about
Critical and independent role for SOCS3 in either myeloid or T cells in resistance to Mycobacterium tuberculosisHematopoietic abnormalities in mice deficient in gp130-mediated STAT signaling.IL-6 trans-signaling via STAT3 directs T cell infiltration in acute inflammation.Naive and activated T cells display differential responsiveness to TL1A that affects Th17 generation, maintenance, and proliferation.Rab8a interacts directly with PI3Kγ to modulate TLR4-driven PI3K and mTOR signalling.Interleukin-27 inhibits ectopic lymphoid-like structure development in early inflammatory arthritis.Innate cellular sources of interleukin-17A regulate macrophage accumulation in cigarette- smoke-induced lung inflammation in mice.STAT3 and STAT1 mediate IL-11-dependent and inflammation-associated gastric tumorigenesis in gp130 receptor mutant mice.Interleukin-6 signaling drives fibrosis in unresolved inflammation.Tying the knot between cytokine and toll-like receptor signaling in gastrointestinal tract cancers.Transcriptional regulation of pattern recognition receptors by Jak/STAT signaling, and the implications for disease pathogenesis.Differential regulation of gastric tumor growth by cytokines that signal exclusively through the coreceptor gp130.IL6 Trans-signaling Promotes KRAS-Driven Lung Carcinogenesis.Differential involvement of gp130 signalling pathways in modulating tobacco carcinogen-induced lung tumourigenesis.Nucleotide oligomerization domain 1 enhances IFN-γ signaling in gastric epithelial cells during Helicobacter pylori infection and exacerbates disease severity.Inflammation modulates the expression of the intestinal mucins MUC2 and MUC4 in gastric tumors.Potential efficacy of interleukin-1β inhibition in lung cancer.Endoscopic ultrasound-guided fine-needle aspirate-derived preclinical pancreatic cancer models reveal panitumumab sensitivity in KRAS wild-type tumors.Myeloid Differentiation Factor 88 Signaling in Bone Marrow-Derived Cells Promotes Gastric Tumorigenesis by Generation of Inflammatory Microenvironment.Investigating the Role of Toll-Like Receptors in Mouse Models of Gastric Cancer.A cell type-specific constitutive point mutant of the common beta-subunit of the human granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin (IL)-3, and IL-5 receptors requires the GM-CSF receptor alpha-subunit for activation.Interacting residues in the extracellular region of the common beta subunit of the human granulocyte-macrophage colony-stimulating factor, interleukin (IL)-3, and IL-5 receptors involved in constitutive activation.Imbalanced gp130 signalling in ApoE-deficient mice protects against atherosclerosis.STAT1 plays a role in TLR signal transduction and inflammatory responses.IL-6/Stat3-driven pulmonary inflammation, but not emphysema, is dependent on interleukin-17A in mice.Differential role of MyD88 and Mal/TIRAP in TLR2-mediated gastric tumourigenesis.The molecular pathogenesis of STAT3-driven gastric tumourigenesis in mice is independent of IL-17.IL-6 trans-signaling modulates TLR4-dependent inflammatory responses via STAT3.Gastric cancer development in mice lacking the SHP2 binding site on the IL-6 family co-receptor gp130.Interleukin-6 promotes pulmonary emphysema associated with apoptosis in mice.STAT3-driven upregulation of TLR2 promotes gastric tumorigenesis independent of tumor inflammation.In vivo evidence that RBM5 is a tumour suppressor in the lung.Hyperactive gp130/STAT3-driven gastric tumourigenesis promotes submucosal tertiary lymphoid structure development.Suppressor of cytokine signaling 3 regulates CD8 T-cell proliferation by inhibition of interleukins 6 and 27.STAT3 activation regulates growth, inflammation, and vascularization in a mouse model of gastric tumorigenesis.LPS hypersensitivity of gp130 mutant mice is independent of elevated haemopoietic TLR4 signaling.Hyperactivation of Stat3 in gp130 mutant mice promotes gastric hyperproliferation and desensitizes TGF-beta signaling.Deregulated Stat3 signaling dissociates pulmonary inflammation from emphysema in gp130 mutant miceFunctional expression cloning reveals proapoptotic role for protein phosphatase 4Pathologic consequences of STAT3 hyperactivation by IL-6 and IL-11 during hematopoiesis and lymphopoiesis
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description
hulumtues
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researcher
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wetenschapper
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հետազոտող
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name
Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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Brendan J. Jenkins
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P106
P1153
7102926924
P21
P31
P496
0000-0002-7552-4656