Serotonin receptor 2 and STAT3 signaling (Mus musculus)

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<?xml version="1.0" encoding="UTF-8"?> <Pathway xmlns="http://pathvisio.org/GPML/2013a" Name="Serotonin Receptor 2 and STAT3 Signaling" Last-Modified="12/1/2011" Organism="Mus musculus"> <Comment Source="WikiPathways-description">This pathway is courtesy of Ariadne Genomics Pathway Studio.</Comment> <Comment Source="WikiPathways-category">Cellular Process</Comment> <Comment Source="HomologyConvert">This pathway was inferred from Homo sapiens pathway [http://www.wikipathways.org/index.php?title=Pathway:WP733&amp;oldid=45035 WP733(r45035)] with a 50% conversion rate.</Comment> <Graphics BoardWidth="353.0" BoardHeight="483.0"/> <DataNode TextLabel="serotonin" GraphId="d4a3b" Type="Metabolite"> <Graphics CenterX="183.0" CenterY="89.0" Width="80.0" Height="20.0" ZOrder="32768" FontSize="10" Valign="Middle" Color="00cc00"/> <Xref Database="CAS" ID="50-67-9"/> </DataNode> <DataNode TextLabel="HTR2A" GraphId="afa00" Type="GeneProduct"> <Comment>5-hydroxytryptamine (serotonin) receptor 2A</Comment> <Graphics CenterX="182.0" CenterY="176.0" Width="80.0" Height="20.0" ZOrder="32768" FontSize="10" Valign="Middle" Color="cc0000"/> <Xref Database="" ID=""/> </DataNode> <DataNode TextLabel="Gnaq" GraphId="cafea" Type="GeneProduct"> <Comment>guanine nucleotide binding protein, alpha q polypeptide</Comment> <Graphics CenterX="283.0" CenterY="254.0" Width="80.0" Height="20.0" ZOrder="32768" FontSize="10" Valign="Middle" Color="cc0000"/> <Xref Database="Entrez Gene" ID="14682"/> </DataNode> <DataNode TextLabel="JAK2" GraphId="cacda" Type="GeneProduct"> <Comment>Janus kinase 2</Comment> <Graphics CenterX="182.0" CenterY="336.0" Width="80.0" Height="20.0" ZOrder="32768" FontSize="10" Valign="Middle" Color="cc0000"/> <Xref Database="" ID=""/> </DataNode> <DataNode TextLabel="Stat3" GraphId="ce8ce" Type="GeneProduct"> <Comment>signal transducer and activator of transcription</Comment> <Graphics CenterX="180.0" CenterY="443.0" Width="80.0" Height="20.0" ZOrder="32768" FontSize="10" Valign="Middle" Color="cc0000"/> <Xref Database="Entrez Gene" ID="20848"/> </DataNode> <Interaction GraphId="be6b0"> <Comment>Direct Regulation serotonin --+&gt; HTR2A</Comment> <Comment>8808177 (Organ: blood vessel, CellType: neural) Stimulation of the 5-HT2A receptors by serotonin has been reported to exert an excitatory effect on neocortical neurons in rats and mice, to facilitate ischaemia-induced release of excitatory amino acids and to mediate the vasomotor constrictor component of the response of blood vessels to 5-HT. 5-HT2A receptor antagonists have, therefore, been proposed as potential protectants against the effects of cerebral ischaemia. 14654098 (Organ: hippocampal, CellType: neural) High doses of 5-HT also recruited both 5-HT2 and 5-HT3 receptors, causing an increase in the rate and amplitude of sIPSCs. cOA (1 microM), in the presence of Y 25130, failed to potentiate the 5-HT2 receptor induced enhancement of sIPSCs. 11157082 Since 5-HT enhances GABA release ( Liu and Alreja 1997 ), 5-HT2A receptor blockade of clozapine may directly reduce pallidal GABA release. 10431683 Mirtazapine is an atypical antidepressant with alpha 2 adrenergic antagonist and serotonin 5-HT2 and 5-HT3 receptor-blocking activity. 8627578 Neomycin (3 mM) inhibited maximal 5-HT-induced contraction by approximately 50% without inhibiting [3H]5-HT binding to 5-HT2A receptors. 9016798 (Tissue: crypt) Superfusing 5-HT (10 microM) in the bath solution increased both K+ and Cl- currents, which were antagonized by the presence of ketanserin (1 microM), a selective 5-HT2A antagonist, in the bath solution. 9272731 (Tissue: mesangia) The L-type channel blocker verapamil, however, dose-dependently (0.1-10 microM) and specifically inhibited 5-HT-elicited Ca2+ signals by interference with binding of 5-HT to 5-HT2A receptors. 5-HT-mediated Ca2+ release was reduced by 80% when protein kinase C was activated by the phorbolester TPA (0.1 microM). </Comment> <BiopaxRef>c21</BiopaxRef> <BiopaxRef>c0c</BiopaxRef> <BiopaxRef>fee</BiopaxRef> <BiopaxRef>f4e</BiopaxRef> <BiopaxRef>d34</BiopaxRef> <BiopaxRef>f11</BiopaxRef> <BiopaxRef>afb</BiopaxRef> <Graphics ZOrder="12288" LineThickness="1.0"> <Point X="183.0" Y="99.0" GraphRef="d4a3b" RelX="0.0" RelY="1.0"/> <Point X="182.0" Y="166.0" GraphRef="afa00" RelX="0.0" RelY="-1.0" ArrowHead="Arrow"/> </Graphics> <Xref Database="" ID=""/> </Interaction> <Interaction GraphId="ba2f3"> <Comment>DirectRegulation HTR2A --+&gt; GNAQ</Comment> <Comment>9439849 (Organ: hypothalamic, Tissue: cortex) These results suggest that fluoxetine gradually increases the G-protein coupling of 5-HT2A/2C receptors without altering the levels of Gq- or G11-proteins. 12721328 (Organ: hypothalamic, Tissue: cortex, CellType: neural) These fluoxetine-induced changes in 5-HT2A receptor signaling occur without changing the levels of Galphaq or RGS4 proteins. </Comment> <BiopaxRef>cd8</BiopaxRef> <BiopaxRef>d9a</BiopaxRef> <Graphics ZOrder="12288" LineThickness="1.0"> <Point X="202.0" Y="186.0" GraphRef="afa00" RelX="0.5" RelY="1.0"/> <Point X="283.0" Y="244.0" GraphRef="cafea" RelX="0.0" RelY="-1.0" ArrowHead="mim-necessary-stimulation"/> </Graphics> <Xref Database="" ID=""/> </Interaction> <Interaction GraphId="d2154"> <Comment>Binding HTR2A ---- JAK2</Comment> <Comment>9169451 The blot showing 5-HT 2A receptor-Jak2 kinase association (Fig. 3 A ) was stripped and reprobed with anti-STAT3 antibody. </Comment> <BiopaxRef>b19</BiopaxRef> <Graphics ZOrder="12288" LineThickness="1.0" Color="cc00cc"> <Point X="182.0" Y="186.0" GraphRef="afa00" RelX="0.0" RelY="1.0"/> <Point X="182.0" Y="326.0" GraphRef="cacda" RelX="0.0" RelY="-1.0"/> </Graphics> <Xref Database="" ID=""/> </Interaction> <Interaction GraphId="fe91c"> <Comment>Prot Modification JAK2 --+&gt; STAT3</Comment> <Comment>15156153 Hes proteins associate with JAK2 and STAT3, and facilitate complex formation between JAK2 and STAT3, thus promoting STAT3 phosphorylation and activation. 15688010 Tkip also inhibited constitutive (DU145) and IL-6-induced (LNCaP) activation of STAT3, consistent with the fact that STAT3 activation is mediated by JAK2. 11708838 (Organ: heart, CellLineName: IPC) The results demonstrated extensive phosphorylation of JAK2 and STAT3 in the IPC hearts which was almost completely abolished by an inhibitor of JAK2, AG490. 15155836 (Organ: kidney, CellLineName: 293) Inhibition of c-Src and Janus kinase 2 and 3 activities abolished STAT3 activation induced by Galpha14QL, but no physical association between Galpha14QL and c-Src could be detected by coimmunoprecipitation. 15650183 (Organ: liver) Using a series of inhibitors and dominant negative mutants, we show that HCV-induced activation of STAT-3 is mediated by oxidative stress and influenced by the activation of cellular kinases, including p38 mitogen-activated protein kinase, JNK, JAK-2, and Src. 15151905 (Tissue: endothelial) IL-6 treatment increased the phosphorylation of JAK2, an upstream activator of STAT3. 10891587 (Organ: brain, Tissue: glia, CellType: neural) The PSD fraction also had a janus kinase 2 (Jak2)-like molecule, Jak2, believed to phosphorylate Stat3. </Comment> <BiopaxRef>bfb</BiopaxRef> <BiopaxRef>d8d</BiopaxRef> <BiopaxRef>fe9</BiopaxRef> <BiopaxRef>a3c</BiopaxRef> <BiopaxRef>aa9</BiopaxRef> <BiopaxRef>e0c</BiopaxRef> <BiopaxRef>e51</BiopaxRef> <Graphics ZOrder="12288" LineThickness="1.0" Color="999900"> <Point X="182.0" Y="346.0" GraphRef="cacda" RelX="0.0" RelY="1.0"/> <Point X="180.0" Y="433.0" GraphRef="ce8ce" RelX="0.0" RelY="-1.0" ArrowHead="mim-necessary-stimulation"/> </Graphics> <Xref Database="" ID=""/> </Interaction> <Interaction GraphId="b5b37"> <Comment>Regulation GNAQ --+&gt; JAK2</Comment> <Comment>15640156 (CellLineName: COS-7) Indeed, transfection of a constitutively activated mutant of Galpha(q) (Q209L) in COS-7 cells demonstrated that Galpha(q) is able to associate and activate JAK2. </Comment> <BiopaxRef>f9a</BiopaxRef> 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