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DTSTART;TZID=Europe/Madrid:20161010T150000
DTEND;TZID=Europe/Madrid:20161010T160000
DTSTAMP:20260421T144056
CREATED:20160928T191705Z
LAST-MODIFIED:20160930T122011Z
UID:24759-1476111600-1476115200@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Publishing in the Nature journals
DESCRIPTION:IBEC Seminar: Publishing in the Nature journals\nDr. Alexia-Ileana Zaromytidou (Chief Editor\, Nature Cell Biology)\nAlexia-Ileana Zaromytidou\, Chief Editor of Nature Cell Biology will provide an editor’s perspective on the editorial and publishing process in the Nature journals.\nShe received her PhD from the London Research Institute of Cancer Research UK in London\, UK (now the Francis Crick Institute) in January 2007. Her doctoral work with Richard Treisman centered on the molecular interactions between actin-regulated transcription factors and their coactivators in the context of MAPK and Rho signaling responses. She pursued her postdoctoral research in the lab of Joan Massagué at Memorial Sloan-Kettering Cancer Center in New York\, where she studied how different phosphorylation inputs affect TGFβ/BMP pathway activity to achieve distinct biological outcomes. In September 2010 she joined the editorial team of Nature Cell Biology as the editor responsible for the areas of cancer biology\, mechanobiology\, cell adhesion\, migration and the cytoskeleton\, and became Chief editor of the journal in November 2015.
URL:https://ibecbarcelona.eu/event/24759/
LOCATION:Sala Félix Serratossa\, Parc Científic de Barcelona\, Barcelona\, Spain
CATEGORIES:IBEC Seminar
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20161010T150000
DTEND;TZID=Europe/Madrid:20161010T160000
DTSTAMP:20260421T144056
CREATED:20160928T191705Z
LAST-MODIFIED:20160928T191705Z
UID:95918-1476111600-1476115200@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Publishing in the Nature journals
DESCRIPTION:IBEC Seminar: Publishing in the Nature journals\nDr. Alexia-Ileana Zaromytidou (Chief Editor\, Nature Cell Biology)\nAlexia-Ileana Zaromytidou\, Chief Editor of Nature Cell Biology will provide an editor’s perspective on the editorial and publishing process in the Nature journals.\nShe received her PhD from the London Research Institute of Cancer Research UK in London\, UK (now the Francis Crick Institute) in January 2007. Her doctoral work with Richard Treisman centered on the molecular interactions between actin-regulated transcription factors and their coactivators in the context of MAPK and Rho signaling responses. She pursued her postdoctoral research in the lab of Joan Massagué at Memorial Sloan-Kettering Cancer Center in New York\, where she studied how different phosphorylation inputs affect TGFβ/BMP pathway activity to achieve distinct biological outcomes. In September 2010 she joined the editorial team of Nature Cell Biology as the editor responsible for the areas of cancer biology\, mechanobiology\, cell adhesion\, migration and the cytoskeleton\, and became Chief editor of the journal in November 2015.
URL:https://ibecbarcelona.eu/event/24759-2/
LOCATION:Sala Félix Serratossa\, Parc Científic de Barcelona\, Barcelona\, Spain
CATEGORIES:IBEC Seminar
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20161013T100000
DTEND;TZID=Europe/Madrid:20161013T110000
DTSTAMP:20260421T144056
CREATED:20161007T133132Z
LAST-MODIFIED:20161007T133132Z
UID:95921-1476352800-1476356400@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Scaling up in Systems Biology: from a minimal cell to microbiomes
DESCRIPTION:Scaling up in Systems Biology: from a minimal cell to microbiomes\nMaria Lluch Senar\, Design of Biological Systems grup\, Centre for Genomic Regulation (CRG)\nUltra-sequencing technologies have allowed the massive identification of human-associated microbiomes. Genome annotations of microbiomes consider conserved ORFs or those encoding for proteins larger than 100aa. However\, growing evidence highlight the existence of a hidden universe of small genes (smORFs) encoding for small peptides (SEPs; <100aa)\, many of them secreted\, being involved in infection and quorum sensing. Also\, in eukaryotes\, small antimicrobial peptides (AMPs) are secreted in response to infection. The interplay between these secreted SEPs is essential to control the different human microbiomes to ensure coexistence rather than weakening the host against opportunistic infections. Thus\, determining the smORFome of bacterial-host ecosystems and studying its role in homeostasis are essential. In this seminar\, I will explain how by using different system biology approaches we discovered this layer of small peptides in Mycoplasma pneumoniae and our future plans to study their role in human microbiomes focusing in female reproductive tract.
URL:https://ibecbarcelona.eu/event/ibec-seminar-scaling-up-in-systems-biology-from-a-minimal-cell-to-microbiomes-2/
CATEGORIES:IBEC Seminar
ORGANIZER;CN="IBEC":MAILTO:www.ibecbarcelona.eu
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20161013T100000
DTEND;TZID=Europe/Madrid:20161013T110000
DTSTAMP:20260421T144056
CREATED:20161007T133132Z
LAST-MODIFIED:20161010T161238Z
UID:24827-1476352800-1476356400@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Scaling up in Systems Biology: from a minimal cell to microbiomes
DESCRIPTION:Scaling up in Systems Biology: from a minimal cell to microbiomes\nMaria Lluch Senar\, Design of Biological Systems grup\, Centre for Genomic Regulation (CRG)\nUltra-sequencing technologies have allowed the massive identification of human-associated microbiomes. Genome annotations of microbiomes consider conserved ORFs or those encoding for proteins larger than 100aa. However\, growing evidence highlight the existence of a hidden universe of small genes (smORFs) encoding for small peptides (SEPs; <100aa)\, many of them secreted\, being involved in infection and quorum sensing. Also\, in eukaryotes\, small antimicrobial peptides (AMPs) are secreted in response to infection. The interplay between these secreted SEPs is essential to control the different human microbiomes to ensure coexistence rather than weakening the host against opportunistic infections. Thus\, determining the smORFome of bacterial-host ecosystems and studying its role in homeostasis are essential. In this seminar\, I will explain how by using different system biology approaches we discovered this layer of small peptides in Mycoplasma pneumoniae and our future plans to study their role in human microbiomes focusing in female reproductive tract.
URL:https://ibecbarcelona.eu/event/ibec-seminar-scaling-up-in-systems-biology-from-a-minimal-cell-to-microbiomes/
CATEGORIES:IBEC Seminar
ORGANIZER;CN="IBEC":MAILTO:www.ibecbarcelona.eu
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20161013T150000
DTEND;TZID=Europe/Madrid:20161013T160000
DTSTAMP:20260421T144056
CREATED:20161006T150918Z
LAST-MODIFIED:20161006T150918Z
UID:95920-1476370800-1476374400@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Targeting fibroblast durotaxis as anti-fibrotic therapy
DESCRIPTION:Targeting fibroblast durotaxis as anti-fibrotic therapy\nDr. David Lagares\, Harvard Medical School\nDysregulated wound repair process in response to chronic tissue injury can lead to the development of tissue fibrosis in most organs. Fibrosis is characterized by accumulation of collagens and other matrix proteins that result in the distortion of tissue architecture\, and ultimately organ failure\, in variety of human diseases including idiopathic pulmonary fibrosis (IPF). Tissue stiffening\, traditionally thought to simply be a consequence of lung fibrosis\, has been recently shown to be a contributing factor to its pathogenesis by inducing fibroblasts differentiation into activated myofibroblasts\, the principal effector cells responsible matrix deposition. \nThe cellular and molecular mechanisms through which increased tissue rigidity drives disease progression remain to be fully elucidated. Using atomic force microscopy (AFM) to mechanically characterize the “topography”\, i.e. the spatial distribution\, of alterations in matrix stiffness produced in mouse models of lung fibrosis\, we consistently found that stiffness\, rather than being uniformly elevated in lung fibrotic tissues from animals models\, rises and falls in spatial gradients between “peaks” and “valleys.” We hypothesize that the stiffness “peaks” represent areas in which the fibrotic process was initiated\, or “nucleated”. Once fibrosis is nucleated\, the stiffness gradients leading to these fibrotic peaks are amplified by fibroblast “durotaxis\,” – the directed migration of cells from regions of lower to higher stiffness\, which occurs in the absence of chemoattractant gradients. Using hydrogels that recapitulate the stiffness gradients observed in animal fibrosis models\, we demonstrated durotaxis of lung fibroblasts in time-lapse microscopy studies. In human studies with lung tissues from IPF patients\, AFM revealed similar stiffness topography as we observed in mouse models\, i.e. the presence of focal peaks surrounded by stiffness gradients. Of note\, we have also found that primary lung fibroblasts from IPF patients exhibit greater durotactic responses to stiffness gradients than do control lung fibroblasts. In efforts to identify the molecular pathways involved in cell durotaxis\, we have found that the increased durotaxis of IPF fibroblasts may be attributable\, at least in part\, to increased acetylation of their microtubules. Acetylation of α-tubulin is dependent on α-tubulin acetyltransferase (αTAT1) activity\, which is upregulated in fibrotic fibroblasts compared with controls. siRNA-mediated αTAT1 downregulation in these fibrotic fibroblasts reduced their pro-durotactic phenotype without affecting fibroblast chemotaxis.  In vivo\, αTAT-1-deficient mice were protected from bleomycin-induced lung fibrosis\, as assessed qualitatively by histology and quantitatively by hydroxyproline levels. Together\, we identified a novel mechanism through which gradients of matrix stiffness produced in the injured lung drives the progression of lung fibrosis\, by recruiting additional fibroblasts to sites of injury and incipient fibrosis through durotaxis. We consequently hypothesize that inhibition of fibroblast durotaxis has the potential to be an entirely new therapeutic strategy for IPF and other fibrotic diseases.
URL:https://ibecbarcelona.eu/event/ibec-seminar-targeting-fibroblast-durotaxis-as-anti-fibrotic-therapy-2/
CATEGORIES:IBEC Seminar
ORGANIZER;CN="IBEC":MAILTO:www.ibecbarcelona.eu
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Madrid:20161013T150000
DTEND;TZID=Europe/Madrid:20161013T160000
DTSTAMP:20260421T144056
CREATED:20161006T150918Z
LAST-MODIFIED:20161010T161431Z
UID:24823-1476370800-1476374400@ibecbarcelona.eu
SUMMARY:IBEC Seminar: Targeting fibroblast durotaxis as anti-fibrotic therapy
DESCRIPTION:Targeting fibroblast durotaxis as anti-fibrotic therapy\nDr. David Lagares\, Harvard Medical School\nDysregulated wound repair process in response to chronic tissue injury can lead to the development of tissue fibrosis in most organs. Fibrosis is characterized by accumulation of collagens and other matrix proteins that result in the distortion of tissue architecture\, and ultimately organ failure\, in variety of human diseases including idiopathic pulmonary fibrosis (IPF). Tissue stiffening\, traditionally thought to simply be a consequence of lung fibrosis\, has been recently shown to be a contributing factor to its pathogenesis by inducing fibroblasts differentiation into activated myofibroblasts\, the principal effector cells responsible matrix deposition. \nThe cellular and molecular mechanisms through which increased tissue rigidity drives disease progression remain to be fully elucidated. Using atomic force microscopy (AFM) to mechanically characterize the “topography”\, i.e. the spatial distribution\, of alterations in matrix stiffness produced in mouse models of lung fibrosis\, we consistently found that stiffness\, rather than being uniformly elevated in lung fibrotic tissues from animals models\, rises and falls in spatial gradients between “peaks” and “valleys.” We hypothesize that the stiffness “peaks” represent areas in which the fibrotic process was initiated\, or “nucleated”. Once fibrosis is nucleated\, the stiffness gradients leading to these fibrotic peaks are amplified by fibroblast “durotaxis\,” – the directed migration of cells from regions of lower to higher stiffness\, which occurs in the absence of chemoattractant gradients. Using hydrogels that recapitulate the stiffness gradients observed in animal fibrosis models\, we demonstrated durotaxis of lung fibroblasts in time-lapse microscopy studies. In human studies with lung tissues from IPF patients\, AFM revealed similar stiffness topography as we observed in mouse models\, i.e. the presence of focal peaks surrounded by stiffness gradients. Of note\, we have also found that primary lung fibroblasts from IPF patients exhibit greater durotactic responses to stiffness gradients than do control lung fibroblasts. In efforts to identify the molecular pathways involved in cell durotaxis\, we have found that the increased durotaxis of IPF fibroblasts may be attributable\, at least in part\, to increased acetylation of their microtubules. Acetylation of α-tubulin is dependent on α-tubulin acetyltransferase (αTAT1) activity\, which is upregulated in fibrotic fibroblasts compared with controls. siRNA-mediated αTAT1 downregulation in these fibrotic fibroblasts reduced their pro-durotactic phenotype without affecting fibroblast chemotaxis.  In vivo\, αTAT-1-deficient mice were protected from bleomycin-induced lung fibrosis\, as assessed qualitatively by histology and quantitatively by hydroxyproline levels. Together\, we identified a novel mechanism through which gradients of matrix stiffness produced in the injured lung drives the progression of lung fibrosis\, by recruiting additional fibroblasts to sites of injury and incipient fibrosis through durotaxis. We consequently hypothesize that inhibition of fibroblast durotaxis has the potential to be an entirely new therapeutic strategy for IPF and other fibrotic diseases.
URL:https://ibecbarcelona.eu/event/ibec-seminar-targeting-fibroblast-durotaxis-as-anti-fibrotic-therapy/
CATEGORIES:IBEC Seminar
ORGANIZER;CN="IBEC":MAILTO:www.ibecbarcelona.eu
END:VEVENT
END:VCALENDAR