PMID- 18498249
OWN - NLM
STAT- MEDLINE
DCOM- 20080716
LR  - 20220330
IS  - 1470-8728 (Electronic)
IS  - 0264-6021 (Linking)
VI  - 412
IP  - 3
DP  - 2008 Jun 15
TI  - The cross-talk between NF-kappaB and HIF-1: further evidence for a significant 
      liaison.
PG  - e17-9
LID - 10.1042/BJ20080920 [doi]
AB  - HIF-1 (hypoxia-inducible factor-1) has been shown to essentially control the 
      cellular response to hypoxia. Hypoxia stabilizes the inducible alpha-subunit, 
      preventing post-translational hydroxylation and subsequent degradation via the 
      proteasome. In recent years, clear evidence has emerged that HIF-1alpha is also 
      responsive to many stimuli under normoxic conditions, including thrombin, growth 
      factors, vasoactive peptides, insulin, lipopolysaccharide and cytokines such as 
      TNF-alpha (tumour necrosis factor-alpha), and in many cases reactive oxygen 
      species are involved. One important mechanism underlying these responses is the 
      transcriptional regulation of HIF-1alpha by the redox-sensitive transcription 
      factor NF-kappaB (nuclear factor kappaB), which binds at a distinct element in 
      the proximal promoter of the HIF-1alpha gene. More recently, NF-kappaB binding to 
      this site in the HIF-1alpha promoter has been shown also under hypoxic 
      conditions. Thus these two major pathways regulating the responses to 
      inflammation and oxidative stress on the one hand, and hypoxia on the other hand, 
      appear to be intimately linked. In this issue of the Biochemical Journal, a study 
      by van Uden et al. has supported these findings further, in which they have 
      confirmed the binding of several proteins of the NF-kappaB family at the 
      previously identified consensus site in the HIF-1alpha promoter and shown that 
      TNF-alpha can also transcriptionally induce HIF-1alpha by this previously 
      described pathway. The identification of HIF-1alpha as a target gene of NF-kappaB 
      will have important implications for a variety of disorders related to 
      hypoxia-ischaemia and/or inflammation and oxidative stress.
FAU - Gorlach, Agnes
AU  - Gorlach A
AD  - Experimentelle Kinderkardiologie, Deutsches Herzzentrum Munchen an der 
      Technischen Universitat Munchen, Lazarettstrasse 36, D-80636 Munchen, Germany. 
      goerlach@dhm.mhn.de
FAU - Bonello, Steve
AU  - Bonello S
LA  - eng
PT  - Comment
PT  - Journal Article
PL  - England
TA  - Biochem J
JT  - The Biochemical journal
JID - 2984726R
RN  - 0 (Hypoxia-Inducible Factor 1)
RN  - 0 (NF-kappa B)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
EIN - Biochem J. 2008 Aug 1;413(3):571
CON - Biochem J. 2008 Jun 15;412(3):477-84. PMID: 18393939
MH  - Cell Hypoxia
MH  - Humans
MH  - Hypoxia-Inducible Factor 1/genetics/*metabolism
MH  - Models, Biological
MH  - NF-kappa B/genetics/*metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - *Signal Transduction
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2008/05/24 09:00
MHDA- 2008/07/17 09:00
CRDT- 2008/05/24 09:00
PHST- 2008/05/24 09:00 [pubmed]
PHST- 2008/07/17 09:00 [medline]
PHST- 2008/05/24 09:00 [entrez]
AID - BJ20080920 [pii]
AID - 10.1042/BJ20080920 [doi]
PST - ppublish
SO  - Biochem J. 2008 Jun 15;412(3):e17-9. doi: 10.1042/BJ20080920.