BEGIN:VCALENDAR
VERSION:2.0
PRODID:-// - ECPv6.6.3//NONSGML v1.0//EN
CALSCALE:GREGORIAN
METHOD:PUBLISH
X-ORIGINAL-URL:https://www.biomed.cas.cz
X-WR-CALDESC:Akce na 
REFRESH-INTERVAL;VALUE=DURATION:PT1H
X-Robots-Tag:noindex
X-PUBLISHED-TTL:PT1H
BEGIN:VTIMEZONE
TZID:Europe/Prague
BEGIN:DAYLIGHT
TZOFFSETFROM:+0100
TZOFFSETTO:+0200
TZNAME:CEST
DTSTART:20240331T010000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:+0200
TZOFFSETTO:+0100
TZNAME:CET
DTSTART:20241027T010000
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTART;TZID=Europe/Prague:20240327T150000
DTEND;TZID=Europe/Prague:20240327T160000
DTSTAMP:20260415T081443
CREATED:20240318T080719Z
LAST-MODIFIED:20240318T080719Z
UID:807-1711551600-1711555200@www.biomed.cas.cz
SUMMARY:Seminář Veronika Zimolová\, M.Sc.
DESCRIPTION:“Janus Kinase 2 (JAK2) mutations: implications for blood diseases” \nThe project aims to elucidate the impact of the germline Jak2 R1063H variant on myeloproliferative disorders and its potential implication in myeloid malignancy predisposition. Utilizing a mouse model harboring the Jak2 R1063H mutation\, we observed higher mortality rate\, elevated D-dimer levels indicative of thrombotic events\, and increased platelets counts. Furthermore\, metabolic profiling revealed alterations in platelet bioenergetics and gene expression patterns associated with fatty acid metabolism. Additionally\, we showed aberrations in hematopoietic stem cell functionality\, manifesting as a skewed myeloid progenitor cell expansion and bone marrow remodeling. These findings collectively suggest that Jak2 R1063H variant represents risk factor in the pathogenesis of myeloid cell transformation.
URL:https://www.biomed.cas.cz/event/seminar-veronika-zimolova-m-sc/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
END:VEVENT
END:VCALENDAR