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FGF16 — FGF2

Pathways - manually collected, often from reviews:

• Reactome Reaction: FGF2 → FGF16 (reaction) Carpenter et al., Exp Cell Res 1999, Hart et al., Mol Biol Cell 2001, Wong et al., Proc Natl Acad Sci U S A 2002, Lax et al., Mol Cell 2002, Fong et al., J Biol Chem 2003, Mohammadi et al., Nature 1992, Agazie et al., Oncogene 2003, Ibrahimi et al., Hum Mol Genet 2004, Mohammadi et al., Mol Cell Biol 1991, Dionne et al., EMBO J 1990, Takeda et al., Clin Cancer Res 2007, Ahmed et al., Biochem J 2008, Byron et al., Cancer Res 2008, Schüller et al., Biochem J 2008, Qing et al., J Clin Invest 2009, Turner et al., Nat Rev Cancer 2010, Bai et al., Cancer Res 2010, Dutt et al., PloS one 2011, Wesche et al., Biochem J 2011, Klint et al., J Biol Chem 1995, Wang et al., Mol Cell Biol 1994, Mohammadi et al., Mol Cell Biol 1996, Ong et al., Biochem Biophys Res Commun 1996, Kanai et al., J Biol Chem 1997, Kouhara et al., Cell 1997, Ong et al., Biochem Biophys Res Commun 1997, Hadari et al., Mol Cell Biol 1998, Raffioni et al., J Biol Chem 1998

Text-mined interactions from Literome

Larsson et al., Cancer Res 2000 (Fibrosarcoma...) : Under these conditions, FGF-2 stimulated FGF receptor kinase activity was unaffected
Parenti et al., Am J Physiol Heart Circ Physiol 2001 (Hypertrophy) : ANG II pretreatment also potentiated the increase in inositol phosphate turnover and upregulated the cell expression of fibroblast growth factor ( FGF-2 ) induced by NE. Anti-FGF-2 neutralizing antibodies prevented the potentiating effect of ANG II on NE-induced cell growth
Chikazu et al., J Bone Miner Res 2001 : FGF-2 alone or in combination with sRANKL/ODF did not induce osteoclastogenesis from C7 cells ; however, FGF-2 from lower concentrations ( > or = 10 ( -11 ) M ) significantly decreased osteoclast formation induced by M-CSF in the presence of sRANKL/ODF
Stevens et al., Mol Endocrinol 2003 : Fibroblast growth factor 2 (FGF2) stimulated MAPK in osteoblasts, and pretreatment with T3 for 6 h induced a more rapid response to FGF that was increased in magnitude by 2- to 3-fold
Damon et al., Exp Cell Res 1992 : These observations suggest ( i ) that acidic and basic FGF activate a protein kinase, possibly protein kinase C, resulting in the phosphorylation of peptide T3 of TH ; ( ii ) that the FGFs and NGF share some but not all second messenger systems ; ( iii ) that heparin potentiates aFGF actions and inhibits bFGF actions in PC12 cells via distinct mechanisms ; ( iv ) that heparin does not potentiate the neurite outgrowth promoting activity of aFGF by enhancing binding to its PC12 cell surface receptor ; and ( v ) that heparin may coordinately regulate several activities of bFGF ( induction of protein phosphorylation, ODC and neurite outgrowth ) via a common mechanism, most likely by inhibiting the productive binding of bFGF to its PC12 cell surface receptor
Yasui et al., Digestion 2004 : Furthermore, FGF-2 dose-dependently induced FGF-2 mRNA expression in these cells
Flott-Rahmel et al., Neuroreport 1992 : Basic FGF mRNA induction by bFGF was investigated in cell cultures from rat brain, i.e. postnatal day 2 cortex and embryonic day 18 hippocampus
Weickert et al., Neuroscience 2005 : The anatomical distribution of these two FGF family members suggests that bFGF is endogenously positioned to be involved in ongoing neurogenesis in the adult hippocampus, and that FGF trophic signaling to differentiated neurons could involve the release of astrocytic bFGF acting on neuronal FGFR1 in the normal adult human hippocampus
Baguma-Nibasheka et al., Leuk Res 2005 (Leukemia) : A natural antisense RNA ( FGF-AS ) has been implicated in the posttranscriptional regulation of FGF-2 mRNA expression
Yamanaka et al., Cutis 2005 (Leg Ulcer...) : Endothelial cell FGF receptors are directly stimulated by bFGF ; also, bFGF promotes the regeneration of capillary-rich granulation tissue
Haines et al., Dev Biol 2006 : We confirmed this by showing that all FLRTs can interact with FGFR1 and FLRTs can be induced by the activation of FGF signalling by FGF-2
Crumley et al., Oncogene 1991 : High-affinity binding and activation of a truncated FGF receptor by both aFGF and bFGF
Black et al., Am J Physiol Cell Physiol 2008 : In addition, FGF-2 mediated increases in FGF-2 expression and PASMC proliferation were attenuated by inhibition of phosphatidylinositol 3-kinase, Akt, and NADPH oxidase
Saito et al., Biochem Biophys Res Commun 1991 (Mammary Neoplasms, Experimental) : Since we had previously shown that both basic fibroblast growth factor (bFGF) and testosterone stimulate the growth of mouse mammary carcinoma cells ( SC-3 ) in serum-free culture, we tested the effect of bFGF or testosterone on FGF receptor mRNA levels ... Northern blot analyses revealed that stimulation with bFGF resulted in a 5-fold increase in FGF receptor mRNA levels at 6-8 h followed by a decline to the unstimulated levels at 24 h. Simultaneous addition of cycloheximide blocked bFGF induced accumulation of FGF receptor mRNA, although exposure of SC-3 cells to cycloheximide alone caused marginal increase in its basal level
Naik et al., Cell Adh Migr 2008 (Neoplasms) : We have previously shown that in endothelial cells, JAM-A regulates basic fibroblast growth factor , ( FGF-2 ) -induced angiogenesis via augmenting endothelial cell migration
Eiselleova et al., Stem Cells 2009 : The transcription program that is responsible for the pluripotency of human ESCs ( hESCs ) is believed to be comaintained by exogenous fibroblast growth factor-2 (FGF-2) , which activates FGF receptors ( FGFRs ) and stimulates the mitogen activated protein kinase ( MAPK ) pathway
MacFarlane et al., Mol Endocrinol 2010 : In the present study, we examined the role of the endogenous FGF-AS transcript in the regulation of FGF-2 expression in the human lung adenocarcinoma cell line Seg-1
Matsumoto et al., Genes Cells 2013 : In cultured cardiomyocytes, Fgf16 expression was promoted by Fgf2
Hayward et al., In Vitro Cell Dev Biol Anim 1995 (Aneuploidy) : In serum-free culture in plastic dishes epidermal growth factor (EGF), transforming growth factor (TGF)-alpha, fibroblast growth factor (FGF) 1 ( aFGF ), and FGF 7 ( KGF ) induced increased proliferation in these cells whereas FGF 2 ( bFGF ), TGF-beta 1, and TGF-beta 2 inhibited proliferative activity
Bikfalvi et al., J Cell Biol 1995 : These results indicate that increased cell migration and FGF receptor down-regulation are mediated by the extracellular interaction of 18-kD bFGF with its cell surface receptor
Quarto et al., J Cell Sci 1994 : It is noteworthy that HSPG binding protects FGF-2 from denaturation and proteolytic degradation, provides a matrix bound or cell-surface reservoir of this factor for the cells and is required for the activation of FGF high-affinity receptors
Kenagy et al., Thromb Res 1995 : PDGF, bFGF and serum increased tPA ( serum > PDGF > FGF )
Zuber et al., J Cell Physiol 1997 : Cysteine-rich FGF receptor regulates intracellular FGF-1 and FGF-2 levels
Moy et al., Biochemistry 1997 : To gain insight into the mechanism of activation of the FGF receptor by FGF-2 and heparin, we have used NMR, dynamic light scattering, and HSPG-deficient cells and cell-free systems
Guillonneau et al., Exp Cell Res 1997 : In addition, in response to exogenous FGF2 , FGF1 is secreted in significant amounts into the extracellular medium at a rate comparable to FGF1 accumulation within the cell