https://www.selleckchem.com/products/abt-199.html
H150Y, p.L187P) overexpression. GBP1 promoted β-catenin translocation into the cytosol and suppressed the formation of cellular adhesion complexes. Suppression of cell-cell adhesion restored the thyroid primordium growth defect observed in gbp1-deficient zebrafish embryos. This study provides further understanding regarding thyroid development and shows that defective cellular remodeling could cause congenital hypothyroidism. This study provides further understanding regarding thyroid development and shows that defective cellular remode
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