Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P05109 (S100A8)
 1,212 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Binding of nuclear proteins from wild oat aleurone protoplasts to the promoter regions of two gibberellin-regulated wheat alpha-amylase genes (alpha-Amy1/18 and alpha-Amy2/54) has been studied by gel retardation and DNase 1 footprinting. Gel retardation studies using 300-430 bp fragments of the promoters showed similar binding characteristics with nuclear extracts from both gibberellin A1-treated and untreated protoplasts. DNase 1 footprints localised binding of nuclear proteins from gibberellin A1-treated aleurone protoplasts to regions in both promoters. Similar sequence elements in the promoter regions of both genes were protected from digestion although the location and number of footprints in each promoter region were different. Each footprint contained either a sequence similar to the cAMP and/or phorbol ester response elements, or a hyphenated palindrome sequence. The presence of cAMP and/or phorbol ester response element-like sequences in the footprints suggests that transcription factors of the bZIP type may be involved in the expression of alpha-amylase genes in aleurone cells. Footprints containing hyphenated palindrome sequences, found in the promoter regions of both genes, suggest the possible involvement of other classes of transcription factor. The conserved alpha-amylase promoter sequence TAA-CAGA was also shown to bind nuclear protein in the alpha-Amy2/54 promoter. These observations are discussed in relation to alpha-amylase gene expression in aleurone and to functional data concerning these genes.
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PMID:Aleurone nuclear proteins bind to similar elements in the promoter regions of two gibberellin-regulated alpha-amylase genes. 151 Nov 35

A human oncodevelopmental protein (ODP) with a molecular size of 28 kDa was isolated, employing malignant ascitic fluid of an advanced mixed mesodermal tumor of the uterus, by anti-ODP coupled Affi-Gel 10 column chromatography, followed by preparative PAGE. The final preparation obtained with this procedure gave a single band exhibiting reactivity with an anti-ODP antibody on analytical sodium dodecyl sulfate-PAGE. The sequence of the first 20 N-terminal amino acids of this protein is identical with those of both the cystic fibrosis protein and Ca-binding protein MRP8 except at position 17, for which no result was obtained. Sequence analysis suggested that the protein shows 90% sequence homology with both these proteins.
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PMID:Isolation of an ascitic oncodevelopmental protein exhibiting high sequence homology with calcium-binding protein MRP8. 769 42

S100A8 (A8) has roles in inflammation, differentiation and development and is associated with oxidative defense. Murine A8 (mA8) is up-regulated in macrophages, fibroblasts, and microvascular endothelial cells by LPS. Glucocorticoids (GCs) amplified LPS-induced mA8 in these cells. Relative to stimulation by LPS, GCs increased mA8 gene transcription and mRNA half-life. Enhancement required new protein synthesis, IL-10 and products of the cyclooxygenase-2 pathway, and both ERK1/2 and p38 MAPK. Protein kinase A positively and protein kinase C negatively regulated this process. Promoter analysis indicated element(s) essential for LPS and dexamethasone enhancement colocated within the region -178 to 0 bp. In the absence of glucocorticoid response elements, NF1 motif at -58 is a candidate for mediation of enhancement. Gel shift analysis detected no differences between LPS- and LPS/dexamethasone-treated complexes within this region. GCs increased constitutive levels of A8 and S100A9 (A9) mRNA in human monocytes. The synovial membrane of rheumatoid patients treated with high dose i.v. methylprednisolone contained higher numbers of A8/A9-positive macrophages than pre- or posttreatment samples. Results support the proposal that A8 has anti-inflammatory properties that may be independent of hetero-complex formation with A9 and may also enable localized defense in the absence of overriding deleterious host responses.
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PMID:Regulation of S100A8 by glucocorticoids. 1569 68

The goal of this investigation was to study the regulation of acid-sensing ion channel (ASIC)3 expression by TGFbeta in the nucleus pulposus cells of the intervertebral disc. Analysis of human nucleus pulposus tissue indicated decreased ASIC3 and elevated TGFbeta expression in the degenerate state. In a parallel study, treatment of nucleus pulposus cells with TGFbeta resulted in decreased expression of ASIC3 mRNA and protein. Suppression of ASIC3 promoter activity was evident when the nucleus pulposus cells were treated with TGFbeta or co-transfected with the constitutively active ALK5 or a smad3 construct. On the other hand, co-transfection of dominant negative smad3 or smad7 restored ASIC3 promoter activity. We validated the role of smad3 in controlling ASIC3 expression using cells derived from smad3-null mice. ASIC3 promoter activity in the null cells was 2- to 3-fold higher than the wildtype cells. Moreover, expression of smad3 in null cells decreased ASIC3 promoter activity by almost 50%. Further studies using deletion constructs and trichostatin A treatment showed that the full-length smad3 was necessary, and the suppression involved recruitment of histone deacetylase to the promoter. To determine the mechanism, we evaluated the rat ASIC3 promoter sequence and noted the presence of two smad interacting CAGA box motifs. Gel-shift and supershift analysis indicated that smad3 protein was bound to this motif. Chromatin immunoprecipitation analysis confirmed that smad3 bound both the CAGA elements. Results of these studies clearly show that TGFbeta is highly expressed in the degenerate disc and through smad3 serves as a negative regulator of ASIC3 expression.
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PMID:SMAD3 functions as a transcriptional repressor of acid-sensing ion channel 3 (ASIC3) in nucleus pulposus cells of the intervertebral disc. 1846 73