Contribution of the STAT1alpha and STAT1beta isoforms to IFN-gamma mediated innate immunity

ABSTRACT: The transcription factor STAT1 is essential for interferon- (IFN) mediated protective immunity in humans and mice. Two splice isoforms of STAT1, STAT1M-NM-1 and STAT1M-NM-2, differ with regard to a C-terminal transactivation domain, which is absent in STAT1M-NM-2. Dimers of STAT1M-NM-2 are therefore considered transcriptionally inactive and potential competitive inhibitors of STAT1M-NM-1. Contrasting this view, generation and analysis of mice deficient for either STAT1M-NM-1 or STAT1M-NM-2 demonstrated transcriptional activity of the STAT1M-NM-2 isoform and its enhancement of innate immunity. Gene expression profiling in primary cells revealed overlapping, but also non-redundant and gene-specific activities of STAT1M-NM-1 and STAT1M-NM-2 in response to IFNM-NM-3. Consistently, both isoform

ORGANISM(S): Mus musculus

SUBMITTER: Claus Vogl 

PROVIDER: E-GEOD-48970 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress