Expertise

Hub members Have many expertise, covering most of the fields in bioinformatics and biostatistics. You'll find below a non-exhaustive list of these expertise

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Searched keyword : Pathway Analysis

Related people (3)

Quentin GIAI-GIANETTO


Since September 2016, I am a research engineer in the Bioinformatics and Biostatistics HUB of the Institut Pasteur and detached in the Proteomics facility. I have a PhD in Signal Processing from the Ecole Nationale Supérieure des Télécommunications de Bretagne (Telecom Bretagne) and a Master in Mathematics with a specialty in Statistical Engineering from Rennes 1 University. After my PhD, I was a research and teaching assistant in Mathematics at the Institut National des Sciences Appliquées (INSA) of Rennes, then I worked as a consultant for public local authorities in the company Ressources Consultants Finances. I started working in the field of Proteomics in October 2014 in the EDyP laboratory located in Grenoble (http://www.edyp.fr/). I have been working on the improvement of statistical analysis of bottom-up proteomics data. Today, most of the projects I work on consist of detecting changes in protein abundances using discovery-driven mass spectrometry. I am interested in the development of new methodologies to optimize proteomics data analysis pipelines, from the identification of peptides/proteins to their quantification and the interpretation of results. For this purpose, I worked on several R packages which can be downloaded from the CRAN and Bioconductor: cp4p (https://cran.r-project.org/web/packages/cp4p/index.html), imp4p (https://cran.r-project.org/web/packages/imp4p/index.html), DAPAR (http://bioconductor.org/packages/release/bioc/html/DAPAR.html) and its GUI ProStar.


Keywords
Machine learningModelingPathway AnalysisProteomicsStatistical inferenceBiostatisticsApplication of mathematics in sciencesData and text miningData integrationStatistical experiment designMultidimensional data analysis
Organisms
Non applicable
Projects (1)

Violaine SAINT-ANDRÉ

Group : DETACHED - Detached : Labex milieu intérieur

After graduating from Paris VI University with a PhD in Genetics on the “Role of histone protein post-translational modifications in splicing regulation” that I performed in the Epigenetic Regulation unit at the Institut Pasteur, I carried out two post-doctoral experiences. I first worked for three years as a postdoctoral associate of the Whitehead Institute for Biomedical Research/MIT in Cambridge (USA). My main project consisted in the integration of genomic and epigenomic data in order to predict the transcription factors that are potentially at the core of the regulation of the cell-type specific gene expression programs. I then joined the Institut Curie where I deepened my experience in multi-omics data analyses and integration to identify non-coding RNAs involved in cancer progression. I have recently joined the HUB-C3BI of the Institut Pasteur where I am performing high-throughput data integration to better understand biological complexity and contribute to precision medicine development.


Keywords
ATAC-seqChIP-seqEpigenomicsNon coding RNAPathway AnalysisRNA-seqSingle CellSystems BiologyTool DevelopmentTranscriptomicsData integrationGraph theory and analysisCell biology and developmental biology
Organisms
Human
Projects (1)

Related projects (10)

Gene ontology analysis of RNAseq data from uninfected and Leishmania-infected mouse macrophages

Gene ontology analysis of RNAseq data from uninfected and Leishmania-infected mouse macrophages.  Scientific context During the course of cutaneous or visceral disease in humans or experimental animal models, the resolution of leishmanial infections or the control of parasite growth is dependent on appropriate innate and adaptive immune responses developed by the parasitized host. Leishmania largely evades and subverts these responses by its intracellular life style inside the mammalian host, where the parasites develop into amastigotes mainly within macrophages (BMDMs). We have focused our interest in the BMDM inflammasome and the way Leishmania amastigotes interfere or subvert BMDM inflammatory responses. Our recent data are in favor of an absence of stimulation, even a down-regulation of the inflammasome in BMDMs harboring replicating amastigotes at the gene and protein expression levels. To go further on this, we have performed RNAseq experiments on uninfected and infected BMDMs. This project was done at the “Transcriptome and Epigenome” platform and in close collaboration with the C3BI for normalization and statistical analysis procedures. Objective In the present proposal we will perform a deep analysis of the repartition of modulated genes between the different conditions using these RNAseq data. Using C3Bi expertise we will classify known functions of modulated genes into GO aspects i.e. molecular function, cellular component and biological process, visualize gene annotations and perform statistical analyses for the distribution of the annotated genes over the GO hierarchy for the different gene lists analyzed. Hopefully, these analyses will bring us a better understanding of the mechanisms underlying the subversion of BMDM functions in the innate and adaptive immune response to Leishmania infection which is a prerequisite to design novel anti-parasitic intervention strategies targeting the infected host cell rather than the parasite.



Project status : Closed

Study of the early pathogenesis during Lassa fever in cynomolgus monkeys and its correlation with the outcome

Because of their increasing incidence, dramatic severity, lack of treatment or vaccine, complicated diagnosis, misreading of the pathogenesis, and need for a maximum containment, Viral Hemorrhagic Fevers (VHF) constitute a major public health problem. There is therefore an urgent need to further study VHF to understand the pathogenesis of the severe disease and the host responses involved in their control or in the dramatic damages. Among VHF, Lassa fever (LF) is probably the most worrying one because of its endemicity and the large number of cases. LF is caused by the Old-World arenavirus Lassa virus (LASV). It is endemic to West Africa and is responsible for 300,000 cases and 5,000 to 6,000 deaths each year. We propose here to study the pathogenesis of VHF by using LF in cynomolgus monkeys as a paradigm, with a particular emphasis on the very early events. The viral tropism, pathophysiological mechanisms, and immune responses will be studied during the course of infection, including the incubation period. Powerful approaches will be used to (1) identify early biological markers of infection, to be able to confirm infection and isolate patients; (2) determine the viral tropism and dynamics during the course of infection to understand the natural history of virus into its host. (3) characterize the early pathogenic events that lead to the severe hemorrhagic syndrome to fully understand the pathophysiogenesis of VHF and identify new therapeutic targets. (4) identify the immune responses involved in the control of infection or in the fatal outcome, to reveal the involvement of immunopathological mechanisms and help to design a vaccine approach. This ambitious and unprecedented project will allow to develop therapeutic and prophylactic approaches but also to identify early biological markers of infection and improve the early diagnosis to optimize the management of outbreaks in the field and increase the survival rate in patients.



Project status : In Progress

Gene expression profiling in Kupffer cells

The liver is the biggest internal organ that is responsible for metabolism, detoxification and the defense between the host and the external environment. Thus the liver is also an immune organ, which constantly confronts conflicting demands of immunity against pathogens and tolerance to antigens metabolized locally and bacteria products derived from the gut. In homeostasis, many mechanisms ensure suppression of immune response in the liver, which include low expression levels of MHC molecules in liver antigen presenting cells (APC), increased expression of inhibitory molecules and sustained expression of suppressive cytokines such as IL-10 and TGF-b. Thus, several pathogens including hepatitis B virus (HBV) shrewdly exploit the tolerant immune environment in the liver to establish chronic infection. However, inflammation can elicit efficient immune response. To investigate immune response to HBV in the context of inflammation, we used Mdr2-/- mice, which develop cholestatic inflammation in the liver. We show that after injection of HBV to the mice, WT animals develop chronic infection whereas Mdr2-/- mice eliminate the virus. We detected robust viral-specific antibody production in Mdr2-/- mice but not in WT mice. Kupffer cells (KC) are liver-resident macrophages and important APCs, expressing MHC I, MHC II and costimulatory molecules required for T cell activation. The efficient immune response against HBV observed in Mdr2-/- mice prompts us to profile gene expression in Kupffer cells derived from these mice and compare to those from WT mice at the naïve state.



Project status : In Progress