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UID:944@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20210210T130000

DTEND;TZID=Asia/Jerusalem:20210210T140000

DTSTAMP:20210802T125904Z

URL:https://biology.technion.ac.il/en/seminars/msc-gradutae-seminar-sewar-
 zbidat-2/

SUMMARY:Msc Gradutae seminar-Sewar Zbidat [No Categories]
DESCRIPTION:Location:   \n Affiliation: \n Host:\n Insulinreceptor turnover
  in fasting is dependent on b-dystroglycan deglycosylationFasting exertsva
 rious physiological effects\, most notably\, reduced signaling through the
 insulin receptor. Insulin receptor activity requires association withDystr
 ophin Glycoprotein Complex (DGC)\, and fasting induces autophagic clearanc
 eof this co-assembly. We showed that insulin receptor turnover during fast
 ingrequires deglycosylation of b-dystroglycan.Removal of N-linked glycans 
 on b-dystroglycanis catalyzed by the lysosomal enzymes HexA and Man2b1 bec
 ause theirdownregulation in atrophying muscles prevented b-dystroglycandeg
 lycosylation and insulin receptor-DGC loss. Surprisingly\, the lysosomalen
 zyme NAGLU\, which cannot process N-linked glycosylation\, also facilitate
 d b-dystroglycan deglycosylation and insulinreceptor loss. Furthermore\, M
 an2b1 andHexA were induced in fasting by the transcriptional complex PPAR-
 g/RXR-a\, but not whenNAGLU or RXR-a were downregulated.By promoting PPAR-
 g O-GlcNAcylation\,NAGLU facilitates PPAR-g/RXR-a-mediated Man2b1 and HexA
  induction and b-dystroglycandeglycosylation. Accordingly\, downregulation
  of NAGLU or RXR-a during fasting blocked b-dystroglycan deglycosylation\,
  and consequentlyinsulin receptor-DGC co-assemblies accumulated on the mus
 cle membrane. Thus\,NAGLU mediates physiological adaptation to fasting by 
 promoting b-dystroglycan deglycosylation.https://technion.zoom.us/j/912491
 61095The seminarwill be given in English 

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