Results 81 to 90 of about 2,930,787 (173)

Genetic variation of aggrecanase-2 (ADAMTS5) in susceptibility to osteoarthritis

open access: yes, 2019
Aggrecanase-2 (ADAMTS5) gene is responsible for aggrecan degradation that may contribute to cartilage destruction in a mouse osteoarthritis (OA) model. We aimed to investigate the effects of ADAMTS5 gene polymorphisms on OA risk in a Chinese population ...
Yong Huang   +7 more
core   +2 more sources

Lactoferrin Deficiency During Lactation Causes Adult Obesity‐Related Metabolic Disease Through Persistent Adipose Dysfunction Driven by Impaired Adipocyte Development

open access: yesAdvanced Science, Volume 13, Issue 44, 7 August 2026.
Lactational lactoferrin deficiency exerts lasting effects on epididymal adipose tissue development from lactation into adulthood: it impairs adipocyte hyperplasia and induces pathological hypertrophy, resulting in lower body weight yet exacerbated metabolic dysfunction under a high‐fat diet in adulthood.
Qin An   +11 more
wiley   +1 more source

The Zonal Architecture of the Mandibular Condyle Requires ADAMTS5

open access: yes, 2018
Temporomandibular joint (TMJ) osteoarthritis (TMJOA) disrupts extracellular matrix (ECM) homeostasis, leading to cartilage degradation. Upregulated a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)–5 leads to cleavage of its ...
C.B. Kern, S.E. Cisewski, A.W. Rogers
core   +1 more source

Determinants of versican-V1 proteoglycan processing by the metalloproteinase ADAMTS5 [PDF]

open access: yes, 2014
Proteolysis of the Glu(441)-Ala(442) bond in the glycosaminoglycan (GAG) β domain of the versican-V1 variant by a disintegrin-like and metalloproteinase domain with thrombospondin type 1 motif (ADAMTS) proteases is required for proper embryo ...
Dours-Zimmermann, Maria T   +7 more
core   +1 more source

Eugenol preserves chondrocyte extracellular matrix homeostasis by modulating the ALK1/ALK5-associated TGF-β/Smad signaling axis

open access: yesFrontiers in Pharmacology
Osteoarthritis (OA) is characterized by inflammatory and catabolic disruption of cartilage extracellular matrix (ECM) homeostasis. An increased relative abundance of activin receptor-like kinase 1 (ALK1) relative to ALK5, together with altered Smad ...
Yongcan Wang   +9 more
doaj   +1 more source

ADAMTS5-mediated aggrecanolysis in murine epiphyseal chondrocyte cultures [PDF]

open access: yes, 2006
SummaryObjectiveAggrecan degradation by aggrecanases [a disintegrin and metalloproteinase with thrombospondin-like motifs (ADAMTS) 1, 4, 5, 8, 9, 15] is considered to initiate much of the cartilage pathology seen in human arthritis, however, the ...
Osborn, B.   +5 more
core   +1 more source

Protein-RNA interactions: a structural analysis [PDF]

open access: yes, 2001
A detailed computational analysis of 32 protein-RNA complexes is presented. A number of physical and chemical properties of the intermolecular interfaces are calculated and compared with those observed in protein-double-stranded DNA and protein-single ...
Daley, DT   +9 more
core  

Peroxisomal membrane proteins insert into the endoplasmic reticulum [PDF]

open access: yes, 2010
We show that a comprehensive set of 16 peroxisomal membrane proteins (PMPs) encompassing all types of membrane topologies first target to the endoplasmic reticulum (ER) in Saccharomyces cerevisiae.
Sub Cellular Protein Chemistry   +4 more
core   +1 more source

Rivaroxaban suppresses factor Xa–Driven PAR-2–ERK inflammatory, catabolic, osteoclastogenic, and mitochondrial dysfunction signaling in osteoarthritis-relevant chondrocytes: a drug-repurposing strategy for joint inflammation

open access: yesFrontiers in Pharmacology
BackgroundOsteoarthritis (OA) is increasingly recognised as an inflammation-driven whole-joint disease in which cartilage catabolism, osteochondral remodelling, and mitochondrial dysfunction drive structural progression.
Rajashree Patnaik   +5 more
doaj   +1 more source

Galnt1 is required for normal heart valve development and cardiac function.

open access: yesPLoS ONE, 2015
Congenital heart valve defects in humans occur in approximately 2% of live births and are a major source of compromised cardiac function. In this study we demonstrate that normal heart valve development and cardiac function are dependent upon Galnt1, the
E Tian   +8 more
doaj   +1 more source

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