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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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DTSTART:20260329T010000
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BEGIN:VEVENT
DTSTART;TZID=Europe/Prague:20260204T150000
DTEND;TZID=Europe/Prague:20260204T160000
DTSTAMP:20260417T154059
CREATED:20260115T104013Z
LAST-MODIFIED:20260115T104013Z
UID:2480-1770217200-1770220800@www.biomed.cas.cz
SUMMARY:Seminář Susana Minguet
DESCRIPTION:“Harnessing TCR Discoveries for the Next Generation of Immunotherapies” \nRecent advances in synthetic immunology and CAR T cell engineering have highlighted the critical importance of signaling diversity for optimizing anti-tumor responses. Our work outlines the design of innovative cell-based cancer immunotherapies rooted in a molecular understanding of T cell activation via the T cell receptor complex (TCR–CD3). I will discuss how modulating receptor signaling interfaces and precisely recruiting kinases and adaptors can advance both fundamental immunology and translational therapies. Key noncanonical interactions between specific components of the TCR–CD3 complex and the Src-kinase Lck fine-tune T cell activation; when implemented in chimeric antigen receptors (CARs)\, these mechanisms improved in vivo tumor control and reduced T cell exhaustion. Supporting our rational design of next-generation CAR T cells\, we demonstrated that harnessing CD3 chain diversity\, rather than simply increasing signaling strength\, enabled the generation of CAR T cells with enhanced anti-tumor efficacy and safety profiles.
URL:https://www.biomed.cas.cz/event/seminar-susana-minguet/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
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BEGIN:VEVENT
DTSTART;TZID=Europe/Prague:20260211T150000
DTEND;TZID=Europe/Prague:20260211T160000
DTSTAMP:20260417T154059
CREATED:20260129T104523Z
LAST-MODIFIED:20260129T104523Z
UID:2482-1770822000-1770825600@www.biomed.cas.cz
SUMMARY:Seminář Lucie Janečková
DESCRIPTION:“NG2-lineage cell plasticity in ischemic brain repair: Roles of Wnt signaling” \nFocal cerebral ischemia (FCI) leads to neuronal loss followed by extensive tissue remodeling\, in which glial and vascular cell populations play indispensable roles. Among these\, NG2 glia and perivascular NG2⁺ cells represent highly plastic cell types that actively participate in post-ischemic responses\, yet their functional heterogeneity and regulatory mechanisms remain poorly understood. In this lecture\, I will present our work investigating how these cell populations respond to ischemic injury and how modulation of Wnt/β-catenin signaling reshapes their cellular states and functions. By combining lineage tracing\, transcriptomic analyses\, and imaging approaches\, we uncover changes in oligodendrocyte differentiation\, perivascular cell behavior\, and their contributions to tissue repair and regeneration. Finally\, I will introduce an ongoing spatial transcriptomics study aimed at mapping cellular organization in the ischemic periphery and glial scar\, highlighting emerging spatial patterns and open questions in brain regeneration.
URL:https://www.biomed.cas.cz/event/seminar-lucie-janeckova/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
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BEGIN:VEVENT
DTSTART;TZID=Europe/Prague:20260218T150000
DTEND;TZID=Europe/Prague:20260218T160000
DTSTAMP:20260417T154059
CREATED:20260209T151442Z
LAST-MODIFIED:20260209T151442Z
UID:2484-1771426800-1771430400@www.biomed.cas.cz
SUMMARY:Seminář Pranav Gulati
DESCRIPTION:“Initiating Mechanisms of Autoinflammatory Osteomyelitis: dysregulated neutrophil recruitment and tyrosine kinase signaling” \nAutoinflammatory diseases result from inappropriate activation of the innate immune system in the absence of infection. Loss of PSTPIP2\, a membrane adaptor protein\, leads to the development of one such disease Chronic Multifocal Osteomyelitis (CMO)\, an autoinflammatory disease in mice which serves as a model for Chronic Recurrent Multifocal Osteomyelitis (CRMO) in humans. Neutrophils are essential for murine CMO initiation and contribute to tissue damage\, but the early events that trigger their pathogenic activity remain poorly defined. Our work shows that early alterations in neutrophil signaling and migration precede both classical inflammatory cytokine responses and the appearance of overt disease symptoms. Pharmacological inhibition of some of these early pathways reduces disease severity and neutrophil activation. Together\, these findings identify the initiating mechanisms of sterile bone inflammation in the mouse model of autoinflammatory osteomyelitis and provide potential targets for therapeutic intervention.
URL:https://www.biomed.cas.cz/event/seminar-pranav-gulati/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
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BEGIN:VEVENT
DTSTART;TZID=Europe/Prague:20260225T150000
DTEND;TZID=Europe/Prague:20260225T160000
DTSTAMP:20260417T154059
CREATED:20260216T074449Z
LAST-MODIFIED:20260216T074449Z
UID:2486-1772031600-1772035200@www.biomed.cas.cz
SUMMARY:Seminář Poulami Banik
DESCRIPTION:“Characterization and targeted rescue of a novel PRPF31 mutation in retinitis pigmentosa” \nRetinitis pigmentosa (RP) is an inherited retinal disease characterized by photoreceptor loss. Mutations in the PRPF31 gene cause approximately 10% of cases of autosomal dominant RP. In this project\, we characterize a novel intronic pathogenic variant in the PRPF31 gene. We provide evidence that the novel RP mutation activates a cryptic splice site\, inducing the expression of an abnormal transcript. The resulting protein is unstable\, and patient cells exhibit lower expression of PRPF31 and other splicing factors. To correct aberrant RNA splicing\, we applied modified antisense oligonucleotides (ASOs) to improve PRPF31 splicing in patient cells. We differentiated the patients‘ induced pluripotent stem cells (iPSCs) into retinal pigment epithelium (RPE) cells and demonstrated that ASO treatment improves PRPF31 splicing and increases PRPF31 protein levels in patient’s RPE cells. These findings suggest that ASO-based splicing correction is a promising therapy for this currently untreatable disease.
URL:https://www.biomed.cas.cz/event/seminar-poulami-banik/
LOCATION:Posluchárna Milana Haška / Milan Hašek Auditorium
ORGANIZER;CN="%C3%9AMG":MAILTO:leona.krausova@img.cas.cz
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