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X-ORIGINAL-URL:https://www.biomed.cas.cz
X-WR-CALDESC:Akce na 
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TZID:Europe/Prague
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TZOFFSETFROM:+0100
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TZNAME:CEST
DTSTART:20260329T010000
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DTSTART:20261025T010000
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BEGIN:VEVENT
DTSTART;VALUE=DATE:20260303
DTEND;VALUE=DATE:20260304
DTSTAMP:20260418T025558
CREATED:20260223T091618Z
LAST-MODIFIED:20260223T091618Z
UID:2491-1772496000-1772582399@www.biomed.cas.cz
SUMMARY:BD Biosciences – Lunch and Learn Seminar
DESCRIPTION:Dear colleagues\, \nWe would like to invite you to join Lunch & Learn seminar focused on Panel Design Strategy in Flow Cytometry. This session is designed to support anyone involved in planning\, optimizing\, or performing multicolor flow cytometry experiments by providing both conceptual guidance and practical demonstrations. \n  \nMore information and registration. \nFlyer \n  \nRegistration is free. \n  \nBest regards \n  \n— \n\n\n\n\n\n\nMatyáš Šíma\, Ph.D.
URL:https://www.biomed.cas.cz/event/bd-biosciences-lunch-and-learn-seminar/
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Prague:20260304T150000
DTEND;TZID=Europe/Prague:20260304T160000
DTSTAMP:20260418T025558
CREATED:20260225T130603Z
LAST-MODIFIED:20260225T130603Z
UID:2494-1772636400-1772640000@www.biomed.cas.cz
SUMMARY:Seminář Vladimír Varga
DESCRIPTION:“Towards understanding life cycle of Trypanosoma brucei” \nTrypanosoma brucei is a unicellular eukaryotic parasite of mammals causing sleeping sickness in humans. T. brucei is transmitted by the tsetse fly. In the fly trypanosomes migrate from the gut to salivary glands\, which is associated with a defined sequence of changes to cells of the parasite. We have established an in vitro approach enabling us for the first time to study these life cycle transitions during initial stages of trypanosome migration. Hence\, we were able to describe associated changes to trypanosome morphology\, cell cycle\, motility as well as to its proteome and metabolome. This revealed that the initial life cycle transitions represent a continuous plastic process rather than a sequence of irreversible decisions. Furthermore\, it let to identification of a molecule in the trypanosome environment\, which is critical for triggering cell cycle arrest during these transitions. Thus\, our work opens new possibilities to understand complex biology of this important human parasite.
URL:https://www.biomed.cas.cz/event/seminar-vladimir-varga/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Prague:20260311T150000
DTEND;TZID=Europe/Prague:20260311T160000
DTSTAMP:20260418T025558
CREATED:20260302T081531Z
LAST-MODIFIED:20260302T081531Z
UID:2496-1773241200-1773244800@www.biomed.cas.cz
SUMMARY:Seminář Diego André Florian Joseph
DESCRIPTION:“The Fall of the Helicase of Dicer” \nDicer is an RNase III endoribonuclease that processes pre-miRNAs and dsRNAs into small RNAs of ~21–28 nt\, serving the miRNA and RNAi pathways. In mammals\, Dicer’s ability to process long dsRNA is constrained by its helicase domain. Consequently\, the miRNA pathway predominates\, and RNAi is considered vestigial. This constraint comes from a crucial interaction between the HEL1 subdomain of Dicer and its catalytic domain\, which maintains Dicer in a “closed” conformation\, making it highly selective. In the absence of HEL1\, Dicer adopts an “open” conformation that reduces substrate selectivity and activates RNAi. Until now\, this was the only interaction known to confer substrate selectivity and restrict RNAi activity. Here\, we show that Dicer contains an additional region within its helicase that contributes to substrate selectivity. Analysis of Dicer’s AlphaFold structure revealed four major intrinsically disordered regions (IDRs) adopting loop-like conformations. IDR1 is enriched in negatively charged residues and is predicted to interact with the positively charged RNA substrate channel of Dicer. Removal of IDR1 recapitulates the phenotype observed in the absence of HEL1\, suggesting that HEL1 subdomain is not the only region in Dicer responsible for substrate selectivity.
URL:https://www.biomed.cas.cz/event/seminar-diego-andre-florian-joseph/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Prague:20260318T150000
DTEND;TZID=Europe/Prague:20260318T160000
DTSTAMP:20260418T025558
CREATED:20260305T070841Z
LAST-MODIFIED:20260408T101238Z
UID:2499-1773846000-1773849600@www.biomed.cas.cz
SUMMARY:Seminář Srikant Ojha
DESCRIPTION:“Plectin Loss Disrupts Mechanotransduction and Attenuates\nHepatic Stellate Cell Activation” \nLiver fibrosis\, a hallmark of fibroproliferative disorders that contribute to nearly 45% of global mortality\, is primarily driven by the activation of hepatic stellate cells (HSCs). In response to injury-induced tissue stiffening\, HSCs undergo mechanosignaling-dependent activation and deposit excessive extracellular matrix (ECM)\, perpetuating a self-sustaining fibrotic loop. We sought to disrupt this process by targeting plectin\, a cytolinker protein central to mechanotransduction. Using an HSC-specific plectin knockout (KO) mouse model\, we observed significantly reduced ECM accumulation following carbon tetrachloride–induced injury. In vitro\, plectin-deficient HSCs displayed impaired proliferation\, migration\, and focal adhesion formation. Single-cell transcriptomics further revealed attenuated activation signatures in KO HSCs. Together\, our findings establish plectin as a key regulator of HSC mechanosignaling and highlight its potential as a therapeutic target to alleviate liver fibrosis.
URL:https://www.biomed.cas.cz/event/seminar-srikant-ojha/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Prague:20260325T150000
DTEND;TZID=Europe/Prague:20260325T160000
DTSTAMP:20260418T025558
CREATED:20260316T072314Z
LAST-MODIFIED:20260408T101231Z
UID:2501-1774450800-1774454400@www.biomed.cas.cz
SUMMARY:Seminář Michael Sixt
DESCRIPTION:“Mechanic and energetic principles of leukocyte locomotion” \nDuring metazoan development\, immune surveillance and cancer dissemination\, cells migrate in complex three-dimensional (3D) microenvironments. These are crowded by cells and extracellular matrix\, generating mazes of differently sized spaces typically smaller than the diameter of the migrating cell. Most mesenchymal and epithelial cells actively generate their migratory path using pericellular tissue proteolysis and transmit traction forces via specific adhesion receptors. On the contrary\, amoeboid cells such as leukocytes employ non-destructive strategies of locomotion and do not hold on to extracellular substrates. This raises the question how these extremely fast cells negotiate dense tissues. We discovered that leukocytes are able to migrate in the total absence of transmembrane force coupling. Instead\, active deformations of the cell body can impose normal forces on the substrate and thereby generate propulsion. We are actively investigating how these normal forces are triggered and generated by the collective activity of the actin and microtuble cytoskeleton and develop new approaches to measure the energetic demands of the process.
URL:https://www.biomed.cas.cz/event/seminar-michael-sixt/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
END:VEVENT
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