SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "L773:1350 9047 srt2:(1995-1999)"

Sökning: L773:1350 9047 > (1995-1999)

  • Resultat 1-18 av 18
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  •  
2.
  • Burgess, D H, et al. (författare)
  • Human skeletal muscle cytosols are refractory to cytochrome c-dependent activation of type-II caspases and lack APAF-1.
  • 1999
  • Ingår i: Cell Death and Differentiation. - : Springer Science and Business Media LLC. - 1350-9047 .- 1476-5403. ; 6:3, s. 256-61
  • Tidskriftsartikel (refereegranskat)abstract
    • Apoptotic regulatory mechanisms in skeletal muscle have not been revealed. This is despite indications that remnant apoptotic events are detected following exercise, muscle injury and the progression of dystrophinopathies. The recent elicitation of a cytochrome c-mediated induction of caspases has led to speculation regarding a cytochrome c mechanism in muscle. We demonstrate that cytosols from skeletal muscle biopsies from healthy human volunteers lack the ability to activate type-II caspases by a cytochrome c-mediated pathway despite the confirmed presence of both procaspase-3 and -9. This was not due to the presence of an endogenous inhibitor, as the muscle cytosols enhanced caspase activity when added to a control cytosol, subsequently activated by cytochrome c and dATP. In addition, we demonstrate that muscle cytosols lack the apoptosis protease activator protein-1 (APAF-1), both at the protein and mRNA levels. These data indicate that human skeletal muscle cells will be refractory to mitochondrial-mediated events leading to apoptosis and thus can escape a major pro-apoptotic regulatory mechanism. This may reflect an evolutionary adaptation of cell survival in the presence of the profusion of mitochondria required for energy generation in motility.
  •  
3.
  •  
4.
  •  
5.
  • Gorman, AM, et al. (författare)
  • Challenging the dogmas
  • 1999
  • Ingår i: Cell death and differentiation. - : Springer Science and Business Media LLC. - 1350-9047 .- 1476-5403. ; 6:2, s. 207-11
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
  •  
6.
  •  
7.
  •  
8.
  • Orrenius, S, et al. (författare)
  • Mitochondria as the focus of apoptosis research
  • 1997
  • Ingår i: Cell death and differentiation. - : Springer Science and Business Media LLC. - 1350-9047 .- 1476-5403. ; 4:6, s. 427-428
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
  •  
9.
  •  
10.
  •  
11.
  •  
12.
  • Samali, A, et al. (författare)
  • Apoptosis: cell death defined by caspase activation
  • 1999
  • Ingår i: Cell death and differentiation. - : Springer Science and Business Media LLC. - 1350-9047 .- 1476-5403. ; 6:6, s. 495-496
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
  •  
13.
  • Schulze-Osthoff, Klaus, et al. (författare)
  • Role of ICE-related and other proteases in Fas-mediated apoptosis
  • 1996
  • Ingår i: Cell Death and Differentiation. - 1350-9047 .- 1476-5403. ; 3:2, s. 177-184
  • Forskningsöversikt (refereegranskat)abstract
    • Interleukin-1 beta-converting enzyme (ICE)-like proteases comprise a novel family of unusual cysteine proteases which have been implicated in programmed cell death in both invertebrates and mammals. Current available evidence indicates a role of ICE proteases as central executioners of apoptosis triggered by the cell surface receptor Fas (APO-1). The presence of multiple mammalian ICE proteases with partially overlapping but distinct activities suggests a complex proteolytic cascade which is induced upon Fas ligation. The precise role of single members of the ICE family in Fas-mediated apoptosis, however, is still unclear. Here, we summarize the present knowledge about the relevance of ICE proteases, their potential targets, and interaction with unrelated proteases in cell death mediated by Fas and other apoptotic stimuli.
  •  
14.
  •  
15.
  •  
16.
  •  
17.
  •  
18.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-18 av 18

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