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DTSTART:20190331T030000
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DTSTART:20181028T020000
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BEGIN:VEVENT
DTSTAMP:20260405T191544Z
UID:5c3726ad4cd61983431462@ist.ac.at
DTSTART:20190114T143000
DTEND:20190114T153000
DESCRIPTION:Speaker: Da-Neng Wang\nhosted by Daria Siekhaus\nAbstract: In t
 he neuron\, citrate functions as an energy source and a precursor for lipi
 d synthesis. The concentration of cytosolic citrate partially depends on d
 irect import across the plasma membrane via the Na+-dependent citrate tran
 sporter (NaCT). Mutations in NaCT (encoded by the SLC13A5 gene) cause earl
 y onset epilepsy encephalopathy and developmental delays\, and the disease
  is thus named SLC13A5 Deficiency. Based on their cellular expression patt
 erns\, the mutations have been classified as Type I and Type II mutations.
  NaCT and its bacterial homologs belong to the divalent anion/sodium sympo
 rter family. Our lab previously determined the crystal structure of a bact
 erial NaCT homolog (VcINDY). The structure reveals a VcINDY dimer\, where 
 each monomer consists of an anchoring domain and a transport domain. This 
 VcINDY structure\, and the transport mechanism it suggested\, have proven 
 to be largely applicable to human NaCT and can explain the molecular defec
 ts caused by SLC13A5 mutations.
LOCATION:Mondi Seminar Room 3\, Central Building\, ISTA
ORGANIZER:amally@ist.ac.at
SUMMARY:Da-Neng Wang: What a bacterial carboxylate transporter structure ha
 s told us about the pathogenesis of early-onset epileptic encephalopathy
URL:https://talks-calendar.ista.ac.at/events/1740
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