fgf2 การใช้

• With no FGF2, there is a partial sex reversal.
• CXCL12, FGF2 and GDNF all communicate via a network to mediate SSC functions.
• This was achieved by establishing the signalling required to create a thyroid lineage, namely BMP4 and FGF2.
• Recent evidence has shown that low levels of FGF2 play a key role in the incidence of excessive anxiety.
• Also in conjunction with FGF2 it can produce progenitor thyroid cells from pluripotent stem cells in mice and hmans.
• As president of StemCulture, LLC . she is currently working on a new study involving a new product, StemBeads FGF2.
• As such, upregulation of GADD45b leads to increased demethylation, increased BDNF and FGF2, and ultimately more neural progenitor cells.
• Perlecan can also promote growth factor ( e . g ., FGF2 ) activity and thus stimulate endothelial growth and re-generation.
• The AER is known to express FGF2, FGF4, FGF8, and FGF9, while the limb bud mesenchyme expresses FGF2 and FGF10.
• The AER is known to express FGF2, FGF4, FGF8, and FGF9, while the limb bud mesenchyme expresses FGF2 and FGF10.
• Sulf2 also upregulated glypican-3, which is commonly overexpressed in HCC, by increasing ERK, AKT activation through enhanced FGF2 signaling.
• Growth factors such as FGF2, HGF, EGF, VEGF, neuregulins and others interact with syndecans [ 1, 2, 8 ].
• Functionally, Sulfs cooperatively desulfate HS 6-O present on activated satellite cells to suppress FGF2 signaling and therefore promote myogenic differentiation to regenerate muscle.
• FGF1 and FGF2 stimulate angiogenesis and the proliferation of fibroblasts that give rise to granulation tissue, which fills up a wound space / cavity early in the wound-healing process.
• Genes expressed in the early dental epithelium in mice such as Bmp4, Bmp7, Dlx2, Dlx5, Fgf1, Fgf2, Fgf4, Fgf8, Lef1, Gli2, and Gli3 are also potential candidates.
• GDNF and FGF2 are both required to activate the phosphoinositide 3-kinase ( PI3K )-Akt pathway, and the mitogen-activated protein kinase / ERK1 kinase1 ( MEK ) pathway, which potentiate SSC proliferation and survival.
• This expression is seen in the distal end of the limb buds, where cells are still undifferentiated and dividing, and appears to be under the regulation of retinoic acid, FGF2, FGF4, and BMP-2  known to regulate limb patterning.
• Moreover, FGF signaling inhibition dramatically reduces revascularization, hitting upon one of the hallmarks of cancers, angiogenesis, and reduces tumor burden in human tumors that depend on autocrine FGF signaling based on FGF2 upregulation following the common VEGFR-2 therapy for breast cancer.
• Gene expression profiling revealed the prevalence of specific fibroblast growth factors ( FGFs ) and FGF receptors in NSCLC cell lines, and found that FGF2, FGF9 and their receptors encompass a growth factor autocrine loop that is active in a subset of gefitinib-resistant NSCLC cell lines.
• Not long after FGF1 and FGF2 were isolated, another group isolated a pair of heparin-binding growth factors that they named HBGF-1 and HBGF-2, while a third group isolated a pair of growth factors that caused proliferation of cells in a bioassay containing blood vessel endothelium cells, which they called ECGF1 and ECGF2.