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TZID:Asia/Kolkata
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DTSTART:20250101T000000
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BEGIN:VEVENT
DTSTART;TZID=Asia/Kolkata:20250313T140000
DTEND;TZID=Asia/Kolkata:20250313T150000
DTSTAMP:20260610T232955
CREATED:20250311T070224Z
LAST-MODIFIED:20250311T070224Z
UID:4395505-1741874400-1741878000@be.iisc.ac.in
SUMMARY:BE Seminar: Harnessing Nanoscale Cellular Communication for Designing Next-Generation Therapeutics by Dr. Tanmoy Saha\,
DESCRIPTION:Speaker: Dr. Tanmoy Saha\, MSc\, PhD. \nInstructor\, Harvard Medical School \nAssociate Bioengineer\, Brigham and Women’s Hospital \nDate: 13th March\nTime: 2.00 PM\nVenue: TCS Smart X Building\, Seminar Hall – (G F – 22) \nTitle: Harnessing Nanoscale Cellular Communication for Designing Next-Generation Therapeutics \nAbstract: Aberrant intercellular communication underlies disease progression. For example\, cancer cells communicate with neighboring cells to exchange organelles\, proteins\, metabolites\, and ions\, which helps them gain survival advantages. He is interested in three different types of communication: (i) transmembrane ionic communication\, (ii) extracellular protein-mediated communication\, and (iii) intercellular nanoscale physical communication. \nCells maintain an ionic homeostasis with the extracellular environment using ion channels and transporters. He has developed a variety of unimolecular and supramolecular artificial chloride channels (ACT). The ACTs are robust supramolecular architecture made up of small molecules. This helps in a better understanding of ion transport activity and modulating ionic communication in cells. He has performed structure-activity relationships to identify the best ACT. He introduced the first-ever example of ACT\, which can induce apoptosis in cancer cells by disrupting ionic homeostasis. \nCancer cells use extracellular proteins\, known as immune checkpoints\, to send kill-me-not signals to T cells and macrophages. Immunotherapy has made a paradigm shift in cancer treatment by blocking such interactions using monoclonal antibodies. However\, more than 70% of cancer patients do not respond to immunotherapy. He has introduced immunoengineered nanotherapeutics that serve as a platform technology to deliver a combination of pharmacological drugs and biologics to cancer cells. This nanotherapeutic can block more than one immune checkpoint and activate both innate and adaptive immunity. This has shown increased therapeutic efficacy in syngeneic lung cancer\, which is not responsive to traditional immunotherapy and monotherapies. \nFurthermore\, they investigated a novel mechanism of immune evasion by cancer cells through nanoscale physical communication. They have used high-resolution electron and optical microscopy to identify the nanoscale communication of the cancer cells with T cells and hijack mitochondria. The transfer of mitochondria metabolically empowers the cancer cells and increases their proliferation\, metastasis\, and drug resistance. In contrast\, the T cell population depletes because of metabolic deactivation. Blocking the nanotube-mediated mitochondria transfer by pharmacological inhibitors has shown potential therapeutic implications in increasing intrinsic T cell immune response and elevating therapeutic efficacy in combination with traditional immunotherapy. Moreover\, they have shown elevating the immune response by supercharging T cells with exogenous mitochondria. Hence\, a mechanistic understanding of cellular communication and novel therapeutic strategies are critical to offer better therapeutic outcomes in cancer and other chronic diseases. \nAbout the Speaker: Dr. Saha is an entry-level faculty at Harvard Medical School and an Associate Bioengineer at Brigham and Women’s Hospital. He has received PhD from the Indian Institute of Science Education and Research Pune and received the best thesis award from the chemistry department. Dr. Saha’s. major research direction is to develop tools to study cellular communication and introduce novel therapeutic strategies. He has published his research in prestigious journals\, including Nature Nanotechnology\, Science Advances\, J. Am. Chem. Soc.\, Cell\, PNAS\, etc. He has received independent research grants from the Department of Defense and Melanoma Research Alliance.
URL:https://be.iisc.ac.in/event/be-seminar-harnessing-nanoscale-cellular-communication-for-designing-next-generation-therapeutics-by-dr-tanmoy-saha/
LOCATION:TCS Smart-X Hub Building\, IISc
CATEGORIES:Seminar
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DTSTART;TZID=Asia/Kolkata:20250313T160000
DTEND;TZID=Asia/Kolkata:20250313T170000
DTSTAMP:20260610T232955
CREATED:20250311T070053Z
LAST-MODIFIED:20250311T070053Z
UID:4395503-1741881600-1741885200@be.iisc.ac.in
SUMMARY:BE Seminar: Modeling complex phenotypes supported by gene regulatory networks by Dr. Tomas Gedeon
DESCRIPTION:Speaker: Dr. Tomas Gedeon\nDate: 13th March\nTime: 4.00 PM\nVenue: TCS Smart X Building\, Classroom 03 – (G F – 12) \nTitle: Modeling complex phenotypes supported by gene regulatory networks \nAbstract: Gene regulatory networks with more than a few genes can support different phenotypes in different conditions. These conditions may be external inputs like intercellular signaling\, resource abundance\, or internal variability like abundance of ribosomes\, RNAP\, or even copy number of different enzymes. The different conditions can be modeled as changes in the parameters of a gene network model. \nThe mathematical challenge is to develop methods to describe\, search\, and analyze the behavior of models across large sets of parameters. He will illustrate the use of the techniques that we developed\, which are based on combining discrete Boolean approaches with differential equations models\, on three problems: \nThe first problem studies a problem where naive CD4+ cells differentiate into Th1\, Th2\, Th17\, and Treg subsets which mutually inhibit each other. in their model\, they compare the prevalence\, across all parameters\, of a fully differentiated cell type to a cell type that combines characteristics of two of the four types. They find that such a type of hybrid occurs\nmore frequently. This suggests that differentiation to four types likely happens in a two-step process\, rather than in a single step. The model is general and conclusions may apply to other differentiation processes. \nThe second problem concerns the ability of the same cell cycle network in yeast to support two phenotypes: (a) regular cell cycle\, and (b) endocycling\, where the cell duplicates the genome but does not go through mitosis. Endocycling can be induced experimentally by knocking down mitotic cyclin and they use the data to show that\, indeed\, a single network in different parameter regimes\, can support these different phenotypes. \nThe third problem concerns the gap gene network in Drosophila. Maternal gradients provide cell-specific input into the gap gene network along the head-to-tail axis. They investigate if this varying input\, interpreted as varying specification of parameters of the gap gene network\, is sufficient to explain different states that the network reaches in different segments\, which lays down the segmentation plan for the animal. \nIf interest and time remain\, He will explain a bit of the mathematics that allows us to do this type of analysis. \nAbout the Speaker: Dr. Tomas Gedeon is a Professor of Mathematics at Montana State University who specializes in mathematical modeling of biological systems\, especially those arising in cellular and molecular biology. His most recent interest is to develop new methods to understand the behavior of gene regulatory networks with applications to apply understanding of cell cycle and behavior of developmental networks across time and space. He obtained his undergraduate degree from Comenius University in his native Slovakia in 1989 and a PhD in Mathematics from Georgia Institute of Technology in 1994.
URL:https://be.iisc.ac.in/event/be-seminar-modeling-complex-phenotypes-supported-by-gene-regulatory-networks-by-dr-tomas-gedeon/
LOCATION:IDR Building – G12: Classroom 3
CATEGORIES:Seminar
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