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Lung-specific MCEMP1 acts as an adaptor for KIT to promote SCF-mediated mast cell proliferation [Lung RNA-seq]

ABSTRACT: Lung-specific MCEMP1 acts as an adaptor for KIT to promote SCF-mediated mast cell proliferation [Lung RNA-seq]

PROVIDER: PRJNA808600 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18076669.fastq.gz	Fastqsanger.gz
	SRR18076670.fastq.gz	Fastqsanger.gz
	SRR18076671.fastq.gz	Fastqsanger.gz
	SRR18076672.fastq.gz	Fastqsanger.gz
	SRR18076673.fastq.gz	Fastqsanger.gz

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Lung-specific MCEMP1 acts as an adaptor for KIT to promote SCF-mediated mast cell proliferation

Project description:Lung-specific MCEMP1 acts as an adaptor for KIT to promote SCF-mediated mast cell proliferation

| PRJNA808599 | ENA

Lung-specific MCEMP1 acts as an adaptor for KIT to promote SCF-mediated mast cell proliferation [PCMC RNA-seq]

Project description:Lung-specific MCEMP1 acts as an adaptor for KIT to promote SCF-mediated mast cell proliferation [PCMC RNA-seq]

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Lung-specific MCEMP1 acts as an adaptor for KIT to promote SCF-mediated mast cell proliferation [PCMC RNA-seq]

Project description:We analyzed transcriptomic changes in Mcemp1-/- Peritoneal cell-derived mast cells (PCMC) versus Mcemp1 wild-type PCMC cultured with SCF and IL-3 for 9-days.

2023-03-13 | GSE197041 | GEO

Global phosphoproteomics elicited by the SCF/KIT axis in human skin mast cells unveil capicua as a potent KIT repressor

Project description:Global phosphoproteomics can reveal signaling cascades in unprecedented detail. The SCF/KIT axis represents a vital hematopoietic receptor tyrosine kinase (RTK) system with gain-of-function mutations prompting the development of mastocytosis and leukemia. Here, we employed a label-free phosphoproteomics profiling strategy to provide the first comprehensive portrayal of SCF-triggered phosphosignaling. Employing untransformed skin-derived mast cells expressing vast amounts of KIT, we uncover around 10,500 class-I-phosphosites following ligand-induced KIT dimerization. Apart from STAT5, the MEK/ERK cascade (including upstream and downstream events) stood out as highly stimulatable by SCF compared to less impacted PI3K/Akt>p38>JNK, a pattern validated by time-resolved immunoblotting. Direct comparison between MEK/ERKÕs and PI3KÕs support of basic programs (anti-apoptosis, cell cycle progression) revealed equipotency with substantial redundancy between the modules. In functional outputs, ERK showed dominance over PI3K regarding cytokine stimulation (TNF-a, IL-8, LIF, OSM) and was the only contributor in the induction of immediate early genes (Fos, JunB, Egr1). Our proteome-wide screen also found Å1,000 phosphosites currently undescribed in databases, pertaining to multiple protein classes. Among candidates, capicua (and components of its network) experienced massive phosphorylation by SCF. Perturbation with capicua by RNA interference unveiled its function as a potent KIT repressor, whose deregulation may contribute to the development of mastocytosis. We demonstrate the utility of an unbiased approach to uncover single protein entities and entire networks activated by RTKs, that can be surveyed experimentally. This rich resource enhances our understanding of RTK-elicited signaling networks and can serve as a benchmark to identify pathological processes, e.g. under circumstances of KIT deregulation.

2022-11-15 | PXD028252 | Pride

Mast cell microRNAs regulated by KIT signaling

2011-01-25 | GSE26783 | GEO

Mast cell microRNAs regulated by KIT signaling

Project description:Objective is to identify microRNAs regulated by KIT signaling in mast cells. miRNA profiles of murine bone marrow derived mast cells with and without SCF treatment were compared. In addition, miRNA profiles of the P815 mutant KIT cell line with and without the KIT inhibitor, imatinib, were compared. We identified miRNAs that were differentially regulated by KIT signals. Two systems were used to identify microRNAs regulated by KIT. RNA was collected from primary murine bone marrow derived mast cells (BMMC) treated and not treated with KIT ligand (SCF). In addition, RNA was harvested from the P815 (activating KIT mutation positive) cell line treated and not treated with the KIT inhibitor, imatinib. Samples were harvested after 24 hours of treatment

2011-01-25 | E-GEOD-26783 | biostudies-arrayexpress

Global phosphoproteomics in SCF stimulated human skin mast cells

2022-03-31 | PXD028245 | Pride

Lung-specific MCEMP1 acts as an adaptor for KIT to promote SCF-mediated mast cell proliferation [Lung RNA-seq]

Project description:We analyzed the lung transcriptome of Mcemp1-/- mice versus wild-type mice in ovalbumin (OVA)-induced asthma model by RNA sequencing.

2023-03-13 | GSE197040 | GEO

SCF -licensed induction of a mucosal mast cell-like transcriptional program by TGF-b

Project description:This study evaluates the effects of 72h stimulus with stem cell factor (SCF) (100 ng/mL) and TGF-b (1 ng/mL or 10 ng/mL), both alone and in combination, on the transcriptome of bone marrow-derived cultured mast cells (BMMCs) grown in IL-3 for 6-8 weeks. Through this approach, we find that SCF dramatically enhances TGF-b mediated upregulation of signature genes associated with mucosal mast cells, including transcripts encoding the proteases mMCP-1 (Mcpt1) and mMCP-2 (Mcpt2). Replicates indicate biologic duplicates. Samples were sequenced on an Illumina NextSeq 500.

2020-08-03 | GSE155571 | GEO

Lung-specific MCEMP1 functions as an adaptor for KIT to promote SCF-mediated mast cell proliferation.

Project description:Lung mast cells are important in host defense, and excessive proliferation or activation of these cells can cause chronic inflammatory disorders like asthma. Two parallel pathways induced by KIT-stem cell factor (SCF) and FcεRI-immunoglobulin E interactions are critical for the proliferation and activation of mast cells, respectively. Here, we report that mast cell-expressed membrane protein1 (MCEMP1), a lung-specific surface protein, functions as an adaptor for KIT, which promotes SCF-mediated mast cell proliferation. MCEMP1 elicits intracellular signaling through its cytoplasmic immunoreceptor tyrosine-based activation motif and forms a complex with KIT to enhance its autophosphorylation and activation. Consequently, MCEMP1 deficiency impairs SCF-induced peritoneal mast cell proliferation in vitro and lung mast cell expansion in vivo. Mcemp1-deficient mice exhibit reduced airway inflammation and lung impairment in chronic asthma mouse models. This study shows lung-specific MCEMP1 as an adaptor for KIT to facilitate SCF-mediated mast cell proliferation.

| S-EPMC10090139 | biostudies-literature

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