RGD Reference Report - Role of Erk1/2 activation in prion disease pathogenesis: absence of CCR1 leads to increased Erk1/2 activation and accelerated disease progression. - Rat Genome Database

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Role of Erk1/2 activation in prion disease pathogenesis: absence of CCR1 leads to increased Erk1/2 activation and accelerated disease progression.

Authors: LaCasse, RA  Striebel, JF  Favara, C  Kercher, L  Chesebro, B 
Citation: LaCasse RA, etal., J Neuroimmunol. 2008 May 30;196(1-2):16-26. Epub 2008 Apr 8.
RGD ID: 5688145
Pubmed: PMID:18396336   (View Abstract at PubMed)
PMCID: PMC2532820   (View Article at PubMed Central)
DOI: DOI:10.1016/j.jneuroim.2008.02.009   (Journal Full-text)

Prion diseases are neurodegenerative infections with gliosis and vacuolation. The mechanisms of degeneration remain unclear, but chemokines may be important. In current experiments CCR1 knock-out (KO) mice succumbed more rapidly to scrapie infection than WT controls. Infected KO mice had upregulation of CCL3, a CCR1 ligand, and CCR5, a receptor with specificity for CCL3. Both infected KO and WT mice had upregulation of CCR5-mediated signaling involving activation of Erk1/2 in astrocytes; however, activation was earlier in KO mice suggesting a role in pathogenesis. In both mouse strains activation of the Erk1/2 pathway may lead to astrocyte dysfunction resulting in neurodegeneration.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CCR1Humanscrapie  ISOCcr1 (Mus musculus) RGD 
Ccr1Ratscrapie  ISOCcr1 (Mus musculus) RGD 
Ccr1Mousescrapie  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ccr1  (C-C motif chemokine receptor 1)

Genes (Mus musculus)
Ccr1  (C-C motif chemokine receptor 1)

Genes (Homo sapiens)
CCR1  (C-C motif chemokine receptor 1)


Additional Information