

Fibronectin (FN), a major extracellular matrix component, enables integrin-mediated cell adhesion via binding of α5β1, αIIbβ3 and αv-class integrins to an RGD-motif. An additional linkage for α5 and αIIb is the synergy site located in close proximity to the RGD motif. We report that mice with a dysfunctional FN-synergy motif (Fn1syn/syn) suffer from surprisingly mild platelet adhesion and bleeding defects due to delayed thrombus formation after vessel injury. Additional loss of β3 integrins dramatically aggravates the bleedings and severely compromises smooth muscle cell coverage of the vasculature leading to embryonic lethality. Cell-based studies revealed that the synergy site is dispensa…

0301 basic medicineMouseQH301-705.5extracellular matrixScienceExtracellular matrix componentIntegrinHemorrhageGeneral Biochemistry Genetics and Molecular BiologyExtracellular matrixMice03 medical and health sciencesfibronectinAnimalsBiology (General)Cell adhesionRGD motifMice KnockoutGeneral Immunology and MicrobiologybiologyCell adhesion moleculeChemistryGeneral NeuroscienceQRThrombosiscell adhesionCell BiologyGeneral MedicineFibronectinsCell biologyFibronectinCrosstalk (biology)030104 developmental biologymechanosignalingImmunologyintegrinsbiology.proteinMedicineResearch ArticleeLife
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MFAP5 Loss-of-Function Mutations Underscore the Involvement of Matrix Alteration in the Pathogenesis of Familial Thoracic Aortic Aneurysms and Dissec…

2014

Thoracic aortic aneurysm and dissection (TAAD) is an autosomal-dominant disorder with major life-threatening complications. The disease displays great genetic heterogeneity with some forms allelic to Marfan and Loeys-Dietz syndrome, and an important number of cases still remain unexplained at the molecular level. Through whole-exome sequencing of affected members in a large TAAD-affected family, we identified the c.472CT (p.Arg158(∗)) nonsense mutation in MFAP5 encoding the extracellular matrix component MAGP-2. This protein interacts with elastin fibers and the microfibrillar network. Mutation screening of 403 additional probands identified an additional missense mutation of MFAP5 (c.62GT …

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesAdolescentExtracellular matrix componentNonsense mutationHaploinsufficiencyThoracic aortic aneurysmPathogenesisContractile ProteinsReportGeneticsmedicineHumansMissense mutationGenetics(clinical)ExomeChildGenetics (clinical)AgedGlycoproteinsAged 80 and overGeneticsAortic Aneurysm ThoracicbiologyGenetic heterogeneitySequence Analysis DNAFibroblastsMiddle Agedmedicine.diseasePedigree3. Good healthAortic DissectionAmino Acid SubstitutionCodon Nonsensebiology.proteinIntercellular Signaling Peptides and ProteinsFemaleHaploinsufficiencyElastinThe American Journal of Human Genetics
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