Project description:Matrices of TPM-normalized counts from RNAseq data for the three phase II clinical trials (IMvigor210, POPLAR, IMmotion150) and the phase I clinical trial PCD4989g.
Project description:Bone marrow (BM) mesenchymal stem/stromal cells are non-hematopoietic (CD45-), non-endothelial (CD31-) multipotential cells capable to differentiate into osteoblastes, chondrocytes and adipocytes. In addition, different subpopulations of MSCs and some of their derivatives (early osteoblastic lineage cells) were shown to form HSC-niche. This makes a complex picture of the relationship between MSCs and HSCs. Despite growing data in mice model, few describe the human counterpart. The BM CD200+ and CD271+ fractions were previously shown to be enriched in native MSCs in human. Herein, we found heterogeneity in expression of CD200 within CD45-/CD31-/CD271+ human BM fraction. We thus selected CD200+ and CD200- cells from CD45-/CD31-/CD271+ BM samples and we analyzed their transcriptome. The differential display of gene expression between these two types of BM fractions will give new insights in the identification of native human MSCs.
Project description:In BRE-GFP transgenic mice BMP activated cells are marked by GFP expression. Analysis of GFP+ and GFP- LSK-SLAM HSC enriched fractions from fetal liver and adult bone marrow shows the interinsic differences in the genetic program of these two HSC enriched fractions. RNAseq of GFP+ and GFP- LSK-SLAM cells from BRE-GFP transgenic mice Fetal liver and adult bone marrow
Project description:Basement membranes (BMs) are ubiquitous extracellular matrices whose composition remains elusive, limiting our understanding of BM regulation and function. By developing a bioinformatic and in vivo discovery pipeline, we define a network of over 220 human proteins localized to BMs. More than 100 BM-network genes associate with human phenotypes and by screening over 63,000 germline genomic sequences from families with rare disorders, we discovered novel predicted loss-of-function variants in MATN2. Biochemical analyses suggest that MATN2 interacts with many BM proteins, and we found that depletion of MATN2 affected levels of core BM components in human podocyte-derived extracellular matrix.