FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2023654094> ?p ?o ?g. }

• W2023654094 endingPage "89" @default.
• W2023654094 startingPage "81" @default.
• W2023654094 abstract "Accelerated bone loss leading to osteopenia, osteoporosis, and bone fracture is a major health problem that is increasingly common in human immunodeficiency virus (HIV)-infected patients. The underlying pathogenesis is unclear but occurs in both treatment naïve and individuals receiving antiretroviral therapies. We developed an HIV-1 transgenic rat that exhibits many key features of HIV disease including HIV-1-induced changes in bone mineral density (BMD). A key determinant in the rate of bone loss is the differentiation of osteoclasts, the cells responsible for bone resorption. We found HIV-1 transgenic osteoclast precursors (OCP) express higher levels of suppressor of cytokine signaling-1 (SOCS-1) and TNF receptor-associated factor 6 (TRAF6) and are resistant to interferon-gamma (IFN-γ) mediated suppression of osteoclast differentiation. Our data suggest that dysregulated SOCS-1 expression by HIV-1 transgenic OCP promotes osteoclastogenesis leading to the accelerated bone loss observed in this animal model. We propose that elevated SOCS-1 expression in OCP antagonizes the inhibitory effects of IFN-γ and enhances receptor activator of NF-kB ligand (RANKL) signaling that drives osteoclast differentiation and activation. Understanding the molecular mechanisms of HIV-associated BMD changes has the potential to detect and treat bone metabolism disturbances early and improve the quality of life in patients." @default.
• W2023654094 created "2016-06-24" @default.
• W2023654094 creator A5004888041 @default.
• W2023654094 creator A5007403554 @default.
• W2023654094 creator A5020680454 @default.
• W2023654094 creator A5036310839 @default.
• W2023654094 creator A5040770925 @default.
• W2023654094 creator A5043058839 @default.
• W2023654094 creator A5058691136 @default.
• W2023654094 creator A5070049123 @default.
• W2023654094 creator A5081718779 @default.
• W2023654094 date "2014-01-10" @default.
• W2023654094 modified "2023-09-24" @default.
• W2023654094 title "Elevated suppressor of cytokine signaling-1 (SOCS-1): a mechanism for dysregulated osteoclastogenesis in HIV transgenic rats" @default.
• W2023654094 cites W1533939550 @default.
• W2023654094 cites W1534645474 @default.
• W2023654094 cites W1639854378 @default.
• W2023654094 cites W1677043489 @default.
• W2023654094 cites W1927367897 @default.
• W2023654094 cites W1966258975 @default.
• W2023654094 cites W1967502057 @default.
• W2023654094 cites W1970370575 @default.
• W2023654094 cites W1980106277 @default.
• W2023654094 cites W1982395713 @default.
• W2023654094 cites W1989353060 @default.
• W2023654094 cites W1992026462 @default.
• W2023654094 cites W1992431645 @default.
• W2023654094 cites W1993015636 @default.
• W2023654094 cites W1997722036 @default.
• W2023654094 cites W2000647744 @default.
• W2023654094 cites W2001294602 @default.
• W2023654094 cites W2014225480 @default.
• W2023654094 cites W2017372504 @default.
• W2023654094 cites W2024932182 @default.
• W2023654094 cites W2025683142 @default.
• W2023654094 cites W2026501885 @default.
• W2023654094 cites W2031157573 @default.
• W2023654094 cites W2037299986 @default.
• W2023654094 cites W2039415019 @default.
• W2023654094 cites W2041581343 @default.
• W2023654094 cites W2048299560 @default.
• W2023654094 cites W2055558890 @default.
• W2023654094 cites W2058277858 @default.
• W2023654094 cites W2062709781 @default.
• W2023654094 cites W2065140364 @default.
• W2023654094 cites W2067631076 @default.
• W2023654094 cites W2075416173 @default.
• W2023654094 cites W2078047860 @default.
• W2023654094 cites W2078517976 @default.
• W2023654094 cites W2082407676 @default.
• W2023654094 cites W2086811903 @default.
• W2023654094 cites W2087665466 @default.
• W2023654094 cites W2090569295 @default.
• W2023654094 cites W2093252878 @default.
• W2023654094 cites W2094996679 @default.
• W2023654094 cites W2100359187 @default.
• W2023654094 cites W2110400973 @default.
• W2023654094 cites W2110555227 @default.
• W2023654094 cites W2114323760 @default.
• W2023654094 cites W2119049249 @default.
• W2023654094 cites W2120837197 @default.
• W2023654094 cites W2128513451 @default.
• W2023654094 cites W2132408993 @default.
• W2023654094 cites W2132933661 @default.
• W2023654094 cites W2139996507 @default.
• W2023654094 cites W2140317538 @default.
• W2023654094 cites W2149384715 @default.
• W2023654094 cites W2155081622 @default.
• W2023654094 cites W2155638837 @default.
• W2023654094 cites W2155886462 @default.
• W2023654094 cites W2165600338 @default.
• W2023654094 cites W2167886526 @default.
• W2023654094 cites W2170206314 @default.
• W2023654094 cites W2321505964 @default.
• W2023654094 doi "https://doi.org/10.1111/2049-632x.12117" @default.
• W2023654094 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4048640" @default.
• W2023654094 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24376119" @default.
• W2023654094 hasPublicationYear "2014" @default.
• W2023654094 type Work @default.
• W2023654094 sameAs 2023654094 @default.
• W2023654094 citedByCount "9" @default.
• W2023654094 countsByYear W20236540942016 @default.
• W2023654094 countsByYear W20236540942018 @default.
• W2023654094 countsByYear W20236540942020 @default.
• W2023654094 countsByYear W20236540942021 @default.
• W2023654094 countsByYear W20236540942022 @default.
• W2023654094 crossrefType "journal-article" @default.
• W2023654094 hasAuthorship W2023654094A5004888041 @default.
• W2023654094 hasAuthorship W2023654094A5007403554 @default.
• W2023654094 hasAuthorship W2023654094A5020680454 @default.
• W2023654094 hasAuthorship W2023654094A5036310839 @default.
• W2023654094 hasAuthorship W2023654094A5040770925 @default.
• W2023654094 hasAuthorship W2023654094A5043058839 @default.
• W2023654094 hasAuthorship W2023654094A5058691136 @default.
• W2023654094 hasAuthorship W2023654094A5070049123 @default.
• W2023654094 hasAuthorship W2023654094A5081718779 @default.
• W2023654094 hasBestOaLocation W20236540941 @default.
• W2023654094 hasConcept C102230213 @default.

• next