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10.1186/s40478-017-0420-1

http://scihub22266oqcxt.onion/10.1186/s40478-017-0420-1
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C5341362!5341362!28274274
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suck abstract from ncbi


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pmid28274274      Acta+Neuropathol+Commun 2017 ; 5 (ä): ä
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  • A novel form of necrosis, TRIAD, occurs in human Huntington?s disease #MMPMID28274274
  • Yamanishi E; Hasegawa K; Fujita K; Ichinose S; Yagishita S; Murata M; Tagawa K; Akashi T; Eishi Y; Okazawa H
  • Acta Neuropathol Commun 2017[]; 5 (ä): ä PMID28274274show ga
  • We previously reported transcriptional repression-induced atypical cell death of neuron (TRIAD), a new type of necrosis that is mainly regulated by Hippo pathway signaling and distinct from necroptosis regulated by RIP1/3 pathway. Here, we examined the ultrastructural and biochemical features of neuronal cell death in the brains of human HD patients in parallel with the similar analyses using mutant Htt-knock-in (Htt-KI) mice. LATS1 kinase, the critical regulator and marker of TRIAD, is actually activated in cortical neurons of postmortem human HD and of Htt-KI mouse brains, while apoptosis promoter kinase Plk1 was inactivated in human HD brains. Expression levels of YAP/YAPdeltaC were decreased in cortical neurons of human HD brains. Ultra-structural analyses revealed extreme enlargement of endoplasmic reticulum (ER), which characterizes TRIAD, in cortical neurons of human HD and those of Htt-KI mice. These biochemical and morphological results support that TRIAD occurs in human and mouse neurons under the HD pathology.Electronic supplementary material: The online version of this article (doi:10.1186/s40478-017-0420-1) contains supplementary material, which is available to authorized users.
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