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Mus musculus

ABSTRACT: The impact of Tcf1/Lef1 deficiency and prostagladin E (PGE) treatment on leukemic stem cell (LSC) transcriptome

PROVIDER: PRJNA357379 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5110190.fastq.gz	Fastqsanger.gz
	SRR5110200.fastq.gz	Fastqsanger.gz
	SRR5110191.fastq.gz	Fastqsanger.gz
	SRR5110201.fastq.gz	Fastqsanger.gz
	SRR5110192.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:Impact of Tcf1 and Lef1 deficiency on HSCs

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Project description:Impact of Tcf1 and Lef1 deficiency on mature CD8 thymocytes

| PRJNA296433 | ENA

Mus musculus

Project description:Impact of Tcf1 and Lef1 deficiency on follicular helper T (Tfh) cells

| PRJNA277948 | ENA

Mus musculus

Project description:Impact of Tcf1 and Lef1 deficiency on histone marks and Tcf1 binding in CD8 T cells

| PRJNA296434 | ENA

Mus musculus

Project description:Impact of Tcf1 and Lef1 deficiency on mSin3A distribution in CD8 T cells

| PRJNA296437 | ENA

Tcf1 and Lef1 regulate follicular helper T cell function eliciated by vaccination [ATAC-Seq]

Project description:The goal of this study is to determine the impact of Tcf1 and Lef1 deficiency on T follicular helper (Tfh) cells elicited by protein immunization. We demonstrate that although phenotypic Tcf1/Lef1-deficient Tfh cells were able to develop in response to vaccination, they are functionally impaired. Mechanisc studies reveal the direct regulatory effect by Tcf1 and Lef1 on transcriptome and chromatin accessibility in vaccine-elicited Tfh cells. Analysis of chromatin accessibility in WT and Tcf1/Lef1-deficient Tfh cells eliciated by vaccination.

2020-10-19 | GSE146421 | GEO

Tcf1 and Lef1 regulate follicular helper T cell function eliciated by vaccination [RNA-Seq]

2020-10-19 | GSE146425 | GEO

Tcf1 and Lef1 regulate follicular helper T cell function eliciated by vaccination [CUTnRUN]

2020-10-19 | GSE146422 | GEO

Impact of Tcf1/Lef1 deficiency on Treg cells

Project description:Impact of Tcf1/Lef1 deficiency on Treg cells

| PRJNA490202 | ENA

The transcription factors TCF1 and LEF1 promote B-1a cell homeostasis and regulatory function.

Project description:B-1 cells are innate-like immune cells found abundantly in serosal cavities and their secreted antibodies are enriched for bacterial recognition1–5. The subset known as “B-1a” repress inflammation by production of regulatory molecules including IL-10 6–8. Unlike conventional B cells, which are produced daily in the bone marrow, B-1a cells are primarily generated from foetal precursors and maintained through self-renewal 9. The mechanisms regulating B-1a homeostasis and function are incompletely understood. Here we demonstrate that serosal cavity mouse and human B-1 cells as well as chronic lymphocytic leukaemia (CLL) B cells express the transcription factors TCF1 and LEF1, and circulating TCF1+LEF1+ B-1 cells increase significantly in patients with bacterial pleural infection. LEF1 is expressed from foetal B-1 progenitors, while TCF1 expression is higher in peripheral B-1a cells. TCF1 and LEF1 deficiency significantly reduces B-1a cells in mice. These transcription factors support B-1a turn-over regulating Myc targets and metabolic pathways. Upon B-1 cell activation, TCF1/LEF1 induce formation of a stem-like population, partly through IL-10 production. TCF/LEF1-deficient B-1 cells proliferate excessively, acquire an exhausted/senescent phenotype, express reduced IL-10 and PD-L1, and fail to suppress brain inflammation. These findings reveal a transcriptional program that links stemness and regulatory potential in B-1a cells.

2025-08-14 | GSE290505 | GEO

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