Amphitheatre Farabeuf, Campus des Cordeliers, 15 rue de l Ecole de Medecine 75006
Lundi 16 Juin 2025    9:00
Invite par: Carla Saleh Annual Scientific Symposium of the Labex IBEID The upcoming Annual Scientific Symposium offers an opportunity to explore the research projects conducted by the IBEID members. Held this year at the ENVA (Ecole nationale veterinaire ... Plus d'infos...
Tags: Financial regulation, LabEx ReFi - European Laboratory on Financial Regulation, Systemic risk, French UMR, French National Centre for Scientific Research
au College de France - Salle D2
11 place Marcelin Berthelot - 75005 Paris
Mercredi 18 Juin 2025    9:30
La premiere reunion du cytoskeleton club de 2025 aura lieu ce mercredi a l’Institut Pasteur : – Charlotte Mallart (post-doc, Minc lab, Institute Jacques Monod) presentera : «Regulation of cytoplasm rheologyby bulk F-Actin networks». – Noemi Zollo (PhD student, Verlhac/ Terret lab, CIRB College de France) presentera : A novel RNP compartment allows mouse oocytes to adapt translational levels during late growth?. Plus d'infos...
Annonce publiée le 14-01-2025
Institut Jacques Monod
Institut Jacques Monod Salle Francois Jacob, 15 rue Helene Brion, Paris, France
Centre de recherche - Paris - Amphitheatre Helene Martel-Massignac (BDD)
Jeudi 19 Juin 2025    11:00
Invite par: Manish KUSHWAHA & Olivier BORKOWSKI Our lab at Imperial College is focused on the engineering of bacteria, mammalian and synthetic cells to advance the applications of synthetic biology. Resource competition between host cells and genetic constructs is one of our main research themes, for its impact on our ability to reliably engineer cellular hosts. In order to tackle resource competition and the cellular burden derived from it, we are currently developing novel tools to address measure and characterise competition in mammalian cells, building on our previous work in bacteria, but also exploring the design of novel gene expression control platforms for low-footprint genetic engineering. Plus d'infos...
Tags: Biotechnology, Appropriate technology, Biocybernetics, Bioinformatics, Synthetic biology, Systems biology, Christopher Voigt
Les galaxies ne voguent pas de façon désordonnée dans l’Univers mais forment un véritable réseau en bulles de savon que l’on appelle la toile cosmique. Cette toile est composée de grands vides entourés par des filaments le long desquels les galaxies se meuvent avant de terminer leur course aux noeuds où de gigantesques amas de galaxies se forment. A l'occasion de cette conférence, nous arpenterons l'Univers sur des milliards d'années lumière afin de comprendre comme se tisse cette toile cosmique, quelles sont ses origines, comment elle influence la naissance et l'évolution des galaxies et en quoi elle représente une sonde cosmologique formidable nous permettant de comprendre l'Histoire et la composition de l’Univers. Plus d'infos...
Annonce publiée le 22-05-2025
Institut Cochin
Salle Rosalind Franklin
Jeudi 19 Juin 2025    12:00
Invite par: Liliana Mancio Silva In this presentation, Professor Hedda Wardemann will describe how we study the clonal evolution of B and T cell responses to Plasmodium falciparum circumsporozoite protein (CSP) at cellular and monoclonal antigen-receptor level to guide ... Plus d'infos...
Tags: Malaria, Plasmodium, Circumsporozoite protein, Isabella Akyinbah Quakyi, David A. Fidock
Annonce publiée le 27-05-2025
Institut Pasteur
Batiment Lwoff , salle Retrovirus,
Jeudi 19 Juin 2025    14:00
Invite par: Manish KUSHWAHA Ribosomes in cells exist in multiple functional states: actively translating, hibernating, inhibited -when perturbed with sublethal doses of drugs. Current theoretical descriptions, based on steady-state growth models, fail to reconcile observed protein synthesis at negligible growth conditions-predicting paradoxically zero active ribosomes despite measurable translation. Here, we present a mechanistic framework that moves beyond the traditional ribosome-centric view by explicitly integrating transcription dynamics and quantifying ribosome usage, thus predicting the physiological costs-both transcriptional and translational-of expressing unnecessary proteins. This approach distinguishes active from inactive ribosome pools, revealing that even at slow growth, a significant fraction of ribosomes actively maintains protein levels against degradation. Our model predicts finely coordinated initiation and elongation rates, stabilizing ribosome densities across varying physiological states, and provides quantitative insights into ribosome sequestration by hibernation factors. Plus d'infos...
Tags: Anonymous, Botnets, Denial-of-service attacks, Internet-based activism, Low Orbit Ion Cannon, Wakanumun, Loc Bouvard
Annonce publiée le 15-05-2025
Paris RNA Club
Auditorium Gallois - 45 rue d Ulm, 75005 Paris
Vendredi 20 Juin 2025    11:00
My group is focused on the discovery of microproteins relevant for cellular plasticity and cancer. Using a computational method for phylogenetic analysis, we have identified 5 novel and evolutionary conserved microproteins dysregulated in cancer and in cellular differentiation/de-differentiation processes. We have experimentally validated their translation and characterized their molecular functions in vitro and in vivo. Our results demonstrate that our newly identified microproteins are novel regulators of cell identity that play important roles in diverse functions such as induction of cellular differentiation, inhibition of EMT and mitochondrial metabolism, all of them under the umbrella of tumor suppression. Our group also hypothesized that the microproteins' small size makes them ideal candidates to be shed by the cell and act as extracellular messengers. We have mined the pancreatic cancer-secreted microproteome for novel regulators of tumor progression and metastasis. Using proteogenomics in patient-derived samples, we have identified hundreds of microproteins secreted -soluble or coated in exosomes- by pancreatic tumors. The characterisation of our top candidates so far has shown that they can extrinsically promote tumor growth and metastasis. Altogether, our data advances our knowledge on the underexplored microproteome and provides pioneering evidence of its role in cancer cell plasticity and tumor communication. Plus d'infos...
Centre de recherche - Paris - Amphitheatre Marie Curie
Vendredi 20 Juin 2025    11:45
Invite par l’equipe Konstantinides, Carlos Estella (Laboratory of stress response and morphogenesis. Centro de Biologia Molecular CSIC-UAM, Madrid, Spain) presentera un seminaire de l’Institut Jacques Monod sur le theme : A cross talk between p53 and the cell cycle regulates apoptotic induction and tumor formation in Drosophila Resume : Cell division is essential for tissue regeneration and organismal survival. However, errors in this process can lead to uncontrolled cell proliferation and cancer. The tumor suppressor gene p53 plays a critical role in maintaining genomic integrity by coordinating cellular responses to stress, such as DNA damage. These responses include cell cycle arrest, DNA repair, senescence, or apoptosis. Importantly, how these responses are precisely coordinated to maintain tissue homeostasis remains poorly understood. To address this challenge, simple genetic models are needed to study the precise regulation of cellular responses triggered by p53 and its role in tumorigenesis. To simplify the study of p53’s functions, we use Drosophila melanogaster, which has a single p53 homolog. Drosophila serves as a powerful genetic model due to its highly conserved pathways and sophisticated genetic tools. Notably, approximately 85% of human cancer-related genes have orthologs in flies. In this seminar I´ll discuss recent work from our laboratory that demonstrated how the cellular context and proliferative status of a cell significantly impact p53’s ability to regulate the various responses triggered by DNA damage. In addition, I´ll present the tumorigenic potential of p53 when its apoptotic role is inhibited. We find that cells with chronic p53 activity that have inhibited its apoptotic potential acquire a persistent activity of the JNK pathway, which drives them into a senescent-like status and induce the non-autonomous overgrowth of the surrounding tissue. These results lead us to propose a model in which cell cycle progression and p53 pro-apoptotic activity are molecularly connected to coordinate the appropriate response after DNA damage. Plus d'infos...
Institut Jacques Monod Salle Francois Jacob, 15 rue Helene Brion, Paris, France
Vendredi 20 Juin 2025    12:00
Invite par: Elizabeth Macintyre amp; Vahid Asnafi Seminar Topic: Mitohormesis and metabolic adaptations in response to therapeutic stress in acute myeloid leukemia Photo credits: DDM-MICHEL VIALA
Plus d'infos...
Invite par: Henrique TEOTÓNIO - 2024-2025 EEB external seminar Abstract : Selection often favours different trait values in males and females, leading to genetic conflicts between the sexes when traits share a genetic basis. Such sexual antagonism has been proposed as a mechanism to maintain genetic polymorphism. However, this notion relies largely on population genetic models of single loci with fixed fitness effects. In this talk, I’ll review recent findings that challenge this view. Specifically, we modelled the evolution of a continuous trait with a shared genetic basis but differing optima in males and females, examining various genetic architectures and fitness landscapes. For autosomal loci, the long-term maintenance of polymorphism requires strong sexual conflict generating unusual sex-specific fitness patterns. More realistic fitness landscapes typically produce stabilising selection, resulting in an evolutionarily stable state dominated by a single homozygous genotype. Thus, genetic variation from sexual antagonism at autosomal loci is likely rare and transient, making it difficult to detect. In contrast, loci tightly linked to the sex-determining region are more conducive to sexually antagonistic variation, generating strong selection to reduce recombination and facilitating the linkage of sexually antagonistic alleles to the sex where they confer advantages. This process can initiate and accelerate sex chromosome evolution. Plus d'infos...
Tags: Evolutionary biology, Sexual selection, Sexual conflict, Polymorphism, Natural selection, Population genetics, Evolution, Intralocus sexual conflict, Interlocus sexual conflict
au College de France - Salle D2
11 place Marcelin Berthelot - 75005 Paris
Lundi 23 Juin 2025    9:00
Les inscription pour le VIP & DIF Day #5 sont ouvertes! Où : Institut Jacques Monod (Amphi Buffon – 15 rue Helene Brion – 75013 Paris)
Quand: Monday 23rd of June 2025. Cette annee, nous aurons le plaisir d’accueillir les deux orateurs principaux suivants : Maria-Cristina Gambetta, University of Lausanne Alper Akay, University of East Anglia Soumettez vos resumes d’affiches ou d’exposes.
https://sites.google.com/view/vipdif/registration-2025
La participation est gratuite mais l’inscription est obligatoire pour tous.
La date limite d’inscription est le 1er juin 2025. Plus d'infos...
Annonce publiée le 20-05-2025
Institut Jacques Monod
Institut Jacques Monod Amphitheatre Buffon, 15 rue Helene Brion, Paris, France
During embryogenesis, precise spatial-temporal patterns from transcription factors (TFs) establish the body plan of the embryo. These TFs function as master regulatory switches controlling genes that instruct cells to adopt specific morphologies and functions to form different organs, tissues, and body segments. For example, TFs from the Homeobox (Hox) family specify the identity of individual body segments along the anterior-posterior axis. However, developmental genes targeted by Hox TFs such as shavenbaby (svb), which terminally fates cells in the ectoderm into trichomes, have enhancers controlled exclusively by low affinity binding sites for the Hox factor Ultrabithorax (Ubx). Moreover, live imaging experiments tracking TF binding in multicellular eukaryotes suggest that TF-DNA interactions are in general short-lived, lasting on average for only a few seconds. Given this stochastic and low-affinity molecular foundation, how can TFs drive efficient gene expression leading to robust phenotype development on the embryo? My work using high- and super-resolution fluorescence microscopy in Drosophila melanogaster embryos showed that svb transcription sites reside in nuclear regions enriched for Ubx. These local environments are co-enriched for specific transcriptional cofactors, thus preserving both regulatory specificity and transcriptional efficiency. Epigenetic modifications, such as H3K4me1, also play an important role in preserving the integrity of these transcriptional microenvironments and regulatory specificity. Finally, genes co-regulated by the same TF can share and reinforce these transcriptional hubs, improving the robustness of gene expression and of phenotype development when embryos are subjected to environmental and genetic stresses. Thus, understanding how the nuclear organization of TFs evolves during embryo development to form and maintain specialized transcriptional hubs, as well as how they can organize stochastic and transient molecular interactions into precise and robust regulatory signals will help decipher how multicellular eukaryotes physically organize their nuclei to shape gene expression. Plus d'infos...
au College de France - Salle D2
11 place Marcelin Berthelot - 75005 Paris
Jeudi 26 Juin 2025    0:00
Invités par Djihad Hadjadj et Benjamin Saint-Pierre. Plus d'infos...
Annonce publiée le 27-03-2025
Institut Cochin
Salle Rosalind Franklin
Jeudi 26 Juin 2025    11:00
Invite par: research axis and Marie-Agnes Petit Tuberculosis(TB), driven primarily by Mycobacterium tuberculosis, continues to pose a severe global health challenge, especially with the rise of multidrug-resistant (MDR) strains. Current treatments are insufficient, creating an urgent demand for new therapeutic options. In our study, we introduce compound X that demonstrates potent efficacy against both actively replicating and dormant M. tuberculosis, including MDR strains. In animal models, compound X exhibits strong in vivo activity, effectively combating both acute and chronic MDR infections. These results highlight compound X as a compelling candidate for advancing the treatment of MDR-TB. Plus d'infos...
Tags: Tuberculosis, Multidrug-resistant tuberculosis, Management of tuberculosis, Mycobacterium tuberculosis, Multiple drug resistance, Extensively drug-resistant tuberculosis, Tuberculosis in Nigeria
Tags: Membrane biology, Lipid bilayer, Lamellar phase, Model lipid bilayer
Annonce publiée le 24-05-2025
Institut Curie
Centre de recherche - Paris - Amphitheatre Marie Curie
Vendredi 04 Juillet 2025    12:00
Invite par: Mario Pende David M. Sabatini studies nutrient sensing and growth control, particularly by the mechanistic Target of Rapamycin (mTOR) pathway. This pathway is the major nutrient-sensitive growth regulator in animals and plays a central role in physiology, metabolism, aging, and cancer. Sabatini discovered the mTOR protein kinase, and most other components of the pathway, including the mTOR-containing complexes mTORC1 and mTORC2, and established them as growth regulators in cells and in vivo. He determined that nutrients signal to mTORC1 through the lysosome-associated Rag GTPases and discovered their many regulators and associated nutrient sensors. In addition to his growth-related work, Sabatini also studies small molecule metabolism and is involved in technology development, such as in generating widely used genome-scale RNAi and CRISPR/Cas9 libraries as well as organellar isolation methods.
Sabatini was born in New York City to Argentine immigrant parents and obtained his bacheloramp; Prague and was previously at MIT.Seminar topic: Nutrient sensing by the mTOR pathwayImage Copyright: Tomas Bellon Plus d'infos...
Tags: Protein complexes, Signal transduction, MTOR, David M. Sabatini, Nutrient sensing, Sirolimus, MTOR inhibitors, Ragulator-Rag complex
Centre de recherche - Paris - Amphitheatre Marie Curie
Mardi 08 Juillet 2025    9:30
During embryogenesis, precise spatial-temporal patterns from transcription factors (TFs) establish the body plan of the embryo. These TFs function as master regulatory switches controlling genes that instruct cells to adopt specific morphologies and functions to form different organs, tissues, and body segments. For example, TFs from the Homeobox (Hox) family specify the identity of individual body segments along the anterior-posterior axis. However, developmental genes targeted by Hox TFs such as shavenbaby (svb), which terminally fates cells in the ectoderm into trichomes, have enhancers controlled exclusively by low affinity binding sites for the Hox factor Ultrabithorax (Ubx). Moreover, live imaging experiments tracking TF binding in multicellular eukaryotes suggest that TF-DNA interactions are in general short-lived, lasting on average for only a few seconds. Given this stochastic and low-affinity molecular foundation, how can TFs drive efficient gene expression leading to robust phenotype development on the embryo? My work using high- and super-resolution fluorescence microscopy in Drosophila melanogaster embryos showed that svb transcription sites reside in nuclear regions enriched for Ubx. These local environments are co-enriched for specific transcriptional cofactors, thus preserving both regulatory specificity and transcriptional efficiency. Epigenetic modifications, such as H3K4me1, also play an important role in preserving the integrity of these transcriptional microenvironments and regulatory specificity. Finally, genes co-regulated by the same TF can share and reinforce these transcriptional hubs, improving the robustness of gene expression and of phenotype development when embryos are subjected to environmental and genetic stresses. Thus, understanding how the nuclear organization of TFs evolves during embryo development to form and maintain specialized transcriptional hubs, as well as how they can organize stochastic and transient molecular interactions into precise and robust regulatory signals will help decipher how multicellular eukaryotes physically organize their nuclei to shape gene expression. Plus d'infos...
Centre de recherche - Paris - Amphitheatre Marie Curie
Mardi 08 Juillet 2025    11:45
Invitee par l’equipe Wassmann, Professor Adele L. Marston (Centre for Cell Biology, University of Edinburgh) presentera un seminaire de l’Institut Jacques Monod sur le theme : Functional organisation of pericentromeres in mitosis and meiosis Resume : Our overall goal is to understand how cells inherit the correct number of chromosomes during mitosis and meiosis. Deviations in chromosome number, called aneuploidy, are a hallmark of cancer and cause birth defects, miscarriages and infertility. Mitosis generates genetically identical daughter cells by evenly segregating the sister chromatids. Meiosis partitions half the genome into gametes through two consecutive segregation events: homologs segregate in meiosis-I, followed by sister chromatids in meiosis-II. Meiosis is especially error-prone: around 1% of human sperm and up to 30% of oocytes are aneuploid. To discover molecular mechanisms, we exploit the tractability of yeast, combined with work in frog, mouse and human oocytes. Our approach is guided by the research question, leading to the employment and development of a wide range of cell biological, genomic, proteomic and biochemical assays. Our group discovered unanticipated roles for pericentromeres, discrete chromosomal domains flanking centromeres, and specialised functions for kinetochores in orienting chromosomes to ensure accurate segregation. In my seminar I will discuss our recent work revealing how pericentromere organization directs accurate chromosome segregation in mitosis and meiosis, in both yeast and oocytes. Plus d'infos...
Tags: Cell cycle, Chromosomes, Cellular processes, DNA replication, In science, Meiosis, Chromosome segregation, Mitosis, Kinetochore, Cell division, Centromere, Sister chromatids
Annonce publiée le 04-06-2025
Institut Jacques Monod
Institut Jacques Monod Salle Francois Jacob, 15 rue Helene Brion, Paris, France
Vendredi 11 Juillet 2025    11:45
Le 11 juillet, Gijsje Koenderink (Department of Bionanoscience, Kavli Institute of Nanoscience Delft, Delft University of Technology) presentera une conference de l’Institut Jacques Monod sur le theme : How cytoskeletal crosstalk makes cells strong Resume : Our bodies are built up of cells and tissues with unique physical properties. Cells and tissues are dynamic but also need to withstand large mechanical loads. This paradoxical mechanical behavior is governed by fibrous protein scaffolds known as the cytoskeleton and the extracellular matrix. Fibrous networks have many advantageous mechanical properties: fibers can form space-filling elastic networks at low volume fractions and they reversibly stress-stiffen, which provides protection from damage. However, it is still poorly understood how biopolymer networks can combine these features with the ability to dynamically adapt their structure and mechanics. In this seminar I will focus on the cytoskeleton: how can the cytoskeleton combine mechanical strength with the ability to dynamically adapt its structure and mechanics? I will summarize our recent insights in this question obtained via quantitative measurements on living cells coupled with experiments on cell-free model systems. I will focus on the role of mechanical crosstalk between the actin, intermediate filament, and septin cytoskeletal networkds, three key determinants of cell mechanics. These three filamentous systems contribute different structural and dynamical properties, but their activities are closely coordinated. I will show that combining cell and cell-free assays allows us to dissect the collaborative and individual roles of the cytoskeletal systems. Our findings may eventually be interesting to guide the search for selective anticancer drugs, since cancer cells often overexpress specific intermediate filaments or septins leading to abnormal mechanical behaviors. Plus d'infos...
Institut Jacques Monod Amphitheatre Buffon, 15 rue Helene Brion, Paris, France
Mardi 26 Aout 2025    0:00
Vijay KUCHROO's research mainly focuses on the regulation of T cell responses in the context of autoimmune disease, to elucidate the role of cytokines and transcription factors in the differentiation of CD4+ T helper subsets and the role of co-stimulatory and co-inhibitory receptors and their ligands in the regulation of autoreactive T cell responses.
The team identified Tim-3 on CD4 + Th1 cells, leading to the discovery of the TIM molecule family. Tim-3 is now recognized as an important co-inhibitory receptor that dampens T cell responses in chronic viral diseases and cancer. Other key discoveries made in his lab include the elucidation of the differentiation factors for Th17, Th9 and Tr1 cells, all of which have a major influence on the development of autoimmunity and tissue inflammation. Vijay Kuchroo is invited by Armelle Blondel. Plus d'infos...
Tags: Immunology, Immune system, T cells, HAVCR2, Vijay Kuchroo, T helper 17 cell, Regulatory B cell, Immune checkpoint
Annonce publiée le 23-05-2025
Institut Cochin
Salle Rosalind Franklin
Jeudi 11 Septembre 2025    0:00
Clear cell renal cell carcinoma (ccRCC) is a prevalent and aggressive subtype of kidney cancer. Immunotherapies that boost the ability of CD8+ T cells to eliminate cancer cells have become a standard of care for ccRCC. However, tumor infiltration of CD8+ T cells can result in contradicting clinical outcomes, potentially due to the functional heterogeneity among tumor-specific CD8+ T cells. In this study, we observed that ccRCC tumors are infiltrated by circulating (Tcirc) and tissue-resident (Trm) memory CD8+ T cells that specifically recognize autologous RCC cells in an HLA class I-dependent manner. Trm cells exhibited higher tumor reactivity but reduced stemness potential and a more exhausted state, whereas Tcirc cells retained higher stemness and cytotoxic potential. Single-cell transcriptomics revealed a rather heterogenous composition of memory populations, including cytotoxic and progenitor Tcirc subsets, as well as multiple Trm subsets, including exhausted Trm cells. TCR and trajectory analyses indicate that circulating progenitors lose their circulation, cytotoxicity and stemness potential within the tumor microenvironment while progressively acquiring a tissue-resident differentiation program followed by a terminal differentiation state. Interestingly, tumor enrichment of Trm and cytotoxic Tcirc cells predicts better survival, while exhausted Trm and total CD8+ T cells predict worse survival in RCC patients. Our findings provide new insights into the differentiation pathways and clinical impact of tumor-specific memory CD8+ T cells infiltrating human RCC tumors. Adoptive T cell therapy (ACT) has demonstrated remarkable efficacy in treating hematological cancers. However, its efficacy against solid tumors remains limited and the emergence of cancer cells that lose expression of targeted antigens promotes resistance to ACT. The mechanisms underlying effective and durable ACT-mediated tumor control are incompletely understood. Here, we show that adoptive transfer of TCR-transgenic CD8+ T cells that efficiently eliminates established murine tumors induces tumor accumulation of CD8+ T cells exhibiting tumor-reactive phenotypes. Interestingly, host CD8+ T cells contributed to ACT-mediated elimination of primary tumors and rejected ACT-resistant melanoma cells lacking the targeted antigen. Mechanistically, ACT induced TNF-?- and dendritic cell-dependent tumor accumulation of endogenous CD8+ T cells and effective tumor elimination. Importantly, although lymphodepleting preconditioning enhanced expansion of transferred cells and ACT-mediated tumor elimination, it impaired host antitumor immunity and abrogated protection against ACT-resistant tumors. Tumor enrichment of transcriptional signatures associated with TNF-? signaling, cross-presenting dendritic cells and tumor-specific CD8+ T cells in correlated with favorable responses to ACT and increased survival in human cancers. Our findings reveal that long-term efficacy of ACT is determined by the interplay between transferred and endogenous CD8+ T cells and is undermined by lymphodepleting preconditioning, which ultimately favors ACT resistance. Plus d'infos...
Analyse de donnees multimodales et modelisation de reseaux pour maitriser les capacites distinctives des cancers Le cours reunira des intervenants de premier plan issus de differents domaines de la biologie des systemes cancereux, de la recherche sur le cancer et de la clinique. Les orateurs invites exposeront diverses approches pour l analyse et l interpretation des donnees omiques, d imagerie et cliniques, en combinant les reseaux de signalisation avec des donnees moleculaires multi-echelles, et en les associant a des donnees cliniques. Les themes abordes comprennent l integration et l analyse de donnees genomiques multimodales, les algorithmes de prediction de la sensibilite aux medicaments, l identification de biomarqueurs et de facteurs de cancer, la stratification des patients, et les applications de la modelisation mathematique et de l analyse d images dans le domaine du cancer. Cette edition comprendra egalement de nouvelles sessions consacrees aux applications actuelles du traitement du langage naturel dans la biologie des systemes computationnels du cancer, a l integration des donnees epigenomiques, ainsi qu aux approches de pharmacologie systemique et de metabolomique. Enfin, un moment fort de la rencontre sera la celebration du 25e anniversaire de la publication de l article fondamental "The hallmarks of cancer" (les capacites distinctives des cancers) de Hanahan et Weinberg (Cell 2000). Plus d'infos...
Annonce publiée le 18-03-2025
Institut Curie
Centre de recherche - Paris - Amphitheatre Helene Martel-Massignac (BDD)
Centre de recherche - Paris - Amphitheatre Helene Martel-Massignac (BDD)
Mercredi 12 Novembre 2025    0:00
L'un des enjeux fondamentaux de la biologie est la comprehension de la relation entre les multiples echelles spatiales et temporelles observees dans un systeme biologique. Des molecules a une fonction cellulaire, d'une collection de cellules a un organisme, ou d'individus a une population, les interactions complexes entre elements singuliers peuvent donner naissance a des proprietes «emergentes» au niveau de l'ensemble. Dans quelle mesure l'ordre spatial et temporel vu au niveau du systeme peut-il etre explique par des proprietes de sous-echelle?ObjectifsCet enseignement a pour objectif de presenter les outils physiques qui ont ete recemment developpes pour decrire cette integration d'echelle (le matin) et de les mettre en application sur des exemples biologiques dans le cadre de seminaires (l'apres-midi). Plus d'infos...
Annonce publiée le 12-06-2025
Institut Curie
Centre de recherche - Paris - Amphitheatre Marie Curie
Vendredi 05 Decembre 2025    11:00