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onsdag 21 november 2018

FOXF2 ( 6p25.3) geenistä, ( Forkhead transcription factor ) 2015 thesis Azadeh Reyahi.

 Geeni  FOXF2(6p25.3) 
 https://www.ncbi.nlm.nih.gov/gene/2295
https://www.sciencedirect.com/science/article/pii/S001216061530333X
Also known as
FKHL6; FREAC2; FREAC-2
Summary
FOXF2 encodes forkhead box F2, one of many human homologues of the Drosophila melanogaster transcription factor forkhead. FOXF2 is expressed in lung and placenta, and has been shown to transcriptionally activate several lung-specific genes. [provided by RefSeq, Jul 2008]
Expression
Biased expression in lung (RPKM 8.4), prostate (RPKM 6.0) and 13 other tissues See more
Orthologs
Preferred Names
forkhead box protein F2
Names
forkhead-like 6
forkhead-related activator 2
forkhead-related protein FKHL6
forkhead-related transcription factor 2
 https://www.ncbi.nlm.nih.gov/protein/NP_001443.1
 Cleft lip and palate : 
  • Cleft lip and cleft palate ongoing research
  • Some of the ongoing research studies on Cleft lip and cleft palate in Singapore are Novel evidence of association with nonsyndromic cleft lip with or without cleft palate was shown for single nucleotide polymorphisms in FOXF2 gene in an Asian population, Congenital midline sinus of the upper lip.
  • Töllö viikolla tuli postista kirje "Operation Smile" . Ruotsalainen projekti jossa kerätäänv aroja  kitalaki-huulihalkiolasten plastiikkakirugiseen kasvokorjaukseen, joka on todella hymyn palauttatja. mainoskessa kerrotiin pienestä pojasta jolla oli  joopa molemmanpuolinen huulihalkio ja  ikätoverit olivat jopa kivittäneet pientä . Hän sai palstiikkakirurgisen korjauksen ja aksvot palautuivat aivaon normaaleiksi. taitavien kirurgien  kräsivällisen operaatiosarjan  avulla.  tästä  saa enemmän tietoja www.operationsmile.se/
Mitä mahdollisuuksia geenikorjauksella on, sen tulevaisuus tietää. Tämä eeni on  monessa ihmistaudissa  osallisena:

Related articles in PubMed





  •  Vuodelta 2015 göteborgilainen väitöskirja

https://gupea.ub.gu.se/handle/2077/40458

Foxf2 gene in development and disease Azadeh Reyahi Department of Chemistry and Molecular Biology, University of Gothenburg, Box 462, SE 405 30, Göteborg, Sweden

Abstract In this thesis I present our recent data on the involvement and the mechanism of action of the forkhead transcription factor Foxf2 in
  • development of the brain microvasculature, 
  • formation of the blood-brain barrier,
  •  control of the intestinal stem cell niche, and 
  • fusion of the secondary palate. 
 The potential clinical significance of these findings is strengthened by a correlation between Foxf2 expression and intestinal adenoma formation, and by association between genetic variants in human FOXF2 and incident stroke. We showed that Foxf2 is expressed in brain pericytes, but not in mural cells of other organs. Foxf2 null mutants have a defective brain vasculature and suffer from intracranial hemorrhage and a leaky blood-brain barrier with increased endothelial vesicular trans-cytosis. Foxf2-/- brain pericytes have diminished Pdgfrβ expression, and the cerebral vasculature a reduced activity of the Tgfβ –Alk5– Smad2/3 signaling pathway, associated with decreased expression of integrins, Tgfb2, Tgfbr2, Alk5 and other pathway components. In a large GWAS performed by an international consortium, we identified a genome-wide significant association of common variants near FOXF2 with risk of stroke. Conditional knockout mice, in which Foxf2 was deleted in healthy adults, developed clinical signs of stroke and exhibited cerebral ischemia, reactive gliosis and microhemorrhage. The animal model results thus corroborate the human genetic association and identifies FOXF2 as a novel risk locus for stroke. In the intestine we showed that Foxf2 is expressed by subepithelial fibroblasts and restricts the size of the stem cell niche, and thereby the number and prolif-eration of Lgr5+ stem cells. Foxf2 is a target of epithelial hedgehog signaling and inhibits the Wnt pathway by increasing the expression of the extracellular Wnt inhibitor Sfrp1. As a consequence, reduced Foxf2 expression significantly increases both initiation and growth of intestinal tumors.
 Reduced proliferation and decreased extracellular matrix production in the neural crest-derived mesenchyme of the palatal shelves was found to be responsible for the cleft palate phenotype in Foxf2 null mutants. Mechanistically, the defect is associated with reduced canonical Tgfβ signaling and integrin expression. The Tgfb2 mRNA level was not affected, but the amount of Tgfβ2 protein was significantly decreased in mutant palatal shelf mesenchyme.


Foxf2 Is Required for Brain Pericyte Differentiation and Development and Maintenance of the Blood-Brain Barrier. Reyahi A1, Nik AM1, Ghiami M1, Gritli-Linde A2, Pontén F3, Johansson BR4, CarlssonP5.
VISA ARTIKEL


Foxf2 in intestinal fibroblasts reduces numbers of Lgr5(+) stem cells and adenoma formation by inhibiting Wnt signaling. Nik AM1, Reyahi A, Pontén F, Carlsson P.
VISA ARTIKEL


FOXF2, a novel risk locus for stroke and small artery disease Ganesh Chauhan, Corey R Arnold, Audrey Y Chu, Myriam Fornage, Azadeh Reyahi, Joshua C Bis, Aki S Havulinna (equal contribution first
authors) ... additional co-authors excluded for brevity... (joint senior
authors:) Lenore J Launer, M Arfan Ikram, Peter Carlsson, Daniel I Chasman, Sarah J Childs, William T Longstreth, Jr, Sudha Seshadri, Stéphanie Debette. Submitted

Foxf2 enhances Tgfβ signaling in secondary palate development Ali M.Nik, Jeanette Astroga-Johansson, Azadeh Reyahi, Mozhgan Ghiami, Fredrik Pontén and Peter Carlsson.

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