Two adjacent nuclear factor-binding domains activate expression from the human PRNP promoter.

ABSTRACT:

Background

The transmissible spongiform encephalopathies (TSEs) comprise a group of fatal degenerative neurological diseases in humans and other mammals. After infection, the cellular prion protein isoform PrPC is converted to the pathological PrPSC scrapie isoform. The continued conversion of PrPC to PrPSC requires de novo endogenous PrP synthesis for disease progression. The human prion protein gene (PRNP) promoter was therefore investigated to identify regulatory elements that could serve as targets for therapeutic intervention.

Findings

The human prion protein gene (PRNP) promoter from position -1593 to +134 relative to the putative transcriptional start site (+1) was analyzed by transient transfection in HeLa cells. Deletions from the 5' end between positions -1593 and

SUBMITTER: Taheny MJ 

PROVIDER: S-EPMC2751769 | biostudies-literature | 2009 Sep

REPOSITORIES: biostudies-literature