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STAT1 is essential for hematopoietic stem cell function and maintains a MHC IIhi stem cell subset that resists myeloablation and neoplastic expansion [LK]

ABSTRACT: STAT1 is essential for hematopoietic stem cell function and maintains a MHC IIhi stem cell subset that resists myeloablation and neoplastic expansion [LK]

PROVIDER: PRJNA750053 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15258061_1.fastq.gz	Fastqsanger.gz
	SRR15258061_2.fastq.gz	Fastqsanger.gz
	SRR15258062_1.fastq.gz	Fastqsanger.gz
	SRR15258062_2.fastq.gz	Fastqsanger.gz
	SRR15258063_1.fastq.gz	Fastqsanger.gz

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STAT1 is essential for hematopoietic stem cell function and maintains a MHC IIhi stem cell subset that resists myeloablation and neoplastic expansion [LK]

Project description:Adult hematopoietic stem cells (HSCs) are predominantly quiescent and can be activated in response to acute stress such as infection or cytotoxic insults. STAT1 is a pivotal mediator of interferon (IFN) signaling and is required for IFN-induced HSC proliferation, but the downstream mechanisms remain unclear and in particular little is known about the role of STAT1 in regulating hematopoietic stem/progenitor cells during homeostasis. Here we show that loss of STAT1 alters the steady state hematopoietic stem and progenitor (HSPC) landscape, impairs HSC function in transplantation assays and delays blood cell regeneration following myeloablation. Under steady state conditions STAT1 was essential for several HSC transcriptional programs including expression of genes involved in virus life cycle, a subset of interferon-stimulated genes, MHC class I genes and genes involved in cell cycle arrest. In addition Stat-1 deficient mice lacked a previously unrecognized quiescent subset of homeostatic HSCs with high levels of MHC II expression (MHC IIhi HSCs). This subset was refractory to 5’-FU induced myeloablation and displayed reduced megakaryocytic potential. Mutant calreticulin, which causes increased megakaryopoiesis in human myeloproliferative neoplasms, gave rise to preferential expansion of MHC IIlo HSCs. These data reveal a STAT1 dependent MHC IIhi quiescent HSC subset and show that STAT1 protects HSCs from proliferative exhaustion.

2022-07-05 | GSE180905 | GEO

STAT1 is essential for hematopoietic stem cell function and maintains a MHC IIhi stem cell subset that resists myeloablation and neoplastic expansion

Project description:STAT1 is essential for hematopoietic stem cell function and maintains a MHC IIhi stem cell subset that resists myeloablation and neoplastic expansion

| PRJNA750055 | ENA

STAT1 is essential for hematopoietic stem cell function and maintains a MHC IIhi stem cell subset that resists myeloablation and neoplastic expansion

2022-07-05 | GSE180904 | GEO

Leptolyngbya iicbica LK strain:LK

Project description:Leptolyngbya iicbica LK strain:LK Transcriptome or Gene expression

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Mouse melanoma cell line B16-F10 treated with G007-LK

Project description:The mouse melanoma cell line B16-F10 provided by American Type Culture Collection (ATCC® CRL-6475™) were treated with DMSO, G007-LK, WNT or G007-LK+WNT, done in triplicates for a total of 12 samples.

2021-07-01 | E-MTAB-8101 | biostudies-arrayexpress

3'-Seq LK Pabpn1 KD in vivo

Project description:Here, we present a 3'-Seq dataset of Pabpn1 KD LK cells and Scr control cells.

2020-03-30 | E-MTAB-8538 | biostudies-arrayexpress

Abnormal Mammary Development in STAT1-null Mice is Stroma-Dependent

Project description:Stat1-null mice (129S6/SvEvTac-Stat1tm1Rds homozygous) uniquely develop estrogen-receptor-positive mammary tumors with incomplete penetrance and long latency. We studied the growth and development of the mammary glands in Stat1-null mice. Stat1-null MGs have faulty branching morphogenesis with abnormal terminal end buds. The Stat1-null MG also fails to sustain growth of 129S6/SvEv wild-type and null epithelium. These abnormalities are partially reversed by added progesterone and prolactin. Transplantation of wild-type bone-marrow into Stat1-null mice does not reverse the mammary gland developmental defects. Media conditioned by Stat1-null epithelium-cleared mammary fat pads does not stimulate epithelial proliferation whereas it is stimulated by conditioned media derived from either wild-type or progesterone and prolactin-treated Stat1-null epithelium-cleared mammary fat pads. Microarrays and multiplex cytokine protein assays showed that the mammary gland of Stat1-null mice had lower levels of growth factors that have been implicated in normal mammary gland growth and development. Transplanted Stat1-null tumors and their isolated cells also grow slower in Stat1-null mammary gland compared to wild-type recipient mammary gland. Stat1-null hosts responded to tumor transplants with granulocytic infiltrates while wild-type hosts show a mononuclear response. These studies demonstrate that growth of normal and neoplastic Stat1-null epithelium primarily depends on the hormonal milieu and factors, such as cytokines, from the mammary stroma. Stat1-null mammary glands were compared to 129SvEv WT mammary glands with respect to development, gene expression profiles, growth factors and histology.

2015-05-01 | E-GEOD-63025 | biostudies-arrayexpress

Combined MEKi (GDC-0973) and WNT (G007-LK) treatment in APC and KRAS mutant HCT-15 cell line

Project description:We report RNAseq data from HCT-15 cells were treated wih control(DMSO), GDC-0973, G007-LK and combined GDC-0973 and G007-LK treatmetn for 24 hours.

2019-04-22 | GSE123807 | GEO

STAT1 regulates immune-mediated intestinal stem cell proliferation and epithelial regeneration

Project description:The role of the immune system in regulating tissue stem cells remains poorly understood, as does the relationship between immune-mediated tissue damage and regeneration. Graft vs. host disease (GVHD) occurring after allogeneic bone marrow transplantation (allo-BMT) involves immune-mediated damage to the intestinal epithelium and its stem cell compartment. To assess impacts of T-cell-driven injury on distinct epithelial constituents, we performed single cell RNA sequencing on intestinal crypts following experimental BMT. Intestinal stem cells (ISCs) from GVHD mice exhibited global transcriptomic changes associated with a substantial Interferon-γ response and upregulation of STAT1. To determine its role in crypt function, STAT1 was deleted within murine intestinal epithelium. Following allo-BMT, STAT1 deficiency resulted in reduced epithelial proliferation and impaired ISC recovery. Similarly, epithelial Interferon-γ receptor deletion also attenuated proliferation and ISC recovery post-transplant. Investigating the mechanistic basis underlying this epithelial response, ISC STAT1 expression in GVHD was found to correlate with upregulation of ISC c-Myc. Furthermore, activated T cells stimulated Interferon-γ- dependent epithelial regeneration in co-cultured organoids, and Interferon-γ directly induced STAT1-dependent c-Myc expression and ISC proliferation. These findings illustrate immunologic regulation of a core tissue stem cell program after damage and support a role for Interferon-γ as a direct contributor to epithelial regeneration.

2024-09-09 | GSE276126 | GEO

A distinct subset of blood stem cells resists regenerative stress to preserve stemness

Project description:A distinct subset of blood stem cells resists regenerative stress to preserve stemness

| PRJNA626094 | ENA