Project description:Thiele2013 - Bone marrow hematopoietic cells
The model of bone marrow hematopoietic cells metabolism is derived from the community-driven global reconstruction of human metabolism (version 2.02, MODEL1109130000
).
This model is described in the article:
A community-driven global reconstruction of human metabolism.
Thiele I, et al
.
Nature Biotechnology
Abstract:
Multiple models of human metabolism have been reconstructed, but each represents only a subset of our knowledge. Here we describe Recon 2, a community-driven,
consensus 'metabolic reconstruction', which is the most comprehensive representation of human metabolism that is applicable to computational modeling. Compared
with its predecessors, the reconstruction has improved topological and functional features, including ~2x more reactions and ~1.7x more unique metabolites. Using
Recon 2 we predicted changes in metabolite biomarkers for 49 inborn errors of metabolism with 77% accuracy when compared to experimental data. Mapping metabolomic
data and drug information onto Recon 2 demonstrates its potential for integrating and analyzing diverse data types. Using protein expression data, we automatically
generated a compendium of 65 cell type-specific models, providing a basis for manual curation or investigation of cell-specific metabolic properties. Recon 2 will
facilitate many future biomedical studies and is freely available at http://humanmetabolism.org/.
This model is hosted on BioModels Database
and identified by: MODEL1310110030
.
To cite BioModels Database, please use: BioModels Database: An enhanced,
curated and annotated resource for published quantitative kinetic models
.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer
to CC0 Public Domain Dedication
for more information.
Project description:Purpose: The goals of this study are to elucidate the underlying mechanism for the regulation of HSC divisions. Methods: Fifteen thousand cells subfractions within the HSC fraction were sorted. These cells were subjected to ATAC-seq using Hi-seq. The sequence reads that passed quality filters were analyzed by FASTX-toolkit.
Project description:Purpose: The goals of this study are to elucidate the underlying mechanism for the regulation of HSC divisions. Methods: One hundred cells of subfractions within the HSC fraction were sorted. These cells were subjected to mRNA sequence using Next-seq. The sequence reads that passed quality filters were analyzed by CLC genomic workbench.
Project description:Purpose: The goals of this study are to elucidate the underlying mechanism for the regulation of HSC divisions. Methods: One hundred thousand cells of subfractions within the HSC fraction were sorted. These cells were subjected to ATAC-sequence by using 10X Genomics Chromium Next GEM Single Cell ATAC Reagent Kits v1.1. The sequence reads that passed quality filters were analyzed by FASTX-toolkit.
Project description:To solve the heterogeniety of human bone marrow non-hematopoietic cells, we perfomed transcriptomic profiling of bone marrow non-hematopoietic cells using scRNAseq.
Project description:Hematopoietic stem cells give rise to all blood lineages, can fully re-populate the bone marrow, and easily outlive the host organism. To better understand how stem cells remain fit during aging, we analyzed the proteome of hematopoietic stem and progenitor cells.
Project description:In the human hematopoietic system, aging is associated with decreased bone marrow cellularity, decreased adaptive immune system function, and increased incidence of anemia and other hematological disorders and malignancies. Recent studies in mice suggest that changes within the hematopoietic stem cell (HSC) population during aging contribute significantly to the manifestation of these age-associated hematopoietic pathologies. While the mouse HSC population has been shown to change both quantitatively and functionally with age, changes in the human HSC and progenitor cell populations during aging have not yet been characterized. Gene expression profiling revealed that aged human HSC transcriptionally up-regulate genes associated with cell cycle, myeloid lineage specification, and myeloid malignancies. These age-associated alterations in the frequency, function, and gene expression profile of human HSC are significantly similar to those changes observed in mouse HSC, suggesting that hematopoietic aging is an evolutionarily conserved process.