PMID- 11677267
OWN - NLM
STAT- MEDLINE
DCOM- 20011204
LR  - 20190630
IS  - 0022-3042 (Print)
IS  - 0022-3042 (Linking)
VI  - 79
IP  - 2
DP  - 2001 Oct
TI  - Binding of nerve growth factor to its p75 receptor in stressed cells induces 
      selective IkappaB-beta degradation and NF-kappaB nuclear translocation.
PG  - 391-9
AB  - Nerve growth factor (NGF) regulates the activity of the transcription factor 
      NF-kappaB (nuclear factor-kappaB) through its low affinity receptor, p75. In the 
      present study we found that NGF binding to p75 induces nuclear translocation of 
      p65 and increases NF-kappaB binding activity in a cell line overexpressing p75, 
      but only after the cells have been subjected to a previous stress. Under 
      physiological conditions, in the absence of stress, NGF is unable to alter p65 
      nuclear levels. Tumor necrosis factor-alpha (TNF-alpha) induces a down-regulation 
      of IkappaB-alpha, -beta and -epsilon both in physiological and in stress, i.e. 
      serum-free, conditions. In contrast, NGF only induces the specific degradation of 
      IkappaB-beta after serum withdrawal, without affecting IkappaB-alpha or -epsilon 
      either in the presence or in the absence of stress. IkappaB-beta consists of 
      several isoforms, whose relative abundance is regulated by serum withdrawal. NGF 
      does not target all the IkappaB-beta isoforms with the same potency, being more 
      effective in reducing the levels of the isoforms up-regulated by serum 
      withdrawal. TRAF-6 is expressed at the same level under both physiological and 
      stress conditions. These results indicate that NGF is able to induce NF-kappaB 
      nuclear translocation by a mechanism that involves specific IkappaB-beta 
      degradation only after the cells have been subjected to a severe stress.
FAU - Cosgaya, J M
AU  - Cosgaya JM
AD  - Department of Neurobiology, Stanford University School of Medicine, Stanford, 
      California 93305, USA.
FAU - Shooter, E M
AU  - Shooter EM
LA  - eng
GR  - NS04270/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Neurochem
JT  - Journal of neurochemistry
JID - 2985190R
RN  - 0 (I-kappa B Proteins)
RN  - 0 (NF-kappa B)
RN  - 0 (Protein Isoforms)
RN  - 0 (Proteins)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 0 (TNF Receptor-Associated Factor 6)
RN  - 9061-61-4 (Nerve Growth Factor)
SB  - IM
MH  - Animals
MH  - Biological Transport/physiology
MH  - Blood Physiological Phenomena
MH  - Cell Line
MH  - I-kappa B Proteins/*metabolism
MH  - Mice
MH  - NF-kappa B/*metabolism
MH  - Nerve Growth Factor/*metabolism/pharmacology
MH  - Protein Isoforms/metabolism
MH  - Proteins/metabolism
MH  - Rats
MH  - Receptor, Nerve Growth Factor
MH  - Receptors, Nerve Growth Factor/*metabolism
MH  - Stress, Physiological/*metabolism/pathology
MH  - TNF Receptor-Associated Factor 6
EDAT- 2001/10/26 10:00
MHDA- 2002/01/05 10:01
CRDT- 2001/10/26 10:00
PHST- 2001/10/26 10:00 [pubmed]
PHST- 2002/01/05 10:01 [medline]
PHST- 2001/10/26 10:00 [entrez]
AID - 10.1046/j.1471-4159.2001.00573.x [doi]
PST - ppublish
SO  - J Neurochem. 2001 Oct;79(2):391-9. doi: 10.1046/j.1471-4159.2001.00573.x.