IndraLab

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JAK2 phosphorylates STAT3. 10 / 462
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"The selective inhibition of JAK2 can prevent STAT3 phosphorylation and dimerization, and several JAK2 inhibitors including AG490, WP1066, and SD-1029 have been reported in recent literature."

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"Mechanistic studies revealed that upon hypoxia‐induced activation, JAK2 phosphorylates STAT3, which then translocates into the nucleus, where it binds to the CCNA2 promoter to transcribe cyclin A2 expression, thereby promoting PASMC hyperplasia along with pulmonary vascular remodelling (Figure xref )."

sparser
"PRP3 overexpression was found to promote the expression level of phosphorylated JAK2 (P < 0.01) and phosphorylated STAT3 (P < 0.01) in HaCaT cells (Fig.  xref )."

sparser
"They could show that mutant JAK2 caused the phosphorylation of STAT3 and STAT5, thereby enhancing PD-L1 promoter activity causing increased PD-L1 protein levels onJAK2 V617F mutant myeloid cells."

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"These tyrosine kinase receptors recruit receptor associated kinases such as Janus kinase 2 (JAK2), which catalyzes the activating phosphorylation of STAT3."

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"The leptin receptor is a member of the class 1 cytokine receptor superfamily, which can activate a number of signal transduction components, including JAK2, which subsequently phosphorylates STAT3 to mediate transcription of a number of genes."

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"SOCS-3 inhibits leptin signaling by binding Ob-Rb and preventing Jak2 phosphorylation of Stat3, and targeting the activated receptor complex for degradation."

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"Since LIF acts through gp130 to activate JAK2, which phosphorylates STAT3, we looked at STAT3 phosphorylation in DRG neurons and found that it was increased."

isi
"Thus, JAK2 downstream signaling proteins phosphorylation of STAT3 at Y705 and S727 as well as STAT3 target protein Mcl-1 expression was decreased with treatment of Lico B."

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"Stat3 is frequently phosphorylated and activated in the majority of breast and ovarian cancers [XREF_BIBR], where cytokines and growth factors such as IL-6 bind to specific receptors and activate JAK2 which, in turn, phosphorylates Stat3 and prompts translocation of pStat3 to the nucleus."
JAK2 phosphorylates STAT3 on Y705. 10 / 103
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No evidence text available

sparser
"Phosphorylation of STAT3 at tyrosine 705 (Y705) by JAK2 is one of the most important and well established cytoplasmic functions of JAK2 xref , xref ."

sparser
"To determine whether JAK2 directly phosphorylates STAT3, we performed an in vitro kinase assay using kinase active JAK2 protein with STAT3 protein we purified from Sf9 insect cells and found that JAK2 phosphorylates STAT3 at Y705 (Fig. 5B)."

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"STAT3 is recruited to the LEPR-B and is phosphorylated by JAK2 on Tyr 705, allowing for STAT3 dimerisation and translocation to the nucleus to mediate gene transcription."

sparser
"Furthermore, treatment of JAK2 clinical medicine AZD1480 to ESCC cells showed similar tendency with Lico B. Thus, JAK2 downstream signaling proteins phosphorylation of STAT3 at Y705 and S727 as well as STAT3 target protein Mcl-1 expression was decreased with treatment of Lico B. Our results suggest that Lico B inhibits ESCC cell growth, arrests cell cycle and induces apoptosis, revealing the underlying mechanism involved in JAK2/STAT3 signaling pathways after Lico B treatment."

sparser
"The activated IL-6/IL-6 receptor/gp130 complex now recruits Janus kinase 2 (JAK2), which directly phosphorylates STAT3 at tyrosine 705 (Tyr705)."

sparser
"JAK2 phosphorylates STAT3 at Y705 to activate its nuclear import and transcriptional activity xref , xref ."

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"IL6 binding activates the phosphorylation of a JAK (mostly JAK2), which in turn will phosphorylate STAT3 on amino acid Y705 [XREF_BIBR]."

No evidence text available

sparser
"Also, JAK2 phosphorylates STAT3 at Tyr705, inducing its dimerization and translocation to the nucleus where it regulates the expression of different proteins involved in cancer progression, such as cyclin D1, COX2, VEGF, and SOCS3, a negative regulator of leptin signaling [ xref , xref ]."
JAK2 phosphorylates STAT3 on tyrosine. 10 / 34
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"Furthermore, our study reveals that PDGF-BB- and bFGF induced proliferation does not affect the osteogenic differentiation potential of hBMMSCs.All of the three GFs activated the hBMMSC ERK1/2 pathway[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Upon activation, STAT3 is phosphorylated by the non receptor protein tyrosine kinases janus kinase 2 (JAK2), leading to the formation of STAT3 dimer and translocation into the nucleus [XREF_BIBR, XREF_BIBR]."

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"Tyrphostin AG490, a specific inhibitor of Jak-2, significantly reduced tyrosine phosphorylation and DNA binding activity of STAT-3 and DNA synthesis induced by 5 (S)-HETE."

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"Additionally, Janus kinase 2 (JAK2) and tyrosine kinase 2 (TYK2) were recruited onto MyD88 to induce the phosphorylation and activation of the transcription factor signal transducer and activator of transcription-3 (STAT-3)."

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"The histamine induced enhancement of activity or tyrosine and serine phosphorylation of STAT3 were suppressed by pyrilamine, but not by cimetidine or thioperamide, which suggests the involvement of H1[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Upon cytokine stimulation, Janus kinase 2 (JAK2) phosphorylates STAT3 at tyrosine residues, which leads to the dimerization of STAT3 via reciprocal interactions between the SH2 domain of one monomer and the phosphorylated tyrosine of the other."

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"Binding of IL-5 to its specific receptor activates JAK2 which leads to the tyrosine phosphorylation of STAT3 proteins."

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"XREF_BIBR SD-1029 appears to act by inhibiting the kinase JAK2, which mediates STAT3 tyrosine phosphorylation in a range of tumor types."

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"WP1066 is a JAK-2 kinase inhibitor that blocks STAT3 tyrosine phosphorylation, and has proapoptotic and antiproliferative activity in a variety of cancers, including glioma [XREF_BIBR, XREF_BIBR]."

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"The stimulation of JAK2 activity then in turn enhances STAT1 and STAT3 Tyr phosphorylation and DNA binding activity, which identifies STAT transcription factors as downstream targets of CER."
Phosphorylated JAK2 phosphorylates STAT3. 9 / 9
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"Results showed that JAK2 inhibitor AG490 could concentration-dependently inhibit phosphorylation of JAK2 and STAT3 inhibitor Stattic could concentration-dependently inhibit phosphorylation of STAT3."

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"Increased JAK2 phosphorylation accompanied increased STAT3 phosphorylation after CD40 ligation."

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"Moreover, 10a selectively inhibited JAK2 and STAT3 phosphorylation as well as IL-6 induced STAT3 phosphorylation."

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"The phosphorylated JAK2 subsequently phosphorylates STAT3, which results in the dimerization and translocation of STAT3 to the nucleus."

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"It is known that JAK2 phosphorylation promotes dimerization and phosphorylation of STAT3 monomers."

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"STAT3 is a downstream target of IL-6, and upon IL-6 binding to the IL-6Ralpha receptor, JAK2 is phosphorylated and initiates the phosphorylation of STAT3."

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"Phosphorylation of JAK2 subsequently triggers the phosphorylation of signal transducer and activator of transcription 3 (STAT3), promoting its dimerization."

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"Hypothalamic phosphorylated Janus kinase 2 (p-JAK2), phosphorylated signal transducer and activator of transcription 3 (p-STAT3), and phosphatidylinositol-3-kinase (PI3K) signaling, and hepatic sterol regulatory element binding protein-1 (SREBP-1) were qualified by Western blotting."

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"Upon IL-6 binding to the IL-6Ralpha, JAK2 is phosphorylated and initiates the phosphorylation of STAT3."
JAK2-V617F phosphorylates STAT3. 5 / 5
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"JAK2 V617F induces constitutive phosphorylation of STAT3 and STAT5, and uses signalling targets such as Ras/MEK/ERK and PI3K and Akt pathways."

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"In addition, the Jak2 V617F mutation contributes to myelofibrosis by constitutively phosphorylating STAT3 and diminishing myeloid cell apoptosis."

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"In ET patients, both JAK2 V617F and CALR Mut bind to TPOR; JAK2 V617F enhances the phosphorylation of STAT1 and STAT3 but CALR Mut promotes STAT3 and STAT5 activation."

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"The JAK2 V617F mutation leads to constitutive STAT3 phosphorylation and potentially leads to inhibition of Stathmin 1 activity via STAT3."

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"The constitutively active JAK2 mutant V617F is found in many patients with myeloproliferative diseases (Levine and Gilliland, 2007), and constitutively phosphorylated STAT3 is found in many solid tumours and haematopoietic malignancies (Lim and Cao, 2006)."
JAK2 leads to the phosphorylation of STAT3 on S727. 3 / 3
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"The phosphorylation of STAT3 at Tyr705 and Ser727 is mediated by the receptor-associated tyrosine kinase JAK2, and both molecules are dephosphorylated by AUY-922 [32]."

rlimsp
"Furthermore, the phosphorylation at Tyr705 of STAT3, which is known to be a phosphorylation site for Janus kinase 2 (JAK2), was completely inhibited by purvalanol A early (3 h) after drug treatment, although the phosphorylation of STAT3 at Ser727, which is a phosphorylation site for Ras/Raf/MEK and extracellular signal-regulated protein kinase 1/2, was still detectable until late (12 h) after treatment."

sparser
"Furthermore, treatment of JAK2 clinical medicine AZD1480 to ESCC cells showed similar tendency with Lico B. Thus, JAK2 downstream signaling proteins phosphorylation of STAT3 at Y705 and S727 as well as STAT3 target protein Mcl-1 expression was decreased with treatment of Lico B. Our results suggest that Lico B inhibits ESCC cell growth, arrests cell cycle and induces apoptosis, revealing the underlying mechanism involved in JAK2/STAT3 signaling pathways after Lico B treatment."
JAK2 leads to the phosphorylation of STAT3 on serine. 3 / 3
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"These results suggest that JAK2 and ERK may mediate tyrosine and serine phosphorylation of STAT3 induced by histamine, respectively, and that both phosphorylations may be required for the activation o[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Furthermore, PDGF-BB-induced STAT3 tyrosine and serine phosphorylation in hBMMSCs are directly mediated by JAK2 and ERK1/2, respectively."

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"Furthermore, our study reveals that PDGF-BB- and bFGF induced proliferation does not affect the osteogenic differentiation potential of hBMMSCs.All of the three GFs activated the hBMMSC ERK1/2 pathway[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
Tyrosine-phosphorylated JAK2 phosphorylates STAT3 on Y705. 3 / 3
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No evidence text available

No evidence text available

No evidence text available
JAK2 phosphorylates STAT3 at position 705. 3 / 3
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sparser
"In primary epithelial cells, oxidized palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine activates tyrosine kinase JAK2, which in turn phosphorylates STAT3 on residue 705."

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"It is currently well characterized that the inflammatory induction of hepcidin expression is mainly mediated by IL-6, which binds to the IL-6 receptor and gp130 and then recruits Janus kinase 2 (JAK2) to phosphorylate STAT3 at tyrosine residue 705 [XREF_BIBR, XREF_BIBR]."

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"In primary epithelial cells, oxidized palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine activates tyrosine kinase JAK2, which in turn phosphorylates STAT3 on residue 705."
Kinase-active JAK2 leads to the phosphorylation of STAT3. 2 / 2
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"Growth arrest or OSM treatment also specifically increases activated (phosphorylated) signal transduction and activators of transcription 3 (STAT3) levels, demonstrating that STAT3, not STAT1 or STAT5, is the downstream target of the activated Janus kinases in MCF-10A"

"JAK2 associates with c-Kit and is phosphorylated after SCF stimulation (Brizzi et al., 1994b). JAK2 activation results in phosphorylation of STAT1?, 3, 5A and 5B"
Kinase-active JAK2 leads to the phosphorylation of STAT3 on Y705. 2 / 2
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"Maximal activation of STAT3 requires phosphorylation at both Tyr705 and Ser727 sites (14). Although JAK2 kinase is shown to be responsible for phosphorylating STAT3 at Tyr705, we have shown that IL-1 receptor associated kinase 1 (IRAK-1) is capable of selectively phosphorylating STAT3 at Ser727 (15)."

"Induction of STAT3 Tyr705 and Ser727 phosphorylations by Galpha(s)QL was suppressed by inhibition of protein kinase A, Janus kinase 2/3, Rac1, c-Jun N-terminal kinase (JNK), or phosphatidylinositol 3-kinase, and a similar profile was observed in response to beta2-adrenergic receptor stimulation"
Modified JAK2 leads to the phosphorylation of STAT3. 2 / 2
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"XREF_FIG shows that over-expression of JAK2-WT and JAK2-V617F increased phosphorylation of JAK2 and STAT3 and the level of Mcl-1."

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"The molecular mechanism by which Jak-2 overexpression induces Stat-3 phosphorylation remains to be determined."
Kinase-active JAK2 leads to the phosphorylation of STAT3 on S727. 1 / 1
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"Induction of STAT3 Tyr705 and Ser727 phosphorylations by Galpha(s)QL was suppressed by inhibition of protein kinase A, Janus kinase 2/3, Rac1, c-Jun N-terminal kinase (JNK), or phosphatidylinositol 3-kinase, and a similar profile was observed in response to beta2-adrenergic receptor stimulation"
JAK2 phosphorylated on an unknown residue, an unknown residue, and an unknown residue phosphorylates STAT3. 1 / 1
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No evidence text available
JAK2 phosphorylates STAT3 on A2. 1 / 1
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"Upon hypoxia‐induced activation, JAK2 phosphorylates STAT3, which transcribes cyclin A2 expression by binding to the CCNA2 promoter, thereby promoting PASMC proliferation."
Mutated JAK2 leads to the phosphorylation of STAT3. 1 / 1
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"These results suggest that mutant JAK2 contributes to MMM pathogenesis by constitutively phosphorylating STAT3 and diminishing myeloid cell apoptosis."