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The influence of the transcription factor EB for BCR-induced gene expression in human Ramos B cells

ABSTRACT: The influence of the transcription factor EB for BCR-induced gene expression in human Ramos B cells

PROVIDER: PRJNA875453 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21380800.fastq.gz	Fastqsanger.gz
	SRR21380801.fastq.gz	Fastqsanger.gz
	SRR21380802.fastq.gz	Fastqsanger.gz
	SRR21380803.fastq.gz	Fastqsanger.gz
	SRR21380804.fastq.gz	Fastqsanger.gz

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The influence of the transcription factor EB for BCR-induced gene expression in murine WEHI-231 B cells

Project description:The influence of the transcription factor EB for BCR-induced gene expression in murine WEHI-231 B cells

| PRJNA875456 | ENA

The influence of the transcription factor EB for BCR-induced gene expression in human Ramos B cells

Project description:To investigate TFEB-dependent expression in BCR-stimulated and resting B cells, CRISPR/Cas9 knockout cell lines were established and subjected to RNA sequencing analysis

2024-06-25 | GSE212456 | GEO

The influence of the transcription factor EB for BCR-induced gene expression in murine WEHI-231 B cells

Project description:To investigate TFEB-dependent expression in BCR-stimulated and resting B cells, CRISPR/Cas9 knockout cell lines were established and subjected to RNA sequencing analysis

2024-06-25 | GSE212457 | GEO

Transcription factor EB sets the stage for fate decisions of antigen-primed B cells in the absence and presence of co-stimulation

Project description:Ligation of the B cell antigen receptor (BCR) initiates humoral immunity. However, mere BCR signaling without appropriate co-stimulation commits B cells to death rather than to differentiation into immune effector cells. How BCR activation depletes potentially autoreactive B cells while simultaneously primes for receiving rescue and differentiation signals from cognate T lymphocytes remains unknown. Here, using a mass spectrometry-based proteomic approach to identify cytosolic/nuclear shuttling elements, we uncover transcription factor EB (TFEB) as a central BCR-controlled rheostat that drives activation-induced apoptosis, and concurrently, promotes the reception of co-stimulatory rescue signals by supporting B cell migration and antigen presentation. CD40 co-stimulation prevents TFEB-driven cell death, while enhancing and prolonging TFEB’s nuclear residency, which hallmarks antigenic experience also of memory B cells. In mice, TFEB shapes the transcriptional landscape of germinal center B cells. Within the germinal center, TFEB facilitates the dark zone entry of light-zone-residing centrocytes through regulation of chemokine receptors and, by balancing the expression of Bcl-2/BH3-only family members, integrates antigen-induced apoptosis with T cell-provided CD40 survival signals. Thus, TFEB reprograms antigen-primed germinal center B cells for cell fate decisions.

2024-08-08 | PXD054505 | Pride

Systematic Analysis of Transcription Program Regulation by Transcription Factor EB (TFEB)

Project description:Systematic Analysis of Transcription Program Regulation by Transcription Factor EB (TFEB)

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Vogesella sp. EB strain:EB

Project description:Vogesella sp. EB strain:EB Genome sequencing and assembly

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Essential role of the transcription factor Bhlhe41 in regulating the self-renewal and BCR repertoire of B-1a cells

Project description:The innate-like B-1a cells provide a first line of defense against pathogens, and yet little is known about their transcriptional control. Here we identified an essential role of the transcription factor Bhlhe41, with a lesser contribution of Bhlhe40, in controlling late stages of B-1a cell differentiation. Bhlhe41/Bhlhe40 mutant B-1a cells were strongly reduced and had an abnormal cell-surface phenotype and altered B-cell receptor (BCR) repertoire, as exemplified by loss of the phosphatidylcholine-specific Vh12/Vk4 BCR. Expression of a pre-rearranged Vh12/Vk4 BCR failed to rescue the mutant phenotype and revealed enhanced proliferation accompanied with increased cell death, implicating Bhlhe41 in controlling the self-renewal of B-1a cells. Bhlhe41 directly repressed the expression of cell cycle regulators and inhibitors of BCR signaling, while activating pro-survival cytokine signaling.

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Transcription Factor EB Controls Metabolic Flexibility during Exercise.

Project description:The transcription factor EB (TFEB) is an essential component of lysosomal biogenesis and autophagy for the adaptive response to food deprivation. To address the physiological function of TFEB in skeletal muscle, we have used muscle-specific gain- and loss-of-function approaches. Here, we show that TFEB controls metabolic flexibility in muscle during exercise and that this action is independent of peroxisome proliferator-activated receptor-γ coactivator1α (PGC1α). Indeed, TFEB translocates into the myonuclei during physical activity and regulates glucose uptake and glycogen content by controlling expression of glucose transporters, glycolytic enzymes, and pathways related to glucose homeostasis. In addition, TFEB induces the expression of genes involved in mitochondrial biogenesis, fatty acid oxidation, and oxidative phosphorylation. This coordinated action optimizes mitochondrial substrate utilization, thus enhancing ATP production and exercise capacity. These findings identify TFEB as a critical mediator of the beneficial effects of exercise on metabolism.

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Project description:EB differentiation study

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2012-09-28 | E-MEXP-3595 | biostudies-arrayexpress

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