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10.1016/j.molmed.2016.04.006

http://scihub22266oqcxt.onion/10.1016/j.molmed.2016.04.006
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suck abstract from ncbi


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pmid27211305
      Trends+Mol+Med 2016 ; 22 (6 ): 511-527
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  • Human TBK1: A Gatekeeper of Neuroinflammation #MMPMID27211305
  • Ahmad L ; Zhang SY ; Casanova JL ; Sancho-Shimizu V
  • Trends Mol Med 2016[Jun]; 22 (6 ): 511-527 PMID27211305 show ga
  • The importance of TANK binding kinase-1 (TBK1), a multimeric kinase that modulates inflammation and autophagy, in human health has been highlighted for the first time by the recent discoveries of mutations in TBK1 that underlie amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), normal tension glaucoma (NTG) or childhood herpes simplex encephalitis (HSE). Gain-of-function of TBK1 are associated with NTG, whereas loss-of-function mutations result in ALS/FTD or in HSE. In light of these new findings, we review the role of TBK1 in these seemingly unrelated, yet allelic diseases, and discuss the role of TBK1 in neuroinflammatory diseases. This discovery has the potential to significantly increase our understanding of the molecular basis of these poorly understood diseases.
  • |Amyotrophic Lateral Sclerosis/genetics/immunology/*metabolism [MESH]
  • |Autophagy [MESH]
  • |Central Nervous System/*metabolism [MESH]
  • |Disease Progression [MESH]
  • |Encephalitis, Herpes Simplex/genetics/immunology/*metabolism [MESH]
  • |Frontotemporal Dementia/genetics/*metabolism [MESH]
  • |Gene Expression [MESH]
  • |Humans [MESH]
  • |Inflammation/*metabolism [MESH]
  • |Interferons/immunology/metabolism [MESH]
  • |Low Tension Glaucoma/genetics/immunology/*metabolism [MESH]
  • |Mutation [MESH]


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