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10.1038/cr.2014.17

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suck abstract from ncbi


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pmid24513853
      Cell+Res 2014 ; 24 (4 ): 417-32
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  • The G??-Src signaling pathway regulates TNF-induced necroptosis via control of necrosome translocation #MMPMID24513853
  • Li L ; Chen W ; Liang Y ; Ma H ; Li W ; Zhou Z ; Li J ; Ding Y ; Ren J ; Lin J ; Han F ; Wu J ; Han J
  • Cell Res 2014[Apr]; 24 (4 ): 417-32 PMID24513853 show ga
  • Formation of multi-component signaling complex necrosomes is essential for tumor necrosis factor ? (TNF)-induced programmed necrosis (also called necroptosis). However, the mechanisms of necroptosis are still largely unknown. We isolated a TNF-resistant L929 mutant cell line generated by retrovirus insertion and identified that disruption of the guanine nucleotide-binding protein ? 10 (G?10) gene is responsible for this phenotype. We further show that G?10 is involved in TNF-induced necroptosis and G?2 is the partner of G?10. Src is the downstream effector of G?2?10 in TNF-induced necroptosis because TNF-induced Src activation was impaired upon G?10 knockdown. G?10 does not affect TNF-induced activation of NF-?B and MAPKs and the formation of necrosomes, but is required for trafficking of necrosomes to their potential functioning site, an unidentified subcellular organelle that can be fractionated into heterotypic membrane fractions. The TNF-induced G??-Src signaling pathway is independent of RIP1/RIP3 kinase activity and necrosome formation, but is required for the necrosome to function.
  • |Amino Acid Sequence [MESH]
  • |Animals [MESH]
  • |Apoptosis/*drug effects/*genetics [MESH]
  • |Base Sequence [MESH]
  • |Biological Transport/drug effects/genetics [MESH]
  • |Cytoplasmic Vesicles/*drug effects/metabolism [MESH]
  • |GTP-Binding Protein beta Subunits/*physiology [MESH]
  • |GTP-Binding Protein gamma Subunits/*physiology [MESH]
  • |HEK293 Cells [MESH]
  • |Humans [MESH]
  • |Mice [MESH]
  • |Molecular Sequence Data [MESH]
  • |Necrosis/chemically induced/genetics [MESH]
  • |Signal Transduction/drug effects/physiology [MESH]
  • |Tumor Cells, Cultured [MESH]
  • |Tumor Necrosis Factor-alpha/*pharmacology [MESH]


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