SwePub
Tyck till om SwePub Sök här!
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "L773:0012 1797 OR L773:1939 327X srt2:(2015-2019)"

Sökning: L773:0012 1797 OR L773:1939 327X > (2015-2019)

  • Resultat 111-115 av 115
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
111.
  • Zhang, C, et al. (författare)
  • Osteoprotegerin Promotes Liver Steatosis by Targeting the ERK-PPAR-γ-CD36 Pathway
  • 2019
  • Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 68:10, s. 1902-1914
  • Tidskriftsartikel (refereegranskat)abstract
    • Previous cross-sectional studies have established that circulating osteoprotegerin (OPG) levels are associated with nonalcoholic fatty liver disease (NAFLD). However, the role of OPG in metabolic diseases, such as diabetes and NAFLD, is still unclear. In the current study, we demonstrated that hepatic OPG expression was downregulated in NAFLD individuals and in obese mice. OPG deficiency decreased lipid accumulation and expression of CD36 and peroxisome proliferator–activated receptor-γ (PPAR-γ) in the livers of OPG−/− mice and cultured cells, respectively, whereas OPG overexpression elicited the opposite effects. The stimulatory role of OPG in lipid accumulation was blocked by CD36 inactivation in hepatocytes isolated from CD36−/− mice. The overexpression of OPG led to a decrease in extracellular signal–regulated kinase (ERK) phosphorylation in the livers of OPG−/− mice and in cultured cells, while OPG deficiency resulted in the opposite effect. The inhibition of PPAR-γ or the activation of ERK blocked the induction of CD36 expression by OPG in cultured cells. Mechanistically, OPG facilitated CD36 expression by acting on PPAR response element (PPRE) present on the CD36 promoter. Taken together, our study revealed that OPG signaling promotes liver steatosis through the ERK–PPAR-γ–CD36 pathway. The downregulation of OPG in NAFLD might be a compensatory response of the body to dampen excess hepatic fat accumulation in obesity.
  •  
112.
  • Zhao, Lue Ping, et al. (författare)
  • Eleven Amino Acids of HLA-DRB1 and Fifteen Amino Acids of HLA-DRB3, 4, and 5 Include Potentially Causal Residues Responsible for the Risk of Childhood Type 1 Diabetes
  • 2019
  • Ingår i: Diabetes. - Arlington, VA, United States : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 68:8, s. 1692-1704
  • Tidskriftsartikel (refereegranskat)abstract
    • Next-generation targeted sequencing of HLA-DRB1 and HLA-DRB3, -DRB4, and -DRB5 (abbreviated as DRB345) provides high resolution of functional variant positions to investigate their associations with type 1 diabetes risk and with autoantibodies against insulin (IAA), GAD65 (GADA), IA-2 (IA-2A), and ZnT8 (ZnT8A). To overcome exceptional DR sequence complexity as a result of high polymorphisms and extended linkage disequilibrium among the DR loci, we applied a novel recursive organizer (ROR) to discover disease-associated amino acid residues. ROR distills disease-associated DR sequences and identifies 11 residues of DRB1, sequences of which retain all significant associations observed by DR genes. Furthermore, all 11 residues locate under/adjoining the peptide-binding groove of DRB1, suggesting a plausible functional mechanism through peptide binding. The 15 residues of DRB345, located respectively in the beta 49-55 homodimerization patch and on the face of the molecule shown to interact with and bind to the accessory molecule CD4, retain their significant disease associations. Further ROR analysis of DR associations with autoantibodies finds that DRB1 residues significantly associated with ZnT8A and DRB345 residues with GADA. The strongest association is between four residues (beta 14, beta 25, beta 71, and beta 73) and IA-2A, in which the sequence ERKA confers a risk association (odds ratio 2.15, P = 10(-18)), and another sequence, ERKG, confers a protective association (odds ratio 0.59, P = 10(-11)), despite a difference of only one amino acid. Because motifs of identified residues capture potentially causal DR associations with type 1 diabetes, this list of residuals is expected to include corresponding causal residues in this study population.
  •  
113.
  •  
114.
  •  
115.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 111-115 av 115
Typ av publikation
tidskriftsartikel (110)
konferensbidrag (4)
forskningsöversikt (1)
Typ av innehåll
refereegranskat (105)
övrigt vetenskapligt/konstnärligt (10)
Författare/redaktör
Korsgren, Olle (12)
Groop, Leif (12)
Lernmark, Åke (11)
Zierath, JR (6)
Lyssenko, Valeriya (6)
Franks, Paul W. (6)
visa fler...
Toppari, Jorma (6)
Nilsson, Peter (5)
Ahlqvist, Emma (5)
Lind, Lars (5)
Wareham, Nicholas J. (5)
Ladenvall, Claes (5)
Langenberg, Claudia (5)
Ingelsson, Erik (5)
Ludvigsson, Johnny (5)
Tuomi, Tiinamaija (4)
Melander, Olle (4)
Ling, Charlotte (4)
McCarthy, Mark I (4)
Eriksson, Olof (4)
Pedersen, Oluf (4)
Hansen, Torben (4)
Scott, Robert A (4)
Boeing, Heiner (3)
Khaw, Kay-Tee (3)
Franks, Paul (3)
Rolandsson, Olov (3)
Krook, A (3)
Salomaa, Veikko (3)
Lee, Hye-Seung (3)
Carlsson, Annelie (3)
Palli, Domenico (3)
Fall, Tove (3)
Vaag, Allan (3)
Grarup, Niels (3)
Orho-Melander, Marju (3)
Hu, Frank B. (3)
Ripatti, Samuli (3)
Gieger, Christian (3)
Strauch, Konstantin (3)
Grarup, N. (3)
Stancakova, A. (3)
Laakso, M. (3)
Hansen, T. (3)
Pedersen, O. (3)
Hattersley, Andrew T (3)
Mahajan, Anubha (3)
Froguel, Philippe (3)
Strawbridge, RJ (3)
Gustafsson, Stefan (3)
visa färre...
Lärosäte
Lunds universitet (46)
Uppsala universitet (38)
Karolinska Institutet (35)
Göteborgs universitet (16)
Umeå universitet (11)
Linköpings universitet (5)
visa fler...
Stockholms universitet (2)
Örebro universitet (1)
Sveriges Lantbruksuniversitet (1)
visa färre...
Språk
Engelska (115)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (91)
Naturvetenskap (3)
Samhällsvetenskap (1)

År

Kungliga biblioteket hanterar dina personuppgifter i enlighet med EU:s dataskyddsförordning (2018), GDPR. Läs mer om hur det funkar här.
Så här hanterar KB dina uppgifter vid användning av denna tjänst.

 
pil uppåt Stäng

Kopiera och spara länken för att återkomma till aktuell vy