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Mus musculus

ABSTRACT: A threshold level of NFATc1 activity is critical for thymocyte differentiation and to prevent leukemia development

PROVIDER: PRJNA318023 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3356107.fastq.gz	Fastqsanger.gz
	SRR3356108.fastq.gz	Fastqsanger.gz

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Similar Datasets

A threshold level of NFATc1 activity is critical for thymocyte differentiation and to prevent leukemia development

Project description:NFATc1 plays a critical role in double-negative thymocyte survival and differentiation. However, the signals that regulate Nfatc1 expression are unknown. Here we show a developmental stage-specific differential expression pattern of Nfatc1 driven by the distal (P1) or proximal (P2) promoters in thymocytes. Whereas, preTCR-negative thymocytes exhibited only P2 promoter-derived Nfatc1b expression, preTCR-positive thymocytes expressed both Nfatc1b and P1 promoter-derived Nfatc1a transcripts. Inducing NFATc1a activity from P1 promoter in preTCR-negative thymocytes, in addition to the NFATc1a from P2 promoter impaired thymocyte development resulting in severe T cell lymphopenia. Additionally, we show that NFATc1 activity suppressed the B-lineage potential of immature thymocytes, and consolidated their differentiation to T cells. Further, in the pTCR-positive DN3 cells, a threshold level of NFATc1 activity was vital in facilitating T cell differentiation and to prevent T-acute lymphoblastic leukemia (T-ALL) development. Altogether, our results show NFATc1 activity is crucial in determining the T cell fate of thymocytes.

2016-04-20 | GSE80138 | GEO

Transcriptional Regulation by NFATc1 during murine thymocyte development

Project description:Transcriptional Regulation by NFATc1 during murine thymocyte development

| PRJNA813437 | ENA

Transcriptional Regulation by NFATc1 during murine thymocyte development [gammadelta_T_cells RNA-seq]

Project description:In thymus hematopoietic precursor cells differentiate into αβ T cells, γδ T cells, mucosa-associated invariant T cells (MAIT), and natural killer T (NKT) cells. We show that both ablation of NFATc1 or its induction during the DN stages of thymocyte development leads to an almost normal thymocyte development but a marked increase in γδ T cells. The γδ cells deficient for NFATc1 acquire an NKT γδ cell phenotype that exhibits the expression of CD4 co-receptor, the NK1.1 marker, the augmented usage of the Vγ1.1 and Vδ6.3 segments, and an increased in IL4 and IFN-γ production.

2023-02-28 | GSE198030 | GEO

Transcriptional Regulation by NFATc1 during murine thymocyte development [BirA RNA-seq]

2023-02-28 | GSE198029 | GEO

Transcriptional Regulation by NFATc1 during murine thymocyte development [ChIP-seq]

2023-02-28 | GSE198028 | GEO

Transcriptional Regulation by NFATc1 during murine thymocyte development [ChIP-seq]

Project description:Transcriptional Regulation by NFATc1 during murine thymocyte development [ChIP-seq]

| PRJNA813442 | ENA

Transcriptional Regulation by NFATc1 during murine thymocyte development [gammadelta_T_cells RNA-seq]

Project description:Transcriptional Regulation by NFATc1 during murine thymocyte development [gammadelta_T_cells RNA-seq]

| PRJNA813440 | ENA

Transcriptional Regulation by NFATc1 during murine thymocyte development [BirA RNA-seq]

Project description:Transcriptional Regulation by NFATc1 during murine thymocyte development [BirA RNA-seq]

| PRJNA813441 | ENA

Myocardial Differentiation is Dependent upon Endocardial Signalling During Early Cardiogenesis in vitro

Project description:The endocardium interacts with the myocardium to promote proliferation and morphogenesis during the later stages of heart development. However, the role of the endocardium in early cardiac ontogeny remains under-explored. Given the shared origin, subsequent juxtaposition, and essential cell-cell interactions of endocardial and myocardial cells throughout heart development, we hypothesized that paracrine signaling from the endocardium to the myocardium is critical for initiating early differentiation of myocardial cells. To test this, we generated an in vitro, endocardial-specific ablation model using the diphtheria toxin receptor under the regulatory elements of the NFATc1 genomic locus (NFATc1-DTR) Early treatment of NFATc1-DTR embryoid bodies with diphtheria toxin efficiently ablated endocardial cells, which significantly attenuated the percent of beating EBs in culture and expression of early and late myocardial differentiation markers. The addition of Bmp2 during endocardial ablation partially rescued myocyte differentiation, maturation and function. Therefore, we conclude that early stages of myocardial differentiation rely on endocardial paracrine signaling mediated in part by Bmp2. Our findings provide novel insight into early endocardial-myocardial interactions that can be explored to promote early myocardial development and growth.

2019-05-01 | GSE119505 | GEO

NFATc1 and NFATc2 regulate glucocorticoid resistance in pediatric T-cell acute lymphoblastic leukemia through modulation of cholesterol biosynthesis and the WNT/β-catenin pathway

Project description:The glucocorticoid (GC) resistance onset in pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL) patients remains one of the biggest challenges in current cancer treatment. The mechanisms driving this resistance are still not fully understood, making it difficult to predict patient outcomes and to develop effective therapies. Our study uncovered critical insights into the biological processes underlying GC resistance, offering potential breakthroughs for future treatments. Building on our previous research on LCK kinase hyperactivation in GC-resistant T-ALL patients, we have now delved deeper into the LCK downstream NFAT transcription factor family's contribution to GC resistance. We discovered that, even at the time of diagnosis, GC resistant T-ALL patients exhibit an intrinsic low glucocorticoid receptor (GR) activity coupled with high NFATc1 and NFATc2 ones. This dysregulation creates a roadblock to effective GC therapy. Indeed, in the absence of either NFATc1 or NFATc2, the normal transcriptional activity of GR is restored, re-sensitizing the leukemia cells to dexamethasone treatment both in vitro and in vivo. This suggests that NFATc1 and NFATc2 are central to driving GC resistance, as they directly regulate crucial pathways like cholesterol biosynthesis and WNT/β-catenin signaling. The identification of NFAT transcription factors as key players in leukemia therapy resistance offers a promising target for future therapeutic strategies, potentially transforming the way we approach treatment for these challenging conditions or autoimmune disorders where glucocorticoids are a cornerstone of treatment.

2025-11-28 | GSE253996 | GEO

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