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Papers In Press, published online ahead of print July 15, 2002
Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm S-17177
Corresponding Author: lorenz.poellinger{at}cmb.ki.se
The Inhibitory PAS (Per/Arnt/Sim) domain protein, IPAS, functions as a dominant negative regulator of hypoxia-inducible transcription factors (HIFs) by forming complexes with these proteins that fail to bind to hypoxia-response elements of target genes. We have observed earlier that IPAS is predominantly expressed in mice in Purkinje cells of the cerebellum and in corneal epithelium of the eye where is appears to play a role in negative regulation of angiogenesis and maintenance of an avascular phenotype. Sequencing of the mouse IPAS genomic structure revealed that IPAS is a splicing variant of the HIF-3
J. Biol. Chem, 10.1074/jbc.C200328200
Submitted on May 31, 2002
Revised on June 25, 2002
Accepted on July 15, 2002
IPAS is an hypoxia-inducible splicing variant of the HIF-3
locus
locus. Thus, in addition to three unique exons (1a, 4a, and 16) IPAS shares three exons (2, 4, and 5) with HIF-3, as well as alternatively spliced variants of exons 3 and 6. In experiments using normal mice and mice exposed to hypoxia (6% O2) for 6 h we observed alternative splicing of the HIF-3 transcript in the heart and lung. The alternatively spliced transcript was only observed under hypoxic conditions, thus defining a novel mechanism of hypoxia-dependent regulation of gene expression. Importantly, this mechanism may establish negative feed back loop regulation of adaptive responses to hypoxia/ischemia in these tissues.
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