BEGIN:VCALENDAR

VERSION:2.0

PRODID:-//wp-events-plugin.com//7.2.2.1//EN

TZID:Asia/Jerusalem

X-WR-TIMEZONE:Asia/Jerusalem
BEGIN:VEVENT

UID:853@biology.technion.ac.il

DTSTART;TZID=Asia/Jerusalem:20190611T130000

DTEND;TZID=Asia/Jerusalem:20190611T140000

DTSTAMP:20210802T125857Z

URL:https://biology.technion.ac.il/en/seminars/phd-graduate-seminar-inbal-
 maniv-2/

SUMMARY:PhD. Graduate Seminar-Inbal Maniv [No Categories]
DESCRIPTION:Location:   \n Affiliation: \n Host:\n ResearchTopic:Mutant Ubi
 quitin Drives theEmergence And Pathogenesis of Alzheimer’s DiseaseAlzhei
 mer’sdisease(AD) is characterized by accumulation of hazardous proteins 
 in the brain. Asthe primary signal of protein clearance in the cell is ubi
 quitin\, defectiveubiquitin signaling could play a pivotal role in the eme
 rgence of this disease.Although the only reported ubiquitin mutation\, UBB
 +1\,can be found in brains of all AD patients\, mouse studies have failed 
 insupplying a causal link with AD pathogenesis. By establishing a 3D neuro
 nalnetwork utilizing human neuronal progenitors\, we demonstrate that UBB+
 1expression alone can initiate the two pathological hallmarks of AD: Abpla
 ques and neurofibrillary tangles.Specifically\, we show that UBB+1competes
 with ubiquitin for the binding to the neuroprotective enzyme UCH-L1 leadin
 g toelevated levels of Amyloid Precursor Protein and amyloid plaque buildu
 p.Importantly\, silencing UBB+1expressionis sufficient to hinder the emerg
 ence of AD hallmarks. Taken together\, UBB+1plays a critical role in drivi
 ng AD development\, serving as a promisingtherapeutic target for the treat
 ment of AD 

END:VEVENT

BEGIN:VTIMEZONE

TZID:Asia/Jerusalem

X-LIC-LOCATION:Asia/Jerusalem

BEGIN:DAYLIGHT

DTSTART:20190329T030000

TZOFFSETFROM:+0200

TZOFFSETTO:+0300

TZNAME:IDT

END:DAYLIGHT

END:VTIMEZONE
END:VCALENDAR