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  <Comment Source="WikiPathways-description">This pathway depicts the downstream signaling of serotonin via receptor 2A, resulting in the activation of STAT3.</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>
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    <Comment>5-hydroxytryptamine (serotonin) receptor 2A</Comment>
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    <Comment>Janus kinase 2</Comment>
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    <Comment>guanine nucleotide binding protein, alpha q polypeptide</Comment>
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    <Comment>signal transducer and activator of transcription</Comment>
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    <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. 
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    <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. 
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    <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). 

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    <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>
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    <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. 

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