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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.

2022-05-06 | GSE201885 | GEO

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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Two Types of Axonal Muscarinic Acetylcholine Receptors Mediate Formation of Saliva Cocktail in the Tick Ixodes ricinus

Project description:The long blood feeding duration of hard ticks relies on the continuous modulation of saliva composition to manipulate host haemostatic and immune systems. While the exogenous muscarinic acetylcholine receptor (mAChR) agonist, pilocarpine, is a potent inducer of tick salivation, the underlying control mechanisms of endogenous stimulation remain unclear. Here, we characterised two pharmacologically distinct types of mAChRs (A and B) in the genome of the Ixodes ricinus tick. A combination of molecular dynamics and directed mutagenesis revealed the atypical muscarinic profile of the type-B receptor. Immunolabelling followed by in vivo pharmacology and proteomic analyses suggested that the composition of secreted saliva is a result of a complex interplay between different central neurons and specific regions of the salivary gland (SG), mediated by distinct axonal mAChR types. This system likely functions upstream of a neuropeptide signalling cascade, ultimately controlling different salivation subunits in SG. Our study describes a unique model of regulation of tick SG activity in a medically relevant tick species. This knowledge holds broader implications for understanding tick-host interactions.

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Antimuscarinic drugs exert beta-arrestin-biased agonism at the muscarinic acetylcholine type 1 receptor

Project description:Antimuscarinic drugs such as pirenzepine (PZ) and muscarinic toxin 7 (MT7), long considered M1 muscarinic acetylcholine receptor (M1R) antagonists, exhibit beta-arrestin-biased agonism. Using HEK293 cells and adult dorsal root ganglion (DRG) neurons, we show that PZ and MT7 selectively recruit beta-arrestin to M1R, activate ERK1/2 signaling, and promote neurite outgrowth without engaging G-alpha-q pathways or receptor internalization. Mass spectrometry identified six key M1R phosphorylation sites (T230, S251, T254, S321, T354, S356) required for beta-arrestin recruitment, with S251/T254 essential for PZ signaling. Casein kinase 2 (CK2), but not GRKs, mediates this phosphorylation; CK2 inhibition blocks beta-arrestin binding, ERK activation, and neurite outgrowth. These findings redefine antimuscarinic drugs as partial, beta-arrestin-biased M1R agonists and identify CK2 as a critical modulator of non-canonical M1R signaling relevant to sensory neuron regeneration and neuropathy therapy.

2025-10-31 | MSV000099707 | MassIVE

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