PMID- 9210478
OWN - NLM
STAT- MEDLINE
DCOM- 19970804
LR  - 20190620
IS  - 0014-2956 (Print)
IS  - 0014-2956 (Linking)
VI  - 246
IP  - 1
DP  - 1997 May 15
TI  - The mouse gene for hypoxia-inducible factor-1alpha--genomic organization, 
      expression and characterization of an alternative first exon and 5' flanking 
      sequence.
PG  - 155-65
AB  - The ubiquitously expressed hypoxia-inducible factor-1 (HIF-1) is involved in 
      expression of a large number of oxygen-regulated genes. HIF-1 is a heterodimer 
      consisting of an alpha and a beta subunit, both belonging to the 
      basic-helix-loop-helix Per-aryl hydrocarbon receptor nuclear translocator-Sim 
      (PAS) family of transcription factors. Whereas HIF-1alpha is a novel member of 
      this family, HIF-1beta is identical to the aryl hydrocarbon receptor nuclear 
      translocator, previously recognized to be involved in xenobiotic metabolism. cDNA 
      cloning revealed that mouse HIF-1alpha can be expressed as two mRNA isoforms 
      containing alternative 5' untranslated regions and two different predicted 
      translational start sites. We cloned and characterized 20.5 kb of the mouse 
      HIF-1alpha gene (Hif1a) containing exon II-XV. The two alternative first exons, 
      I.1 and I.2, are separated from exon II by approximately 24 kb and 17 kb, 
      respectively. We also sequenced Hif1a exon I.1 and flanking regions, and mapped a 
      single exon I.1 transcription initiation site. Reverse transcription PCR analysis 
      of total RNA derived from normoxic and hypoxic mouse hepatoma and fibroblast cell 
      lines suggested that the two alternative mRNA isoforms are constitutively 
      coexpressed in these cells, and that two different promoters drive transcription 
      of HIF-1alpha. A minimal exon I.1 promoter was identified which moderately 
      activated heterologous gene expression, indicating that additional cis-elements 
      are required for efficient HIF-1alpha transcription in vivo.
FAU - Wenger, R H
AU  - Wenger RH
AD  - Institute of Physiology, University of Zurich-Irchel, Switzerland.
FAU - Rolfs, A
AU  - Rolfs A
FAU - Kvietikova, I
AU  - Kvietikova I
FAU - Spielmann, P
AU  - Spielmann P
FAU - Zimmermann, D R
AU  - Zimmermann DR
FAU - Gassmann, M
AU  - Gassmann M
LA  - eng
SI  - GENBANK/Y09085
SI  - GENBANK/Y09086
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Eur J Biochem
JT  - European journal of biochemistry
JID - 0107600
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (DNA, Complementary)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Drosophila Proteins)
RN  - 0 (Hif1a protein, mouse)
RN  - 0 (Hypoxia-Inducible Factor 1)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Nuclear Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transcription Factors)
RN  - 0 (sim protein, Drosophila)
RN  - EC 3.1.30.1 (Single-Strand Specific DNA and RNA Endonucleases)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Basic Helix-Loop-Helix Transcription Factors
MH  - Binding Sites
MH  - *Cell Hypoxia
MH  - Cell Line
MH  - Cloning, Molecular
MH  - DNA, Complementary/chemistry
MH  - DNA-Binding Proteins/chemistry/*genetics
MH  - Drosophila Proteins
MH  - Enhancer Elements, Genetic
MH  - Exons/genetics
MH  - *Gene Expression Regulation
MH  - Genes, Reporter
MH  - Helix-Loop-Helix Motifs/genetics
MH  - Hypoxia-Inducible Factor 1
MH  - Hypoxia-Inducible Factor 1, alpha Subunit
MH  - Mice
MH  - Molecular Sequence Data
MH  - Nuclear Proteins/chemistry/*genetics
MH  - Promoter Regions, Genetic/genetics
MH  - RNA Splicing/genetics
MH  - RNA, Messenger/chemistry
MH  - Sequence Analysis, DNA
MH  - Single-Strand Specific DNA and RNA Endonucleases/metabolism
MH  - Transcription Factors/chemistry/*genetics
MH  - Tumor Cells, Cultured
EDAT- 1997/05/15 00:00
MHDA- 1997/05/15 00:01
CRDT- 1997/05/15 00:00
PHST- 1997/05/15 00:00 [pubmed]
PHST- 1997/05/15 00:01 [medline]
PHST- 1997/05/15 00:00 [entrez]
AID - 10.1111/j.1432-1033.1997.t01-1-00155.x [doi]
PST - ppublish
SO  - Eur J Biochem. 1997 May 15;246(1):155-65. doi: 
      10.1111/j.1432-1033.1997.t01-1-00155.x.