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Role of unphosphorylated transcription factor STAT3 in late cerebral ischemia after subarachnoid hemorrhage.

Samraj, Ajoy K; Müller, Anne H; Grell, Anne-Sofie and Edvinsson, Lars LU (2014) In Journal of Cerebral Blood Flow and Metabolism 34(5). p.759-763
Abstract
Molecular mechanisms behind increased cerebral vasospasm and local inflammation in late cerebral ischemia after subarachnoid hemorrhage (SAH) are poorly elucidated. Using system biology tools and experimental SAH models, we have identified signal transducer and activator of transcription 3 (STAT3) transcription factor as a possible major regulatory molecule. On the basis of the presence of transcription factor binding sequence in the promoters of differentially regulated genes (significant enrichment PE: 6 × 10(5)) and the consistent expression of STAT3 (mRNA, P=0.0159 and Protein, P=0.0467), we hypothesize that unphosphorylated STAT3 may directly DNA bind and probably affect the genes that are involved in inflammation and late cerebral... (More)
Molecular mechanisms behind increased cerebral vasospasm and local inflammation in late cerebral ischemia after subarachnoid hemorrhage (SAH) are poorly elucidated. Using system biology tools and experimental SAH models, we have identified signal transducer and activator of transcription 3 (STAT3) transcription factor as a possible major regulatory molecule. On the basis of the presence of transcription factor binding sequence in the promoters of differentially regulated genes (significant enrichment PE: 6 × 10(5)) and the consistent expression of STAT3 (mRNA, P=0.0159 and Protein, P=0.0467), we hypothesize that unphosphorylated STAT3 may directly DNA bind and probably affect the genes that are involved in inflammation and late cerebral ischemia to influence the pathologic progression of SAH.Journal of Cerebral Blood Flow & Metabolism advance online publication, 12 February 2014; doi:10.1038/jcbfm.2014.15. (Less)
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Contribution to journal
publication status
published
subject
in
Journal of Cerebral Blood Flow and Metabolism
volume
34
issue
5
pages
759 - 763
publisher
Nature Publishing Group
external identifiers
  • pmid:24517975
  • wos:000335430700004
  • scopus:84899968109
ISSN
1559-7016
DOI
10.1038/jcbfm.2014.15
language
English
LU publication?
yes
id
d752c235-025f-4e94-a2d0-1b3881d98653 (old id 4334848)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24517975?dopt=Abstract
date added to LUP
2014-03-06 10:43:57
date last changed
2017-11-05 03:08:58
@article{d752c235-025f-4e94-a2d0-1b3881d98653,
  abstract     = {Molecular mechanisms behind increased cerebral vasospasm and local inflammation in late cerebral ischemia after subarachnoid hemorrhage (SAH) are poorly elucidated. Using system biology tools and experimental SAH models, we have identified signal transducer and activator of transcription 3 (STAT3) transcription factor as a possible major regulatory molecule. On the basis of the presence of transcription factor binding sequence in the promoters of differentially regulated genes (significant enrichment PE: 6 × 10(5)) and the consistent expression of STAT3 (mRNA, P=0.0159 and Protein, P=0.0467), we hypothesize that unphosphorylated STAT3 may directly DNA bind and probably affect the genes that are involved in inflammation and late cerebral ischemia to influence the pathologic progression of SAH.Journal of Cerebral Blood Flow & Metabolism advance online publication, 12 February 2014; doi:10.1038/jcbfm.2014.15.},
  author       = {Samraj, Ajoy K and Müller, Anne H and Grell, Anne-Sofie and Edvinsson, Lars},
  issn         = {1559-7016},
  language     = {eng},
  number       = {5},
  pages        = {759--763},
  publisher    = {Nature Publishing Group},
  series       = {Journal of Cerebral Blood Flow and Metabolism},
  title        = {Role of unphosphorylated transcription factor STAT3 in late cerebral ischemia after subarachnoid hemorrhage.},
  url          = {http://dx.doi.org/10.1038/jcbfm.2014.15},
  volume       = {34},
  year         = {2014},
}