Altered versican cleavage in ADAMTS5 deficient mice; a novel etiology of myxomatous valve disease.
about
The ADAMTS (A Disintegrin and Metalloproteinase with Thrombospondin motifs) familyRegulated proteolytic processing of Reelin through interplay of tissue plasminogen activator (tPA), ADAMTS-4, ADAMTS-5, and their modulatorsGalnt1 is required for normal heart valve development and cardiac functionLumican deficiency results in cardiomyocyte hypertrophy with altered collagen assemblyADAMTS5 Is a Critical Regulator of Virus-Specific T Cell ImmunityBiosynthesis and expression of a disintegrin-like and metalloproteinase domain with thrombospondin-1 repeats-15: a novel versican-cleaving proteoglycanaseDevelopment of a monoclonal anti-ADAMTS-5 antibody that specifically blocks the interaction with LRP1.ADAMTS4 and ADAMTS5 knockout mice are protected from versican but not aggrecan or brevican proteolysis during spinal cord injury.The multiple, complex roles of versican and its proteolytic turnover by ADAMTS proteases during embryogenesis.Isolation and purification of versican and analysis of versican proteolysis.Anti-ADAMTS5 monoclonal antibodies: implications for aggrecanase inhibition in osteoarthritis.Deficient signaling via Alk2 (Acvr1) leads to bicuspid aortic valve development.Determinants of versican-V1 proteoglycan processing by the metalloproteinase ADAMTS5BMP-2 induces versican and hyaluronan that contribute to post-EMT AV cushion cell migration.Imbalanced expression of Vcan mRNA splice form proteins alters heart morphology and cellular protein profiles.Pericellular versican regulates the fibroblast-myofibroblast transition: a role for ADAMTS5 protease-mediated proteolysisSmall leucine-rich proteoglycans exhibit unique spatiotemporal expression profiles during cardiac valve development.Insufficient versican cleavage and Smad2 phosphorylation results in bicuspid aortic and pulmonary valvesAntibody-based exosite inhibitors of ADAMTS-5 (aggrecanase-2)ADAMTS9-Mediated Extracellular Matrix Dynamics Regulates Umbilical Cord Vascular Smooth Muscle Differentiation and RotationMaladaptive matrix remodeling and regional biomechanical dysfunction in a mouse model of aortic valve disease.Translational development of an ADAMTS-5 antibody for osteoarthritis disease modification.The cerebral cavernous malformation pathway controls cardiac development via regulation of endocardial MEKK3 signaling and KLF expression.Monoclonal antibodies for the treatment of osteoarthritis.Wave mice: a new tool in the quest to characterize aortic valvular disease etiologies.Endocardial Brg1 disruption illustrates the developmental origins of semilunar valve disease.LRP-1-mediated endocytosis regulates extracellular activity of ADAMTS-5 in articular cartilageVersican processing by a disintegrin-like and metalloproteinase domain with thrombospondin-1 repeats proteinases-5 and -15 facilitates myoblast fusion.Endothelial deletion of ADAM17 in mice results in defective remodeling of the semilunar valves and cardiac dysfunction in adults.Tbx20 acts upstream of Wnt signaling to regulate endocardial cushion formation and valve remodeling during mouse cardiogenesis.Review of molecular and mechanical interactions in the aortic valve and aorta: implications for the shared pathogenesis of aortic valve disease and aortopathy.BMP2 expression in the endocardial lineage is required for AV endocardial cushion maturation and remodeling.Challenges and opportunities for the future of monoclonal antibody development: Improving safety assessment and reducing animal use.Hyaluronidase 2 Deficiency Causes Increased Mesenchymal Cells, Congenital Heart Defects, and Heart Failure.Transcriptional induction of ADAMTS5 protein by nuclear factor-κB (NF-κB) family member RelA/p65 in chondrocytes during osteoarthritis development.Activation of Mouse Cumulus-Oocyte Complex Maturation In Vitro Through EGF-Like Activity of Versican.Comparative Transcriptomic Profiling and Gene Expression for Myxomatous Mitral Valve Disease in the Dog and Human.The ADAMTS5 Metzincin Regulates Zebrafish Somite Differentiation.ADAMTS5 Deficiency in Calcified Aortic Valves Is Associated With Elevated Pro-Osteogenic Activity in Valvular Interstitial Cells.Massive aggrecan and versican accumulation in thoracic aortic aneurysm and dissection.
P2860
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P2860
Altered versican cleavage in ADAMTS5 deficient mice; a novel etiology of myxomatous valve disease.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Altered versican cleavage in A ...... y of myxomatous valve disease.
@ast
Altered versican cleavage in A ...... y of myxomatous valve disease.
@en
type
label
Altered versican cleavage in A ...... y of myxomatous valve disease.
@ast
Altered versican cleavage in A ...... y of myxomatous valve disease.
@en
prefLabel
Altered versican cleavage in A ...... y of myxomatous valve disease.
@ast
Altered versican cleavage in A ...... y of myxomatous valve disease.
@en
P2093
P2860
P1476
Altered versican cleavage in A ...... y of myxomatous valve disease.
@en
P2093
A Megan Diminich
Alexandria Bahan
Andy Wessels
Christine B Kern
Courtney M Nelson
Daniel R McCulloch
Deidra Weber
Jessica D McGarity
Loren E Dupuis
Suneel S Apte
P2860
P304
P356
10.1016/J.YDBIO.2011.06.041
P407
P577
2011-07-01T00:00:00Z