RGD Reference Report - Huntingtin is degraded to small fragments by calpain after ischemic injury. - Rat Genome Database

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Huntingtin is degraded to small fragments by calpain after ischemic injury.

Authors: Kim, M  Roh, JK  Yoon, BW  Kang, L  Kim, YJ  Aronin, N  DiFiglia, M 
Citation: Kim M, etal., Exp Neurol 2003 Sep;183(1):109-15.
RGD ID: 1304431
Pubmed: PMID:12957494   (View Abstract at PubMed)

The gene defect in Huntington's disease (HD) causes a polyglutamine expansion in the N-terminal region of huntingtin (N-htt). In vitro studies suggest that mutant N-htt fragments can aggregate and cause cell death in HD. The physiological and pathological conditions that affect htt proteolysis in the brain are unclear. We examined htt expression by Western blot in the rat brain after transient ischemic injury, which causes striatal neurodegeneration similar to that seen in HD and activates proteases including calcium-dependent calpains. Focal brain ischemia reduced levels of full-length htt in the infarcted cortex and striatum and increased expression of a 55-kDa N-htt fragment that was also produced by treating control brain extracts with calpain. N-htt fragments between 65 and 80 kDa also rose after injury, but these fragments were not as long-lived as the 55-kDa N-htt fragment. The results suggest that after ischemic injury full-length htt is degraded in degenerating neurons and an N-htt fragment accumulates.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
transient cerebral ischemia  ISOHtt (Rattus norvegicus)1304431; 1304431protein:increased degradation:brainRGD 
transient cerebral ischemia  IEP 1304431protein:increased degradation:brainRGD 

Objects Annotated

Genes (Rattus norvegicus)
Htt  (huntingtin)

Genes (Mus musculus)
Htt  (huntingtin)

Genes (Homo sapiens)
HTT  (huntingtin)


Additional Information