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FGF9
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Fibroblast growth factor 9 precursor (FGF-9) (Glia-activating factor) (GAF) (Heparin-binding growth factor 9) (HBGF-9) ==Publications== {{medline-entry |title=[[FGFR3]] is a negative regulator of the expansion of pancreatic epithelial cells. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/17192470 |abstract=Fibroblast growth factors (FGFs) and their receptors (FGFRs) are key signaling molecules for pancreas development. Although [[FGFR3]] is a crucial developmental gene, acting as a negative regulator of bone formation, its participation remains unexplored in pancreatic organogenesis. We found that [[FGFR3]] was expressed in the epithelia in both mouse embryonic and adult regenerating pancreata but was absent in normal adult islets. In [[FGFR3]] knockout mice, we observed an increase in the proliferation of epithelial cells in neonates, leading to a marked increase in islet areas in adults. In vitro studies showed that [[FGF9]] is a very potent ligand for [[FGFR3]] and activates extracellular signal-related kinases (ERKs) in pancreatic cell lines. Moreover, [[FGFR3]] blockade or [[FGFR3]] deficiency led to increased proliferation of pancreatic epithelial cells in vivo. This was accompanied by an increase in the proportion of potential islet progenitor cells. Thus, our results show that [[FGFR3]] signaling inhibits the expansion of the immature pancreatic epithelium. Consequently, this study suggests that [[FGFR3]] participates in regulating pancreatic growth during the emergence of mature islet cells. |mesh-terms=* Aging * Animals * Animals, Newborn * Cell Line * Epithelial Cells * Islets of Langerhans * Mice * Mice, Inbred NOD * Mice, Knockout * Pancreas * Receptor, Fibroblast Growth Factor, Type 3 * Regeneration * Signal Transduction |full-text-url=https://sci-hub.do/10.2337/db05-1073 }} {{medline-entry |title=Expression of fibroblast growth factors and their receptors during full-thickness skin wound healing in young and aged mice. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/16079254 |abstract=The highly ordered process of wound healing involves the coordinated regulation of cell proliferation and migration and tissue remodeling, predominantly by polypeptide growth factors. Consequently, the slowing of wound healing that occurs in the aged may be related to changes in the activity of these various regulatory factors. To gain additional insight into these issues, we quantified the absolute copy numbers of mRNAs encoding all the fibroblast growth factors (FGFs), their receptors (FGFRs) and two other growth factors in the dorsal skin of young and aged mice during the healing of full-thickness skin excisional wounds. In young adult mice (8 weeks old), [[FGF7]], [[FGF10]] and [[FGF22]] mRNAs were all strongly expressed in healthy skin, and levels of [[FGF7]] and 10 but not 22 increased 2- to 3.5-fold over differing time courses after wounding. The levels of [[FGF9]], 16, 18 and especially 23 mRNAs were moderate or low in healthy skin but increased 2- to 33-fold after wounding. Among the four FGFRs, expression of only [[FGFR1]] mRNA was augmented during wound healing. Expression of transforming growth factor-beta and hepatocyte growth factor was also high in healthy skin and was upregulated during healing. Notably, in aged mice (35 weeks old), where healing proceeded more slowly than in the young, both the basal and wound-induced mRNA expression of most of these genes was reduced. While these results confirm the established notion that [[FGFR2]] IIIB ligands ([[FGF7]] and [[FGF10]]) are important for wound healing, they also suggest that decreased expression of multiple FGF ligands contributes to the slowing of wound healing in aged mice and indicate the potential importance of further study of the involvement of [[FGF9]], 16, 18 and 23 in the wound healing process. |mesh-terms=* Actins * Aging * Animals * Fibroblast Growth Factors * Gene Expression * Glyceraldehyde-3-Phosphate Dehydrogenases * Hepatocyte Growth Factor * Male * Mice * Mice, Mutant Strains * RNA, Messenger * Receptors, Fibroblast Growth Factor * Skin * Transforming Growth Factor beta * Wound Healing |full-text-url=https://sci-hub.do/10.1677/joe.1.06055 }} {{medline-entry |title=Expression and possible function of fibroblast growth factor 9 ([[FGF9]]) and its cognate receptors [[FGFR2]] and [[FGFR3]] in postnatal and adult retina. |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/15614790 |abstract=Fibroblast growth factors (FGFs) are important regulators of retinal development and survival. We examined the expression and distribution of [[FGF9]] and its preferred receptors [[FGFR2]]IIIc and [[FGFR3]]IIIc in this tissue. [[FGF9]] transcripts in whole rat retina were detected by RT-PCR but were not present in purified cultured Muller glia. Transcripts appeared as 3.2-kb and 4.0-kb bands on Northern blots, and Western blotting of whole retina revealed [[FGF9]]-immunoreactive bands at 30 and 55 kDa. [[FGF9]] mRNA demonstrated a biphasic expression profile, elevated at birth and adulthood, but relatively decreased during terminal retinal differentiation (4-14 days postnatal). Antibody labeling broadly reflected these findings: staining in vivo was observed mainly in the inner retina (and outer plexiform layer in adults) whereas [[FGF9]] was not detectable in cultured Muller glia. In adults, [[FGF9]] in situ hybridization also showed a detectable signal in inner retina. [[FGFR2]]IIIc and [[FGFR3]]IIIc were detected by RT-PCR, and Western blotting showed both FGFRs existed as multiple forms between approximately 100-200 kDa. [[FGFR2]] and [[FGFR3]] antibodies showed prominent labeling in the inner retina, especially in proliferating cultured Muller glia. Exogenous [[FGF9]] elicited a dose-dependent increase in Muller glial proliferation in vitro. These data suggest a role for [[FGF9]] in retinal differentiation and maturation, possibly representing a neuronally derived factor acting upon glial (and other) cells. |mesh-terms=* Aging * Animals * Animals, Newborn * Cell Differentiation * Cell Proliferation * Dose-Response Relationship, Drug * Fibroblast Growth Factor 9 * Fibroblast Growth Factors * Gene Expression Regulation, Developmental * Neuroglia * Neurons * Protein Isoforms * Protein-Tyrosine Kinases * RNA, Messenger * Rats * Rats, Wistar * Receptor Protein-Tyrosine Kinases * Receptor, Fibroblast Growth Factor, Type 2 * Receptor, Fibroblast Growth Factor, Type 3 * Receptors, Fibroblast Growth Factor * Retina |full-text-url=https://sci-hub.do/10.1002/jnr.20363 }}
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