Smad4 deficiency in T cells leads to the Th17-associated development of premalignant gastroduodenal lesions in mice.
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The gastrointestinal tumor microenvironmentThe role and regulation of human Th17 cells in tumor immunityThe Justy mutant mouse strain produces a spontaneous murine model of salivary gland cancer with myoepithelial and basal cell differentiationCellular Stress in the Context of an Inflammatory Environment Supports TGF-β-Independent T Helper-17 Differentiation.IL-26 promotes the proliferation and survival of human gastric cancer cells by regulating the balance of STAT1 and STAT3 activationA critical role for transcription factor Smad4 in T cell function that is independent of transforming growth factor β receptor signaling.Two sides of the story? Smad4 loss in pancreatic cancer versus head-and-neck cancerSmad4 represses the generation of memory-precursor effector T cells but is required for the differentiation of central memory T cells.Smad4 inhibits cell migration via suppression of JNK activity in human pancreatic carcinoma PANC-1 cellsMouse models of gastric cancer.Activin receptor-like kinase5 inhibition suppresses mouse melanoma by ubiquitin degradation of Smad4, thereby derepressing eomesodermin in cytotoxic T lymphocytes.Gastric Lgr5(+) stem cells are the cellular origin of invasive intestinal-type gastric cancer in mice.Mouse models for gastric cancer: Matching models to biological questions.Smad4 in T cells plays a protective role in the development of autoimmune Sjögren's syndrome in the nonobese diabetic mouse.Impact of T-cell-specific Smad4 deficiency on the development of autoimmune diabetes in NOD mice.SMAD regulatory networks construct a balanced immune system.Interleukin-23 is sufficient to induce rapid de novo gut tumorigenesis, independent of carcinogens, through activation of innate lymphoid cells.Th17 Cells in Protection from Tumor or Promotion of Tumor ProgressionRecapitulating Human Gastric Cancer Pathogenesis: Experimental Models of Gastric Cancer.Redirecting the focus of cancer immunotherapy to premalignant conditions.Activation of TGF-β-induced non-Smad signaling pathways during Th17 differentiation.Expression of IL-23/Th17-related cytokines in basal cell carcinoma and in the response to medical treatments.Chinese 1 strain of Toxoplasma gondii excreted-secreted antigens negatively modulate Foxp3 via inhibition of the TGFßRII/Smad2/Smad3/Smad4 pathway.Dependency of colorectal cancer on a TGF-β-driven program in stromal cells for metastasis initiation.The role of TGF-β in Th17 differentiation.The Src kinase Fyn is protective in acute chemical-induced colitis and promotes recovery from disease.[Th17 cells and IL-17 are increased in patients with brain metastases from the primary lung cancer].TGF-β in T Cell Biology: Implications for Cancer Immunotherapy.
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P2860
Smad4 deficiency in T cells leads to the Th17-associated development of premalignant gastroduodenal lesions in mice.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Smad4 deficiency in T cells le ...... astroduodenal lesions in mice.
@en
type
label
Smad4 deficiency in T cells le ...... astroduodenal lesions in mice.
@en
prefLabel
Smad4 deficiency in T cells le ...... astroduodenal lesions in mice.
@en
P2093
P2860
P356
P1476
Smad4 deficiency in T cells le ...... astroduodenal lesions in mice.
@en
P2093
Frank Robert Jirik
Jennifer Nancy Hahn
Vincent George Falck
P2860
P304
P356
10.1172/JCI45114
P407
P577
2011-09-01T00:00:00Z