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JAK2 phosphorylates JAK2 on tyrosine. 18 / 19
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"As expected, PRLR and Jak2 activation led to tyrosine phosphorylation of Jak2, PRLR as well as wild type and catalytically inactive form of SHP-2."

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"The EPO responsiveness of the cell lines was assessed through epoetin alpha-induced tyrosine phosphorylation of Janus kinase 2 (JAK2)."

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"Moreover, Gal-3 stimulates either extracellular or intracellular signaling cascades, depending on the cell type, via increased tyrosine phosphorylation of Janus kinase 2 (JAK2) and other signal transd[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Consistent with these observations, we found that deletion of SH2-B impaired leptin-stimulated JAK2 activation and tyrosine phosphorylation of both STAT3 and IRS2 in the hypothalamus."

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"In addition, it has been shown in ovarian cancer and sarcoma cells expressing constitutively active JAK2 that cisplatin significantly inhibited tyrosine phosphorylation and kinase activity of JAK2 in a dose- and time-dependent manner [29]."

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"15 (S)-HETE also induced tyrosine phosphorylation of Janus kinase 2 (Jak2) in VSMCs, and its inhibition substantially reduced STAT3 phosphorylation, MCP-1 expression, and VSMC migration."

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"Indeed JAK2, when activated, mediates the phosphorylation of JAK2 itself and aforementioned three tyrosine residues of Ob-Rb: TyrY985, TyrY1077 and TyrY1138."

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"After the binding of EPO to its cognate receptor (EPOR), EPOR is tyrosine-phosphorylated by Janus kinase 2 (Jak2) and other tyrosine kinases, and thereby recruits various src homology (SH) domain-2-co[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"However, upon GCSF binding, four conserved tyrosine residues in the cytoplasmic domain develop an increased affinity to STAT3, the adapter proteins Src homology and collagen homology (Shc), growth factor receptor bound protein 2, and suppressor of cytokine signaling 3 (SOCS3) after being phosphorylated by JAK1, JAK2, and Tyrosine kinase-2 Tyrosine kinase-2 (TYK2) (17)."

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"In particular, we investigated JAK2 tyrosine kinase activation and phosphorylation (and subsequent activation) of STAT1 and STAT3 transcription factors."

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"Upon binding of leptin to its extracellular domain, homodimerized LepRb undergoes a conformational change that enables the activation of JAK2, which then phosphorylates other tyrosine residues within the LepRb–JAK2 complex to activate downstream signalling cascades (FIG."

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"GH-triggered activation of JAK2 causes GHR and JAK2 tyrosine phosphorylation and induces signaling systems including STATs (most notably STAT5b), ERKs, and PI3-kinase [14–16] ( Fig. 1 )."

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"Furthermore, in vitro treatment of activated T-cells with quercetin in EAE amelioration may be related with IL-12 production inhibition and the blockage of tyrosine phosphorylation of Janus kinase 2 (JAK2), tyrosine kinase 2 (TYK2) and signal transducer and activator of transcription 3 (STAT3), resulting in inhibition of T cell proliferation and Th1 cells differentiation, with parallel INF-γ production decrease reaching up to 87.5% [27]."

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"Interestingly, LY294002 enhanced the TPO induced DNA binding activity of Stat5 without affecting the Jak2 activation and tyrosine phosphorylation of Stat5."

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"Following leptin binding, JAK2 is activated resulting in phosphorylation of JAK2 as well as specific tyrosine residues within the C-terminal domain of ObR."

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"Janus kinase 2 (JAK2) is then activated, resulting in JAK2 autophosphorylation and tyrosine phosphorylation of IL-23R, which in turn result in the recruitment, phosphorylation, homodimerization, and nuclear translocation of signal transducer and activator of transcription 3 (STAT3)."

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"Recently, adaptor molecule containing PH and SH2 domains (APS) was shown to be tyrosine-phosphorylated by Jak2 at its C-terminal tyrosine residue and to interact with c-Cbl [14] ."

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"A 15 min incubation of PRL-naive cells led to substantial tyrosine phosphorylation of Jak 2 and Stat 5a by U-PRL and an essentially equivalent Jak 2 activation by S179D PRL."