SwePub
Sök i SwePub databas

  Utökad sökning

Träfflista för sökning "WFRF:(Andersen Peter) ;mspu:(publicationother)"

Sökning: WFRF:(Andersen Peter) > Annan publikation

  • Resultat 1-10 av 22
Sortera/gruppera träfflistan
   
NumreringReferensOmslagsbildHitta
1.
  •  
2.
  •  
3.
  •  
4.
  •  
5.
  •  
6.
  • Bergemalm, Daniel, 1977-, et al. (författare)
  • Superoxide dismutase-1 and other proteins in inclusions from transgenic amyotrophic lateral sclerosis model mice
  • Annan publikation (övrigt vetenskapligt/konstnärligt)abstract
    • Mutant superoxide dismutase-1 (SOD1) causes amyotrophic lateral sclerosis (ALS) through a cytotoxic mechanism of unknown nature. A hallmark in ALS patients and transgenic mouse models carrying human SOD1 (hSOD1) mutations are hSOD1-immunoreactive inclusions in spinal cord ventral horns. The hSOD1 inclusions may block essential cellular functions or cause toxicity through sequestering of other proteins. Inclusions from 4 different transgenic mouse models were examined after density gradient ultracentrifugation. The inclusions are complex structures with heterogeneous densities and are disrupted by detergents. The aggregated hSOD1 was mainly composed of subunits that lacked the native stabilizing intrasubunit disulfide bond. A proportion of subunits formed hSOD1 oligomers or was bound to other proteins through disulfide bonds. Dense inclusions could be isolated and the protein composition was analyzed using proteomic techniques. Mutant hSOD1 accounted for half of the protein. Ten other proteins were identified. Two were cytoplasmic chaperones, 4 were cytoskeletal proteins, and 4 were proteins that normally reside in the endoplasmic reticulum (ER). The presence of ER proteins in inclusions containing the primarily cytosolic hSOD1 further supports the notion that ER stress is involved in ALS.
  •  
7.
  • Byström, Roberth, 1971-, et al. (författare)
  • Identification of property outliers among ALS-associated SOD1 mutations : Common effect on surface hydrogen bonds
  • Annan publikation (populärvet., debatt m.m.)abstract
    • In good accord with the protein-aggregation hypothesis for neurodegenerative diseaseALS-associated SOD1 mutations are found to reduce structural stability or netrepulsive charge. Moreover there are weak indications that the ALS diseaseprogression is correlated with the degree of mutational impact on the SOD1 structure.A bottleneck for obtaining more conclusive information about these structure-diseaserelationships, however, is the large intrinsic variability in patient survival times andinsufficient disease statistics for the majority of ALS-provoking mutations. As analternative test of the structure-disease relationship we focus here on the SOD1 amutation that appears to be outliers in the data set. The results identify several ALSprovokingmutations whose only effect on apo SOD1 is the elimination orintroduction of a single charge, i.e., D76V/Y, D101N and N139D/K. Thethermodynamic stability and folding behaviour of these mutants are indistinguishablefrom the wildtype control, showing that structurally benign replacements of individualsurface charges are sufficient to trigger ALS. Moreover, D101N is a clear outlier inthe plot of stability loss vs. patient survival time by having too rapid diseaseprogression. Common to the identified mutations is that they truncate conserved saltlinksand/or H-bond networks in the functional loops IV or VII. The results show thatthe local impact of ALS-associated mutations on the SOD1 molecule can sometimesoverrun their global effects on stability and net repulsive charge, and point at theanalysis of property outliers as an efficient strategy for mapping out new ALSprovokingfeatures.
  •  
8.
  •  
9.
  •  
10.
  •  
Skapa referenser, mejla, bekava och länka
  • Resultat 1-10 av 22
Typ av publikation
annan publikation  (22)Ta bort avgränsningen
Typ av innehåll
övrigt vetenskapligt/konstnärligt (18)
populärvet., debatt m.m. (4)
Författare/redaktör
Andersen, Peter M. (11)
Marklund, Stefan L. (11)
Brännström, Thomas (9)
Andersen, Peter M., ... (5)
Forsberg, Karin (5)
Zetterström, Per (4)
visa fler...
Wuolikainen, Anna (4)
Moritz, Thomas (2)
Pedrosa-Domellöf, Fa ... (2)
Marklund, Stefan (2)
Birve, Anna (2)
Andersen, Peter (2)
Nordström, Ulrika (2)
Gilthorpe, Jonathan (2)
Antti, Henrik, 1970- (2)
Behzadi, Arvin, 1994 ... (2)
Tjust, Anton E., 198 ... (2)
Hugelius, Gustaf (1)
Kuhry, Peter (1)
Nilsson, Peter (1)
Danielsson, Jens (1)
Oliveberg, Mikael (1)
Gilthorpe, Jonathan ... (1)
Nilsson, Torbjörn K (1)
Bergemalm, Daniel, 1 ... (1)
Glass, Jonathan D. (1)
Press, R (1)
Hedlund, Eva (1)
Blennow, Kaj (1)
Brandslund, Ivan (1)
Byström, Roberth, 19 ... (1)
Gröbner, Gerhard (1)
Sahlin, Nils-Eric (1)
Weydt, Patrick (1)
Sjöström, Johan (1)
Bergh, Johan (1)
Andersen, Peter Munc ... (1)
Andersen, Sven Jørn (1)
Hansen, Jørn Otto (1)
Jul, Ole (1)
Magnus, Carl (1)
Mortensen, Richard (1)
Nilsson, John Peter (1)
Sylvan, Bo (1)
Zetterberg, Henrik (1)
Wingsle, Gunnar (1)
Eggan, Kevin (1)
Olesen, Mads Nikolaj (1)
Pujol-Calderón, Fani (1)
Madsen, Jonna Skov (1)
visa färre...
Lärosäte
Umeå universitet (20)
Luleå tekniska universitet (1)
Stockholms universitet (1)
Lunds universitet (1)
Språk
Engelska (19)
Odefinierat språk (2)
Svenska (1)
Forskningsämne (UKÄ/SCB)
Medicin och hälsovetenskap (12)
Naturvetenskap (3)
Teknik (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