Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:Q9UID6 (
Kruppel-like
)
147
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Sodium
trisulfide (Na
2
S
3
) releases hydrogen polysulfide (H
2
S
n
) and is useful for the investigation of the effects of H
2
S
n
on the cell functions. In the present study, we first examined the effects of Na
2
S
3
on the gene expression of IEC-6 cells, a rat intestinal epithelial cell line. Microarray analysis and reverse transcription-polymerase chain reaction analysis revealed that Na
2
S
3
increased the gene expression of early growth response 1 (EGR1) and
Kruppel-like
transcription factor 4 (KLF4). It was interesting that U0126, an inhibitor of the activation of extracellular signal-regulated kinase 1 (ERK1), ERK2, and ERK5, inhibited the Na
2
S
3
-induced gene expression of EGR1 and KLF4. Na
2
S
3
activated ERK1 and ERK2 (ERK1/2) within 15 min. In addition to ERK1/2, Na
2
S
3
activated ERK5. We noticed that the electrophoretic mobility of ERK5 was decreased after Na
2
S
3
treatment. Phos-tag analysis and in vitro dephosphorylation of the cell extracts indicated that the gel-shift of ERK5 was due to its phosphorylation. The gel-shift of ERK5 was inhibited completely by both U0126 and ERK5-IN-1, a specific inhibitor of ERK5. From these results, we concluded that the gel-shift of ERK5 was induced through autophosphorylation by activated ERK5 after Na
2
S
3
treatment. The present study suggested that H
2
S
n
affected various functions of intestinal epithelial cells through the activation of the ERK1/2 and ERK5 pathways.
...
PMID:Increased expression of EGR1 and KLF4 by polysulfide via activation of the ERK1/2 and ERK5 pathways in cultured intestinal epithelial cells. 3252 29