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Identification of M3 muscarinic acetylcholine receptor reactive Th17 cells in patients with primary Sjögren’s syndrome

ABSTRACT: Identification of M3 muscarinic acetylcholine receptor reactive Th17 cells in patients with primary Sjögren’s syndrome

PROVIDER: PRJNA626633 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11575703.fastq.gz	Fastqsanger.gz
	SRR11575704.fastq.gz	Fastqsanger.gz
	SRR11575705.fastq.gz	Fastqsanger.gz

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Identification of M3 muscarinic acetylcholine receptor reactive Th17 cells in patients with primary Sjögren’s syndrome

Project description:Previously M3 muscarinic acetylcholine receptore (M3R) reactive Th1 cells were identified, and here, M3R reactive Th17 cells were identified in peripheral blood of primary Sjögren’s syndrome patients using ELISpot method. To assess TCR repertoire overlap between identified M3R reactive Th17 cells, and salivary gland infiltrating T cells, we performed high throughput TCR sequencing of those cells from pSS patient.

2021-04-18 | GSE148966 | GEO

The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

Project description:The M3 muscarinic acetylcholine receptor (CHRM3) is predominantly expressed in the basal epidermal layer where it mediates the effects of the auto/paracrine cytotransmitter acetylcholine. Patients with the autoimmune blistering disease pemphigus develop autoantibodies to CHRM3 and show alterations in keratinocyte adhesion, proliferation and differentiation, suggesting that CHRM3 controls these cellular functions. Chrm3 mice display altered epidermal morphology resembling that seen in patients with pemphigus vulgaris. Here, we characterized the cellular and molecular mechanisms whereby CHRM3 controls epidermal structure and function. We used single cell (sc)RNA-seq to evaluate keratinocyte heterogeneity and identify differentially expressed genes in specific subpopulations of epidermal cells in Chrm3 KO neonatal mice.

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Molecular mechanism of muscarinic acetylcholine receptor M3 interaction with Gq

Project description:Muscarinic acetylcholine receptor M3 (M3) and its downstream effector Gq/11 are critical drug development targets given their involvement in numerous physiological processes and diseases. Although a cryo-electron microscopy study previously defined the structure of the M3-miniGq complex, the lack of information on the intracellular loop 3 (ICL3) of M3 and α-helical domain (AHD) of Gαq has made it difficult to comprehend the molecular mechanism of M3-Gq coupling fully. Here, we present the molecular mechanism underlying the dynamic interactions between the wild-type full-length M3 and heterotrimeric Gq using hydrogen-deuterium exchange mass spectrometry and NanoLuc Binary Technology-based cell systems. This study suggests potential binding interfaces between M3 and Gq in pre-assembled and fully active nucleotide-free complexes. In addition to well-known binding interfaces, we observed the interaction of long ICL3 with Gβγ. Furthermore, M3 ICL3 negatively affected M3-Gq coupling, and the Gαq AHD underwent unique conformational changes during M3-Gq coupling. Therefore, we propose a comprehensive molecular mechanism of M3-Gq coupling by analyzing previously well-defined binding interfaces and neglected regions, such as M3 ICL3 and the Gαq AHD.

2024-05-22 | PXD042562 | Pride

The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

Project description:The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

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The effect of deletion of muscarinic acetylcholine receptor 4 in Math1 expressing cells in the small intestine

Project description:The muscarinic acetylcholine receptor 4 was inducibly deleted in Math1 expressing lineages and alterations in gene expression evaluated by bulk RNA sequencing

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M3 muscarinic acetylcholine receptor-reactive Th17 cells in primary Sjogren's syndrome.

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Activation of M3 muscarinic ameliorates experimental autoimmune encephalomyelitis by restoring microglial quiescence

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