Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: GSE18737
PROVIDER: PRJNA123807 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:mass spectrometry analysis of aged and adult hematopoietic stem cells, multipotent progenitors and oligopotent progenitors
2021-07-24 | PXD017442 | Pride
Project description:Umbilical cord blood (CB) is a non-invasive, convenient and broadly used source of hematopoietic stem cells (HSCs) for allogeneic stem cell transplantation. However, limiting numbers of HSCs remain a major constraint for its clinical application. One feasible option would be to expand HSCs to improve therapeutic outcome, however available protocols and the molecular mechanisms governing the self-renewal of HSC are unclear. Here we show that ectopic expression of a single miRNA, miR-125a, in purified murine and human multipotent progenitors (MPP) resulted in increased self-renewal and robust long-term multi-lineage repopulation in transplanted recipient mice. Using quantitative proteomics and Western blot analysis, we identified a restricted set of miR-125a targets which revealed the involvement of the MAP kinase signaling pathway in conferring long-term repopulating capacity to multipotent progenitors in human and mice. Our findings offer the innovative potential to use MPP with enhanced self-renewal activity to augment limited sources of HSC to improve clinical protocols.
2017-01-11 | PXD003931 | Pride
Project description:Hamey2017 - Blood stem cell regulatory
network (LMPP network)
This model is described in the article:
Reconstructing blood stem
cell regulatory network models from single-cell molecular
profiles
Fiona K. Hamey, Sonia Nestorowa,
Sarah J. Kinston, David G. Kent, Nicola K. Wilson, and Berthold
Göttgens
Proceedings of the National Academy of
Sciences of the United States of America
Abstract:
Adult blood contains a mixture of mature cell types, each
with specialized functions. Single hematopoietic stem cells
(HSCs) have been functionally shown to generate all mature cell
types for the lifetime of the organism. Differentiation of HSCs
toward alternative lineages must be balanced at the population
level by the fate decisions made by individual cells.
Transcription factors play a key role in regulating these
decisions and operate within organized regulatory programs that
can be modeled as transcriptional regulatory networks. As
dysregulation of single HSC fate decisions is linked to fatal
malignancies such as leukemia, it is important to understand
how these decisions are controlled on a cell-by-cell basis.
Here we developed and applied a network inference method,
exploiting the ability to infer dynamic information from
single-cell snapshot expression data based on expression
profiles of 48 genes in 2,167 blood stem and progenitor cells.
This approach allowed us to infer transcriptional regulatory
network models that recapitulated differentiation of HSCs into
progenitor cell types, focusing on trajectories toward
megakaryocyte–erythrocyte progenitors and lymphoid-primed
multipotent progenitors. By comparing these two models, we
identified and subsequently experimentally validated a
difference in the regulation of nuclear factor, erythroid 2
(Nfe2) and core-binding factor, runt domain, alpha subunit 2,
translocated to, 3 homolog (Cbfa2t3h) by the transcription
factor Gata2. Our approach confirms known aspects of
hematopoiesis, provides hypotheses about regulation of HSC
differentiation, and is widely applicable to other hierarchical
biological systems to uncover regulatory relationships.
This model is hosted on
BioModels Database
and identified by:
MODEL1610060001.
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.
2017-06-09 | MODEL1610060001 | BioModels
Project description:Hamey2017 - Blood stem cell regulatory
network
This model is described in the article:
Reconstructing blood stem
cell regulatory network models from single-cell molecular
profiles
Fiona K. Hamey, Sonia Nestorowa,
Sarah J. Kinston, David G. Kent, Nicola K. Wilson, and Berthold
Göttgens
Proceedings of the National Academy of
Sciences of the United States of America
Abstract:
Adult blood contains a mixture of mature cell types, each
with specialized functions. Single hematopoietic stem cells
(HSCs) have been functionally shown to generate all mature cell
types for the lifetime of the organism. Differentiation of HSCs
toward alternative lineages must be balanced at the population
level by the fate decisions made by individual cells.
Transcription factors play a key role in regulating these
decisions and operate within organized regulatory programs that
can be modeled as transcriptional regulatory networks. As
dysregulation of single HSC fate decisions is linked to fatal
malignancies such as leukemia, it is important to understand
how these decisions are controlled on a cell-by-cell basis.
Here we developed and applied a network inference method,
exploiting the ability to infer dynamic information from
single-cell snapshot expression data based on expression
profiles of 48 genes in 2,167 blood stem and progenitor cells.
This approach allowed us to infer transcriptional regulatory
network models that recapitulated differentiation of HSCs into
progenitor cell types, focusing on trajectories toward
megakaryocyte–erythrocyte progenitors and lymphoid-primed
multipotent progenitors. By comparing these two models, we
identified and subsequently experimentally validated a
difference in the regulation of nuclear factor, erythroid 2
(Nfe2) and core-binding factor, runt domain, alpha subunit 2,
translocated to, 3 homolog (Cbfa2t3h) by the transcription
factor Gata2. Our approach confirms known aspects of
hematopoiesis, provides hypotheses about regulation of HSC
differentiation, and is widely applicable to other hierarchical
biological systems to uncover regulatory relationships.
This model is hosted on
BioModels Database
and identified by:
MODEL1610060000.
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.
2017-06-09 | MODEL1610060000 | BioModels
Project description:Hematopoietic stem cells (HSC) possess life-long self-renewal activity and generate a series of multipotent progenitors that differentiate into lineage-committed progenitors and subsequently mature cells. Recently, functionally distinct stem and progenitor cell types have been identified, however, a systems-wide understanding of the underlying gene regulation is lacking. Here, we present the global transcriptome of ex vivo isolated mouse multipotent hematopoietic stem/progenitor cells (HSPCs, LinnegSca-1+c-Kit+) and myeloid committed precursors (LinnegSca-1-c-Kit+) as revealed by next-generation sequencing (RNA-seq).
2014-10-08 | E-MTAB-1963 | biostudies-arrayexpress
Project description:Hematopoietic stem cells (HSC) possess life-long self-renewal activity and generate a series of multipotent progenitors that differentiate into lineage-committed progenitors and subsequently mature cells. Recently, functionally distinct stem and progenitor cell types have been identified, however, a systems-wide understanding of the underlying gene regulation is lacking. Here, we present the global transcriptome of ex vivo isolated mouse multipotent hematopoietic stem cells (HSC) and multipotent progenitor cells (MPP1-MPP4) as revealed by next-generation sequencing (RNA-seq). A related high-throughput study with DNA methylome data was also conducted, with data deposited at NCBI Gene Expression Omnibus, under accession GSE52709 ( http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE52709 ). An imported copy of the methylome data set can also be found at ArrayExpress: http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-52709.
2014-08-21 | E-MTAB-2262 | biostudies-arrayexpress
Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive proliferation of T-lymphocytes usually associated with oncogenic activation of NOTCH1 signaling. Using a bone marrow transplantation approach, we have modeled murine CD4+ CD8+ T-ALL by overexpressing DNMT3A R882H in Tet2-/- multipotent progenitors. T-ALL derived from NOTCH1 L1601PdelP Tet2-/-, NOTCH1 L1601PdelP Tet2+/+ or TCL1A progenitors were used for comparison, as well as normal Tet2+/+ and Tet2-/- CD4+ CD8+ double positive (DP) thymocytes.
2016-02-24 | E-MTAB-4161 | biostudies-arrayexpress
Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive proliferation of T-lymphocytes usually associated with oncogenic activation of NOTCH1 signaling. Using a bone marrow transplantation approach, we have modeled murine CD4+ CD8+ T-ALL by overexpressing DNMT3A R882H in Tet2-/- multipotent progenitors. T-ALL derived from NOTCH1 L1601PdelP Tet2-/-, NOTCH1 L1601PdelP Tet2+/+ or TCL1A progenitors were used for comparison, as well as normal Tet2+/+ and Tet2-/- CD4+ CD8+ double positive (DP) thymocytes.
2016-02-24 | E-MTAB-4159 | biostudies-arrayexpress
Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive proliferation of T-lymphocytes usually associated with oncogenic activation of NOTCH1 signaling. Using a bone marrow transplantation approach, we have modeled murine CD4+ CD8+ T-ALL by overexpressing DNMT3A R882H in Tet2-/- multipotent progenitors. T-ALL derived from NOTCH1 L1601PdelP Tet2-/-, NOTCH1 L1601PdelP Tet2+/+ or TCL1A progenitors were used for comparison, as well as normal Tet2+/+ and Tet2-/- CD4+ CD8+ double positive (DP) thymocytes.
2016-02-24 | E-MTAB-4158 | biostudies-arrayexpress
Project description:T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive proliferation of T-lymphocytes usually associated with oncogenic activation of NOTCH1 signaling. Using a bone marrow transplantation approach, we have modeled murine CD4+ CD8+ T-ALL by overexpressing DNMT3A R882H in Tet2-/- multipotent progenitors. T-ALL derived from NOTCH1 L1601PdelP Tet2-/-, NOTCH1 L1601PdelP Tet2+/+ or TCL1A progenitors were used for comparison, as well as normal Tet2+/+ and Tet2-/- CD4+ CD8+ double positive (DP) thymocytes.
2016-02-24 | E-MTAB-4157 | biostudies-arrayexpress