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Alterations of Nedd4-2-binding capacity in PY-motif of NaV 1.5 channel underlie long QT syndrome and Brugada syndrome.

Ya WangYuan DuLing LuoPeijing HuGuodong YangTao LiXiu HanAiqun MaTingzhong Wang
Published in: Acta physiologica (Oxford, England) (2020)
Our data suggest that the PY-motif plays an essential role in modifying the expression/function of NaV 1.5 channels through Nedd4-2-mediated ubiquitination. Alterations of NaV 1.5-Nedd4-2 interaction represent a novel pathological mechanism for NaV 1.5 channel diseases caused by SCN5A variants.
Keyphrases
  • poor prognosis
  • case report
  • binding protein
  • copy number
  • electronic health record
  • big data
  • gene expression
  • drug induced
  • dna methylation
  • long non coding rna
  • artificial intelligence
  • data analysis