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SUMMARY:BioE COLLOQUIA SERIES:  "1-Deoxy-Sphingolipids – When Sphingolip
 ids Become Headless"
DTSTART:20190923T121500
DTSTAMP:20260511T072930Z
UID:fd69e9a5391219ccd355ae13c6155fa5b35e3cd03bfbc84eb624a420
CATEGORIES:Conferences - Seminars
DESCRIPTION:Prof. Thorsten Hornemann\, University of Zürich (CH)\nWEEKLY 
 BIOENGINEERING COLLOQUIA SERIES\n(sandwiches served)\n\nAbstract: \n1-Deox
 ySphingolipids (1-deoxySL) are atypical sphingolipids\, which are formed d
 ue to a shift in the substrate preference of the serine palmitoyltransfera
 se (SPT). 1-DeoxySL lack the C1 hydroxyl group of normal sphingolipids\, w
 hich precludes their conversion to complex sphingolipids but also their fu
 rther downstream metabolism. The rare axonal neuropathy HSAN1 is caused by
  pathologically increased 1-deoxySL levels due to mutations in SPT. 1-Deox
 ySLs are toxic to neurons in culture\, induce neurite retraction and disru
 pt neuronal structures\, likely by interfering with regulatory components 
 of the cytoskeleton. At increased L-serine concentrations\, 1-deoxySL form
 ation is significantly suppressed. HSAN1 mice\, which received an L-serine
  enriched diet\, showed normal 1-deoxySL levels and did not develop neurop
 athic symptoms.  1-DeoxySL are also elevated in type 2 diabetes and assoc
 iated with beta cell dysfunction\, wound healing defects and the diabetic 
 sensory neuropathy (DSN).  L-serine supplementation significantly improve
 d neuropathy in diabetic rats. Although 1-deoxySL cannot be degraded by th
 e canonical sphingolipid catabolism\, they appear to be metabolized by a s
 et of desaturases and CYP4F enzymes\, which likely reflects a physiologica
 l detoxification mechanism.  CYP4F expression is reduced in obesity where
 as PPARαantagonists\, such as fibrates\, induce the expression of these e
 nzymes and lower 1-deoxySL levels. Trageting CYP4F enzymes could therefore
  be a novel therapeutic approach in DSN.\n\nResearch overview:\nThe main f
 ield of our research is the influence of sphigolipid metabolism on cellula
 r signalling and apoptosis. Ceramides and metabolites thereof are ubiquito
 us constituents of membrane lipids in mammalian cells and involved in vari
 ous cellular events like apoptosis\, signal transduction and membrane traf
 ficking. A dysfunctuion of the ceramide pathway is the cause for various d
 eseases like HSN1 or Fabry. In our research we investigate the role of de 
 novo sphingolipid synthesis on peripheral neuronal development and axonal 
 regeneration as well as its possible influence in other neurodegenerative 
 diseases like diabetic sensory neuropathy (DSN) or Alzheimer desease. Curr
 ently the main focus of our work is the function and regulation of the ser
 ine-palmitoyltransferase\, a keyenzyme in the de-novo synthesis pathway of
  sphingolipids.
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717
STATUS:CONFIRMED
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