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Fate mapping reveals two pathways of native thrombopoiesis (bulk RNA sequencing)

ABSTRACT: Fate mapping reveals two pathways of native thrombopoiesis (bulk RNA sequencing)

PROVIDER: PRJNA760525 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15713753_1.fastq.gz	Fastqsanger.gz
	SRR15713753_2.fastq.gz	Fastqsanger.gz
	SRR15713754_1.fastq.gz	Fastqsanger.gz
	SRR15713754_2.fastq.gz	Fastqsanger.gz
	SRR15713755_1.fastq.gz	Fastqsanger.gz

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Fate mapping reveals two pathways of native thrombopoiesis (scRNA sequencing)

Project description:Fate mapping reveals two pathways of native thrombopoiesis (scRNA sequencing)

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Fate mapping reveals two pathways of native thrombopoiesis (bulk RNA sequencing)

Project description:Bulk transcriptomes of Megakaryocyte progenitor cells isolated from bone marrow of WT mice; the following cell types were sorted: CD48high Megakaryocyte Progenitor (MkP): lineage- Sca-1- c-kit+ CD41+ CD150+ CD48hi; CD48-/low Megakaryocyte Progenitor (MkP): lineage- Sca-1- c-kit+ CD41+ CD150+ CD48lo

2022-04-28 | GSE183409 | GEO

Fate mapping of hematopoietic stem cells reveals two pathways of native thrombopoiesis.

Project description:Hematopoietic stem cells (HSCs) produce highly diverse cell lineages. Here, we chart native lineage pathways emanating from HSCs and define their physiological regulation by computationally integrating experimental approaches for fate mapping, mitotic tracking, and single-cell RNA sequencing. We find that lineages begin to split when cells leave the tip HSC population, marked by high Sca-1 and CD201 expression. Downstream, HSCs either retain high Sca-1 expression and the ability to generate lymphocytes, or irreversibly reduce Sca-1 level and enter into erythro-myelopoiesis or thrombopoiesis. Thrombopoiesis is the sum of two pathways that make comparable contributions in steady state, a long route via multipotent progenitors and CD48hi megakaryocyte progenitors (MkPs), and a short route from HSCs to developmentally distinct CD48-/lo MkPs. Enhanced thrombopoietin signaling differentially accelerates the short pathway, enabling a rapid response to increasing demand. In sum, we provide a blueprint for mapping physiological differentiation fluxes from HSCs and decipher two functionally distinct pathways of native thrombopoiesis.

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Fate mapping reveals two pathways of native thrombopoiesis (scRNA sequencing)

Project description:Transcriptomes of 1141 single cells isolated from bone marrow of induced R26rtTA/rtTA/Col1A1H2B-GFP/H2B-GFP mice; the following cell types were sorted: Megakaryocyte Progenitor (MkP): lineage- Sca-1- c-kit+ CD41+ CD150+; Multipotent Progenitor (MPP): lineage- Sca-1+ c-kit+ CD48- CD150- ; Hematopoietic Stem Cell (HSC):lineage- Sca-1+ c-kit+ CD48- CD150+; E34 HSC: lineage- Sca-1+ c-kit+ CD48- CD150+ CD201hi CD34-/lo; Restricted hematopoietic progenitor 1 (HPC-1): lineage- Sca-1+ c-kit+ CD48+ CD150-; lineage- kit+ CD41- CD150- cells; lineage- kit+ CD150+ cells.

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Project description:Immune thrombocytopenia (ITP) is a complicated bleeding disease characterized by sharp platelet reduction. As a dominating element involved in ITP, megakaryocytes (MKs) are responsible for thrombopoiesis. However, the mechanism behind the dysregulation of thrombopoiesis in ITP remains undetermined. In this study, we examined the role of YAP1, Yes-associated protein 1, in thrombopoiesis during ITP. We observed a reduced YAP1 expression with cytoskeletal actin misalignment in MKs of ITP patients. Using experimental ITP mice, we showed that YAP1 reduction induced aberrant MK distribution, reduced the percentage of late MKs in total MKs, and caused submaximal platelet recovery. Mechanistically, YAP1 upregulation by GATA1 binding to its promoter promoted MK maturation. Phosphorylated YAP1 facilitated cytoskeletal activation by binding of its WW2 domain to MYH9, facilitating thrombopoiesis. Targeting YAP1 by its activator XMU-MP-1 was sufficient to rescue cytoskeleton defects and thrombopoiesis in YAP1+/- ITP mice and ITP patients. Taken together, these results demonstrate a crucial role for YAP1 in thrombopoiesis, providing a potential for the development of diagnostic markers and therapeutic options for ITP.

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YAP1 regulates thrombopoiesis by binding to MYH9 in immune thrombocytopenia [scRNA-seq]

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2024-07-25 | GSE254764 | GEO

YAP1 regulates thrombopoiesis by binding to MYH9 in immune thrombocytopenia

Project description:YAP1 regulates thrombopoiesis by binding to MYH9 in immune thrombocytopenia

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FATE-NK100 as Monotherapy and in Combination With Monoclonal Antibody in Subjects With Advanced Solid Tumors

Project description:This is a Phase 1, single-dose, open-label, dose-escalation study. The study will be conducted in three parts (i.e. regimens) in an outpatient setting as follows: * Regimen A: FATE-NK100 as a monotherapy in subjects with advanced solid tumor malignancies. * Regimen B: FATE-NK100 in combination with trastuzumab in subjects with human epidermal growth factor receptor 2 positive (HER2+) advanced breast cancer, HER2+ advanced gastric cancer or other advanced HER2+ solid tumors. * Regimen C: FATE-NK100 in combination with cetuximab in subjects with advanced colorectal cancer (CRC) or head and neck squamous cell cancer (HNSCC), or other epidermal growth factor receptor 1 positive (EGFR1+) advanced solid tumors.

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DNA methylation analysis of Conyza canadensis.L in the native and non-native range.

Project description:To understand widespread differences in the DNA methylation patterns of Conyza canadensis leaf samples from its native and non-native ranges. Using Whole Genome Bisulfite Sequencing, we found average read coverages in high mapped reads across native and non-native samples of Conyza canadensis. Using R bioconductor package, we found enrichment score of methylated sites in both native and non-native samples. while analyzing CG, CHG and CHH methylation, we found relatively low CG and CHG methylation across transcriptional units in natives over non-natives. However, differentially methylated regions were found to be 53% hypomethylated and 41% hypermethylated in non-natives on genic regions.

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