p(HGNC:JAK2)

Entity

Name

JAK2

Namespace

hgnc

Namespace Version

20180906

Namespace URL

https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/hgnc-names.belns

JAK-2, also implicated in the neuroprotective pathway, may play a role in linking nAChR action with calcium signaling, because JAK-2 phosphorylates inositol 1,4,5-triphosphate receptors through its activation of FYN (Wallace et al., 2005). PubMed:19293145

Nicotine induced phosphorylation of STAT-3 (signal transducer and activator of transcription 3) in peritoneal macrophages is mediated by an alpha7-dependent activation of JAK-2, as part of the anti-inflammatory action of vagal nerve stimulation (de Jonge et al., 2005). PubMed:19293145

JAK-2, another early target in the nicotine neuroprotection pathway that may mediate signaling between the nAChR and the PI3K pathway (Shaw et al., 2002), may link nAChR activation with the JAK/signal transducer and activator of transcription 3 (STAT-3) protective pathway. JAK-2 is also activated by nicotine in non-neuronal cells such as nAChR-bearing keratinocytes (Arredondo et al., 2006). In a microarray study, expression of 8 of 33 JAK/STAT pathway genes was altered when human bronchial epithelial cells were exposed to 5 microM nicotine for 4 to 10 h (Tsai et al., 2006). Thus, the JAK-2/STAT-3 pathway is activated by exposure to nicotine. PubMed:19293145

JAK-2, another early target in the nicotine neuroprotection pathway that may mediate signaling between the nAChR and the PI3K pathway (Shaw et al., 2002), may link nAChR activation with the JAK/signal transducer and activator of transcription 3 (STAT-3) protective pathway. JAK-2 is also activated by nicotine in non-neuronal cells such as nAChR-bearing keratinocytes (Arredondo et al., 2006). In a microarray study, expression of 8 of 33 JAK/STAT pathway genes was altered when human bronchial epithelial cells were exposed to 5 microM nicotine for 4 to 10 h (Tsai et al., 2006). Thus, the JAK-2/STAT-3 pathway is activated by exposure to nicotine. PubMed:19293145

Furthermore, inhibitors of SRC, a closely related tyrosine kinase, also prevent nicotinic protection of differentiated PC12 cells against serum-deprivation-induced cell death (Li et al., 1999b), and inhibitors of FYN or Janus kinase-2 (JAK-2) block the neuroprotection against Abeta toxicity of therapeutic AChE inhibitors (Takada-Takatori et al., 2006). PubMed:19293145

JAK-2, also implicated in the neuroprotective pathway, may play a role in linking nAChR action with calcium signaling, because JAK-2 phosphorylates inositol 1,4,5-triphosphate receptors through its activation of FYN (Wallace et al., 2005). PubMed:19293145

JAK-2, another early target in the nicotine neuroprotection pathway that may mediate signaling between the nAChR and the PI3K pathway (Shaw et al., 2002), may link nAChR activation with the JAK/signal transducer and activator of transcription 3 (STAT-3) protective pathway. JAK-2 is also activated by nicotine in non-neuronal cells such as nAChR-bearing keratinocytes (Arredondo et al., 2006). In a microarray study, expression of 8 of 33 JAK/STAT pathway genes was altered when human bronchial epithelial cells were exposed to 5 microM nicotine for 4 to 10 h (Tsai et al., 2006). Thus, the JAK-2/STAT-3 pathway is activated by exposure to nicotine. PubMed:19293145

Nicotine induced phosphorylation of STAT-3 (signal transducer and activator of transcription 3) in peritoneal macrophages is mediated by an alpha7-dependent activation of JAK-2, as part of the anti-inflammatory action of vagal nerve stimulation (de Jonge et al., 2005). PubMed:19293145

JAK-2, another early target in the nicotine neuroprotection pathway that may mediate signaling between the nAChR and the PI3K pathway (Shaw et al., 2002), may link nAChR activation with the JAK/signal transducer and activator of transcription 3 (STAT-3) protective pathway. JAK-2 is also activated by nicotine in non-neuronal cells such as nAChR-bearing keratinocytes (Arredondo et al., 2006). In a microarray study, expression of 8 of 33 JAK/STAT pathway genes was altered when human bronchial epithelial cells were exposed to 5 microM nicotine for 4 to 10 h (Tsai et al., 2006). Thus, the JAK-2/STAT-3 pathway is activated by exposure to nicotine. PubMed:19293145

JAK-2, another early target in the nicotine neuroprotection pathway that may mediate signaling between the nAChR and the PI3K pathway (Shaw et al., 2002), may link nAChR activation with the JAK/signal transducer and activator of transcription 3 (STAT-3) protective pathway. JAK-2 is also activated by nicotine in non-neuronal cells such as nAChR-bearing keratinocytes (Arredondo et al., 2006). In a microarray study, expression of 8 of 33 JAK/STAT pathway genes was altered when human bronchial epithelial cells were exposed to 5 microM nicotine for 4 to 10 h (Tsai et al., 2006). Thus, the JAK-2/STAT-3 pathway is activated by exposure to nicotine. PubMed:19293145

JAK-2, also implicated in the neuroprotective pathway, may play a role in linking nAChR action with calcium signaling, because JAK-2 phosphorylates inositol 1,4,5-triphosphate receptors through its activation of FYN (Wallace et al., 2005). PubMed:19293145