PMID- 20686646
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211020
IS  - 1179-2698 (Print)
IS  - 1179-2698 (Electronic)
IS  - 1179-2698 (Linking)
VI  - 1
DP  - 2009 Aug 1
TI  - Expression of transcription factor zinc-binding protein-89 (ZBP-89) is inhibited 
      by inflammatory cytokines.
PG  - 7-12
AB  - Zinc-binding protein-89 (ZBP-89; ZNF148, BERF-1, BFCOL-1) is a zinc-finger 
      transcription factor of the Kruppel family. It has been shown to regulate the 
      expression of a number of genes, acting as either an activator or repressor of 
      gene expression, depending on the context. It is over-expressed in several 
      cancers, but has been shown to be involved in apoptosis and to have a negative 
      influence on cell growth in part by interactions with p53. Previously, ZBP-89 was 
      shown to activate transcription of the matrix metalloproteinase-3 (MMP-3) gene by 
      binding to a polymorphic promoter element in competition with nuclear factor 
      kappaB (NF-kappaB). NF-kappaB is known to be a key regulator of the inflammatory 
      response, but relatively little is known about regulation of ZBP-89. In order to 
      ascertain whether ZBP-89 is regulated during inflammation, we designed 
      experiments to determine whether and to what extent ZBP-89 levels are affected by 
      inflammatory cytokines. Here we show that ZBP-89 mRNA and protein expression are 
      significantly inhibited in human fibroblasts by the inflammatory cytokine 
      interleukin-1beta. Since any change in the levels of ZBP-89 would presumably 
      impact the regulation of MMP-3 and other ZBP-89 target genes, these results 
      provide important insight into mechanisms involved in fine-tuning the immune 
      response.
FAU - Borghaei, Ruth C
AU  - Borghaei RC
AD  - Department of Biochemistry and Molecular Biology, Philadelphia College of 
      Osteopathic Medicine, 4170 City Avenue, Philadelphia, PA 19131, USA.
FAU - Chambers, Mariah
AU  - Chambers M
LA  - eng
GR  - R15 DE016277/DE/NIDCR NIH HHS/United States
GR  - R15 DE016277-02/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PL  - New Zealand
TA  - Pathol Lab Med Int
JT  - Pathology and laboratory medicine international
JID - 101530479
PMC - PMC2913887
MID - NIHMS171948
COIS- The authors report no conflicts of interest in this work.
EDAT- 2010/08/06 06:00
MHDA- 2010/08/06 06:01
PMCR- 2010/08/02
CRDT- 2010/08/06 06:00
PHST- 2010/08/06 06:00 [entrez]
PHST- 2010/08/06 06:00 [pubmed]
PHST- 2010/08/06 06:01 [medline]
PHST- 2010/08/02 00:00 [pmc-release]
AID - 10.2147/plmi.s6249 [doi]
PST - ppublish
SO  - Pathol Lab Med Int. 2009 Aug 1;1:7-12. doi: 10.2147/plmi.s6249.