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FGFR3 — INS

Pathways - manually collected, often from reviews:

• WikiPathways Focal Adhesion-PI3K-Akt-mTOR-signaling pathway: EFNA1/FGF1/FGF11/FGF10/EFNA2/EGF/FGF12/CSF1/ANGPT4/ANGPT2/ANGPT1/VEGFA/EFNA3/EFNA4/EFNA5/FGF14/FGF19/FGF17/FGF18/FGF2/FGF3/FGF4/FGF6/FGF7/FGF8/FGF9/FIGF/HGF/IGF1/INS/INS/KITLG/VEGFC/VEGFB/PDGFB/PGF/PDGFA/NGF/PDGFC/FGF21/FGF22/PDGFD/FGF20/FGF16 → FGFR2/KDR/INSR/FGFR3/IGF1R/KIT/FGFR1/EPHA2/EGFR/CSF1R/FGFR4/FLT1/FLT4/NGFR/MET/PDGFRA/PDGFRB/TEK (activation)
  

Text-mined interactions from Literome

Miura et al., Toxicol Appl Pharmacol 2001 : TPT administration significantly suppressed the insulin secretion induced by 15 and 27.8 mM glucose or 100 microM ACh in the presence of 5.5 mM glucose
Yanagisawa et al., Jpn J Physiol 2001 : The open-state probability ( p ) of K ( + ) channel induced by the application of acetylcholine (ACh) to the bath solution was increased by insulin in the presence of ACh
Nakano et al., Endocrinology 2002 (Calcium Signaling) : We investigated the mechanism by which acetylcholine (ACh) regulates insulin secretion from rat pancreatic beta-cells ... In an extracellular solution with 5.5 mM glucose, ACh increased the rate of insulin secretion from rat islets ... In islets treated with bisindolylmaleimide ( BIM ), a PKC inhibitor, ACh still increased insulin secretion, but the increment was lower than that without BIM ... In the presence of nifedipine, an L-type Ca ( 2+ ) channel blocker, on the other hand, ACh did not increase insulin secretion
Miguel et al., Biochim Biophys Acta 2002 : Acetylcholine (ACh) , a major neurotransmitter from the autonomic nervous system, regulates the cholinergic stimulation of insulin secretion, through interactions with muscarinic receptors ... The present study has characterised the individual involvement of muscarinic receptor subtypes in ACh induced insulin secretion, using clonal beta cells and selective muscarinic receptor antagonists
Miguel et al., Biochem Pharmacol 2003 : GLP-1 ( 20 nM ) and ACh ( 100 microM ) increased insulin secretion by 24-47 %, whereas in combination there was a further 89 % enhancement of insulin release
Kajikuri et al., Jpn J Physiol 1992 : Divalent cation ionophores abolished the increase in [ Ca2+ ] i but not the synthesis of Ins ( 1,4,5 ) P3 induced by subsequent application of 10 microM ACh in Ca ( 2+ ) -free solution, suggesting that the Ca2+ released by Ins ( 1,4,5 ) P3 following application of ACh does not act to accelerate the ACh induced synthesis of Ins ( 1,4,5 ) P3 in smooth muscle of the porcine coronary artery
Lee et al., Biochem J 1992 : The increase in accumulation of Ins ( 1,4,5 ) P3 and Ins ( 1,3,4,5 ) P4 by Li+ was absolutely dependent on the presence of ACh
Chen et al., Am J Physiol Heart Circ Physiol 2006 (Diabetes Mellitus, Type 2...) : No significant changes in fasting glucose ( 156 +/- 11 mg/dl ), insulin ( 14 +/- 2 microU/ml ), SI ( Clamp ) [ 2.71 +/- 0.46 x 10 ( -4 ) dl x kg ( -1 ) x min ( -1 ) / ( microU/ml ) ], or forearm blood flow in response to ACh , SNP, or insulin were observed after vitamin C treatment
Lee et al., Clin Exp Pharmacol Physiol 2006 : 6. The results of the present study suggest that ginsenoside Rh2 has the ability to increase insulin secretion as a result of the release of ACh from nerve terminals that then stimulates muscarinic M ( 3 ) receptors in pancreatic cells
Gautam et al., Diabetes Obes Metab 2007 (Diabetes Mellitus, Type 2...) : Various lines of evidence indicate that acetylcholine (ACh) , the major neurotransmitter of the parasympathetic nervous system, can enhance glucose stimulated insulin secretion from pancreatic beta-cells
Gireesh et al., J Neurosci Res 2008 (Diabetes Mellitus, Experimental) : Acetylcholine (ACh) , a major neurotransmitter from autonomic nervous system, regulates the cholinergic stimulation of insulin secretion, through interactions with muscarinic receptors
Perticone et al., Int J Cardiol 2013 : On univariate analysis, incident diabetes was inversely related with ACh stimulated FBF ( HR=0.65, 95 % CI=0.52-0.82 ; P < 0.001 ) and directly with serum CRP ( HR=1.22, 95 % CI=1.09-1.37 ; P < 0.001 ), HOMA-index ( HR=1.20, 95 % CI=1.05-1.37 ; P=0.007 ), fasting insulin ( HR=1.05, 95 % CI=1.01-1.09 ; P=0.006 ) and age ( HR=1.03, 95 % CI=1.00-1.05 ; P=0.014 )
Ruiz de Azua et al., Life Sci 2012 (Diabetes Mellitus, Type 2) : The activation of these receptors by ACh or other muscarinic agonists leads to the augmentation of glucose induced insulin release via multiple mechanisms
Müller et al., Digestion 1986 : The effects of Ach and GIP on insulin secretion from the rat pancreas were additive at 0.05 X 10 ( -6 ) M Ach and slightly, but not significantly less than additive at 0.25 or 2.5 X 10 ( -6 ) M Ach
Ejiri et al., Diabetes Res Clin Pract 1989 (Myasthenia Gravis) : Atropine suppressed insulin release, and alpha-Btx and anti-Ach.R.Ab potentiated it ; atropine did not suppress glucagon release, while alpha-Btx and anti-Ach.R.Ab raised it
Henquin et al., Endocrinology 1988 : ACh also accelerated 86Rb+ and 45Ca2+ efflux and barely affected basal insulin release ... ACh also accelerated 86Rb+ and 45Ca2+ efflux and strongly potentiated insulin release
Billewicz-Stankiewicz et al., Acta Physiol Pol 1980 : Intraperitoneal insulin caused no changes in the level and synthesis of ACh while in vitro ACh synthesis was increased in the cortex as well as striatum after insulin
Burr et al., Am J Physiol 1976 : Continuous challenge with ACh produces a biphasic insulin release response, both phases of which are reduced when the medium calcium concentration is reduced during stimulation ; when the calcium content is reduced during an initial perifusion period of 30 min and then replaced during subsequent stimulation only the first phase of the response to ACh is affected ; perifusion with epinephrine prior to stimulation with ACh produces enhancement of both phases of ACh induced insulin release when calcium in both media is normal
Gao et al., Endocrinology 1994 : In the presence of 15 mM glucose and 2.5 mM Ca2+, AVP and ACh stimulated inositol phosphate ( IP ) formation, increased cytoplasmic Ca2+ (Cai2+), and potentiated insulin release ... In the absence of extracellular Ca2+, only ACh induced a short lived increase in Cai2+ and insulin ... Under these conditions, the effects of AVP and ACh on IP production and Cai2+ were practically abolished, and only ACh transiently increased insulin release
Ji et al., Cell Calcium 1993 : ACh induced Ins ( 1,4,5 ) P3 production increased rapidly within the first 2 min and continued to rise over the next 20 min. ACh was a much more effective stimulus of inositol phosphate production at native ( up to 35-fold ) than at expressed receptors ( less than 2-fold )
Ito et al., Diabetologia 1995 (Diabetes Mellitus, Experimental) : To elucidate the mechanisms of insensitivity of hormone secretion to glucose in streptozotocin induced diabetic rat islets, we investigated the effects of acetylcholine (ACh) and norepinephrine on insulin and glucagon secretion in response to changes in glucose concentration, using perfused pancreas preparations