NIK overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells. - Wikidata - wikimedia - TriplyDB

NIK overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells.

NIK overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells.

http://www.wikidata.org/entity/Q36825184

about

Roles of tumor necrosis factor receptor associated factor 3 (TRAF3) and TRAF5 in immune cell functions Self-termination of the terminator Inflammation meets cancer, with NF-κB as the matchmaker Non-canonical NF-κB activation and abnormal B cell accumulation in mice expressing ubiquitin protein ligase-inactive c-IAP2.NIK stabilization in osteoclasts results in osteoporosis and enhanced inflammatory osteolysis.Roles of the NF-kappaB pathway in lymphocyte development and function.The noncanonical NF-κB pathway.Negative feedback in noncanonical NF-kappaB signaling modulates NIK stability through IKKalpha-mediated phosphorylation Human TRAF3 adaptor molecule deficiency leads to impaired Toll-like receptor 3 response and susceptibility to herpes simplex encephalitis.Cleavage of NIK by the API2-MALT1 fusion oncoprotein leads to noncanonical NF-kappaB activation BAFF receptor signaling aids the differentiation of immature B cells into transitional B cells following tonic BCR signaling IκB kinase β (IKBKB) mutations in lymphomas that constitutively activate canonical nuclear factor κB (NFκB) signaling.Constitutive BR3 receptor signaling in diffuse, large B-cell lymphomas stabilizes nuclear factor-κB-inducing kinase while activating both canonical and alternative nuclear factor-κB pathways.Mouse hepatocyte overexpression of NF-κB-inducing kinase (NIK) triggers fatal macrophage-dependent liver injury and fibrosis.Biallelic loss-of-function mutation in NIK causes a primary immunodeficiency with multifaceted aberrant lymphoid immunity.NIK signaling in dendritic cells but not in T cells is required for the development of effector T cells and cell-mediated immune responses NF-κB in immunobiology.Signaling by the tumor necrosis factor receptor superfamily in B-cell biology and disease Carboxyl terminus of HSC70-interacting protein (CHIP) down-regulates NF-κB-inducing kinase (NIK) and suppresses NIK-induced liver injury NF-κB–inducing kinase plays an essential T cell–intrinsic role in graft-versus-host disease and lethal autoimmunity in mice An oncogenic role for alternative NF-κB signaling in DLBCL revealed upon deregulated BCL6 expression.AR-regulated TWEAK-FN14 pathway promotes prostate cancer bone metastasis BAFF promotes proliferation of human mesangial cells through interaction with BAFF-R Targeting signaling factors for degradation, an emerging mechanism for TRAF functions K63-linked ubiquitination in kinase activation and cancer.The coding genome of splenic marginal zone lymphoma: activation of NOTCH2 and other pathways regulating marginal zone development.TNFR-associated factor 2 deficiency in B lymphocytes predisposes to chronic lymphocytic leukemia/small lymphocytic lymphoma in mice.Antagonism of inhibitor of apoptosis proteins increases bone metastasis via unexpected osteoclast activation NF-κB–inducing kinase (NIK) promotes hyperglycemia and glucose intolerance in obesity by augmenting glucagon action The immunological contribution of NF-κB within the tumor microenvironment: a potential protective role of zinc as an anti-tumor agent.NF-kappaB p100 limits TNF-induced bone resorption in mice by a TRAF3-dependent mechanism.Murine BAFF-receptor residues 168-175 are essential for optimal CD21/35 expression but dispensable for B cell survival.Context-specific BAFF-R signaling by the NF-κB and PI3K pathways TRAF3 regulates the effector function of regulatory T cells and humoral immune responses.Noncanonical NF-κB signaling is limited by classical NF-κB activity.Noncanonical NF-κB pathway controls the production of type I interferons in antiviral innate immunity.NF-κB inducing kinase: a key regulator in the immune system and in cancer Targeting BAFF in autoimmunity.Non-canonical NF-κB signaling pathway.The kinase NIK as a therapeutic target in multiple myeloma.

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P2860

NIK overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells.

http://www.wikidata.org/entity/Q36825184

description

2008 nî lūn-bûn

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

NIK overexpression amplifies, ...... d survival signals in B cells.

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type

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NIK overexpression amplifies, ...... d survival signals in B cells.

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NIK overexpression amplifies, ...... d survival signals in B cells.

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Proceedings of the National Academy of Sciences of the United States of America

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NIK overexpression amplifies, ...... d survival signals in B cells.

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Dinis P Calado

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Marc Schmidt-Supprian

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Shin-ichi Nishikawa

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Yoshiteru Sasaki

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Yuri Shimizu

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P2860

Specificity of TRAF3 in its negative regulation of the noncanonical NF-kappa B pathway

Regulation of B cell self-tolerance by BAFF

NF-kappaB and the immune response

MAP3K-related kinase involved in NF-kappaB induction by TNF, CD95 and IL-1

Rescue of TRAF3-null mice by p100 NF-kappa B deficiency

NF-kappaB in cancer: from innocent bystander to major culprit

NF-kappaB antiapoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation

Mutations in the NF-kappaB signaling pathway: implications for human disease.

Functions of NF-kappaB1 and NF-kappaB2 in immune cell biology

The role of the BAFF/APRIL system in B cell homeostasis and lymphoid cancers.

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105

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Fabienne Mackay

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