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evaluated the currently known TBK1-mediated phosphorylation sites in the SKICH domains of NDP52 and TAX1BP1 on the basis of their interactions with NAP1
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Results show that TAX1BP1 translocates to mitochondria in response to RNA virus infection and inducibly interacts with the MAVS adaptor protein and indicate that TAX1BP1 functions as an adaptor molecule for Itch to target MAVS during RNA virus infection and thus restrict virus-induced apoptosis.
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TAX1BP1 downregulation by EBV-miR-BART15-3p enhances chemosensitivity of gastric cancer cells to 5-fluorouracil.
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The induction of antibodies to an AQP4 epitope in mice immunized with the TAX1BP1-derived peptide suggests that a latent HTLV-1 infection could lead to TAX1BP1 antigen presentation and the production of anti-AQP4 antibodies in human neuromyelitis optica.
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we demonstrate that myosin VI and TAX1BP1 are recruited to ubiquitylated Salmonella and play a key role in xenophagy
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A protein construct corresponding to the SKICH domain plus the linker region was expressed, purified and crystallized for TAX1BP1.
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RNF11 functions together with TAX1BP1 to restrict antiviral signaling and IFN-beta production.
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Autophagy of Tax1bp1/Ndp52 promotes non-canonical NF-kappaB signalling.
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Allele frequencies of three Alu insertions that are located in MEF2C (two of them) and TAX1BP1 genes significantly differ between cohorts of healthy donors and ALL(acute lymphoblastic leukemia) patients.
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ABIN1 requires its ubiquitin binding domain and cooperates with TAX1BP1 and A20 to restrict antiviral signaling.
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In a link with T cell leukemia virus-1-associated myelopathy/tropical spastic paraparesis, an alphabeta T cell receptor recognizes a self peptide from neuronal protein HuD in context of histocompatibility antigen HLA-A2.
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There is evidence of the association between the TAX1BP1 polymorphism and oral cavity cancer but there are no differences in the distribution of the polymorphism among patients with head and neck cancer and individuals without history of neoplasm.
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results demonstrate TBK1-IKKi to be novel substrates for A20 and further identify a novel mechanism whereby A20 and TAX1BP1 restrict antiviral signaling by disrupting a TRAF3-TBK1-IKKi signaling complex
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myosin VI-T6BP interactions may link membrane trafficking pathways with cell adhesion and cytokine-dependent cell signalling.
