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Sökning: WFRF:(Motiño O) > ACBP/DBI protein ne...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003462naa a2200565 4500
001oai:prod.swepub.kib.ki.se:236191214
003SwePub
008240124s2022 | |||||||||||000 ||eng|
009oai:prod.swepub.kib.ki.se:152471169
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:2361912142 URI
024a https://doi.org/10.1073/pnas.22073441192 DOI
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1524711692 URI
040 a (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Motiño, O4 aut
2451 0a ACBP/DBI protein neutralization confers autophagy-dependent organ protection through inhibition of cell loss, inflammation, and fibrosis
264 c 2022-10-03
264 1b Proceedings of the National Academy of Sciences,c 2022
506 a gratis
520 a Acyl-coenzyme A (CoA)–binding protein (ACBP), also known as diazepam-binding inhibitor (DBI), is an extracellular feedback regulator of autophagy. Here, we report that injection of a monoclonal antibody neutralizing ACBP/DBI (α-DBI) protects the murine liver against ischemia/reperfusion damage, intoxication by acetaminophen and concanavalin A, and nonalcoholic steatohepatitis caused by methionine/choline-deficient diet as well as against liver fibrosis induced by bile duct ligation or carbon tetrachloride. α-DBI downregulated proinflammatory and profibrotic genes and upregulated antioxidant defenses and fatty acid oxidation in the liver. The hepatoprotective effects of α-DBI were mimicked by the induction of ACBP/DBI-specific autoantibodies, an inducibleAcbp/Dbiknockout or a constitutiveGabrg2F77Imutation that abolishes ACBP/DBI binding to the GABAAreceptor. Liver-protective α-DBI effects were lost when autophagy was pharmacologically blocked or genetically inhibited by knockout ofAtg4b. Of note, α-DBI also reduced myocardium infarction and lung fibrosis, supporting the contention that it mediates broad organ-protective effects against multiple insults.
700a Lambertucci, F4 aut
700a Anagnostopoulos, G4 aut
700a Li, S4 aut
700a Nah, J4 aut
700a Castoldi, F4 aut
700a Senovilla, L4 aut
700a Montégut, L4 aut
700a Chen, H4 aut
700a Durand, S4 aut
700a Bourgin, M4 aut
700a Aprahamian, F4 aut
700a Nirmalathasan, N4 aut
700a Alvarez-Valadez, K4 aut
700a Sauvat, A4 aut
700a Carbonnier, V4 aut
700a Djavaheri-Mergny, M4 aut
700a Pietrocola, Fu Karolinska Institutet4 aut
700a Sadoshima, J4 aut
700a Maiuri, MC4 aut
700a Martins, I4 aut
700a Kroemer, G4 aut
710a Karolinska Institutet4 org
773t Proceedings of the National Academy of Sciences of the United States of Americad : Proceedings of the National Academy of Sciencesg 119:41, s. e2207344119-q 119:41<e2207344119-x 1091-6490
773t Proceedings of the National Academy of Sciencesd : Proceedings of the National Academy of Sciencesg 119:41, s. e2207344119-q 119:41<e2207344119-x 0027-8424
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:236191214
8564 8u https://doi.org/10.1073/pnas.2207344119
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:152471169

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