CHRNa1 ELISA kit
- Known as:
- CHRNa1 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-CHRNa1-Hu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- CHRNa1 ELISA kit
Related genes to: CHRNa1 ELISA kit
- Gene:
- CHRNA1 NIH gene
- Name:
- cholinergic receptor nicotinic alpha 1 subunit
- Previous symbol:
- CHRNA
- Synonyms:
- -
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-25
- Date modifiied:
- 2016-02-04
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- Juvenile dermatomyositis (JDM) is a rare systemic autoimmune disease primarily affecting children, with a female predominance. While muscle fiber inflammation has been extensively investigated, the contribution of the neuromuscular junction (NMJ) and its cellular microenvironment to JDM pathogenesis remains poorly understood. This study aimed to characterize NMJ-related gene expression patterns in JDM to identify potential pathogenic mechanisms and candidate biomarkers. - Source: PubMed
Publication date: 2026/09/05
Sanfilippo CristinaCastrogiovanni PaolaImbesi RosaFagone PaoloScuderi GraziaGrosso GiuseppeMusumeci GiuseppeTibullo DanieleVecchio MicheleDi Rosa Michelino - Physical exercise induces neurogenesis in adult and developing animal brains, but how movement promotes neurogenesis remains unclear. Here, we use two independent methods for immobilization, a physical barrier (gel matrix) or a genetic manipulation (CRISPR-Cas9 mutation of ), to completely immobilize zebrafish larvae during postembryonic development. Both immobilization methods result in smaller brains, reduced brain cell proliferation, and accelerated neuronal differentiation. Conversely, exercised fish in a swim tunnel had larger brains, increased brain cell proliferation, and delayed neuronal differentiation. Interestingly, these effects of exercise could be mimicked by increasing neural activity pharmacologically using GABA receptor antagonist pentylenetetrazol, or by artificially activating the dorsal root ganglia (DRG) sensory neurons, which increases swimming. Both promote cell proliferation and delayed neuronal differentiation. Finally, we dissociate the role of muscle contractions from neural activity by artificially activating the DRG neurons in CRISPR- mutants, completely reversing neurogenesis defects that result from muscle paralysis. - Source: PubMed
Publication date: 2026/08/14
Sherlock ShelbyAppel LaurenHall ZacharyPhan Anna - Skeletal muscle atrophy is a secondary complication in the aetiology of injury and chronic disease. Identifying mechanisms that control muscle mass is necessary to characterise atrophy and develop prevention strategies. We aimed to integrate transcriptomic and epigenomic data to identify key regulatory pathways controlled by promoter DNA methylation during muscle unloading. Twenty-one healthy men (20-40 years) completed a 4-week standardised exercise programme prior to a 14-day knee brace immobilisation with dietary control. Skeletal muscle mass and strength were assessed before and after immobilisation and biopsies were collected (m. vastus lateralis) before, at 3 days, and at completion at 14 days. RNA and DNA were isolated and analysed using Illumina RNA sequencing and DNA methylation 850K EPIC BeadChips. The 14-day immobilisation decreased muscle mass (∼9%; P < 0.0001) and strength (∼16%; P < 0.0001). At 3 days, most biological processes (BPs) were upregulated/hypomethylated (157 gene sets); upregulated BPs included cell signalling and protein ubiquitination and downregulated BPs included metabolism. After 14 days, BPs were predominantly downregulated/hypermethylated, including translation and ribosome biogenesis. Across both time points, HDAC4, GADD45A and CHRNA1 emerged as methylation-regulated candidate mediators of atrophy. HDAC4 and GADD45A showed strong correlations primarily at day 3, and CHRNA1 remained significant at both time points, extending prior observations in animals to human skeletal muscle. We have characterised changes in gene expression related to hypo- and hyper-methylation during muscle unloading in humans. These data extend our understanding of the regulatory processes that occur during skeletal muscle atrophy that, at the individual gene level, may be useful in developing strategies for reducing muscle wasting. - Source: PubMed
Publication date: 2026/08/24
Thompson Jamie-Lee MDoering Thomas MBudiono Boris PMackenzie-Shalders Kristen LAshton Kevin JDunn Paul JCoffey Vernon G - Circadian rhythm disruption is increasingly recognized as a contributor to chronic inflammatory disorders; however, its specific significance and underlying mechanisms in chronic obstructive pulmonary disease (COPD) remain unclear. This study aimed to identify circadian rhythm-associated biomarkers in COPD and explore their diagnostic value, immune correlations, and therapeutic potential. - Source: PubMed
Publication date: 2026/07/31
Zhang LanLi ZhifeiXia TianshengYang TingtingFu JiaLu YanXu JiayiHan Kaiyu - Congenital myasthenic syndromes (CMS) are rare genetic disorders caused by pathogenic variants in proteins expressed at the neuromuscular junction. Current literature surrounding adult CMS patients remains limited, primarily derived from Western cohorts. - Source: PubMed
Publication date: 2026/07/17
Hoe Rebecca Hui MinKoh Jasmine ShiminSaini MonicaPrasad KalpanaChan Yee CheunNg Peng SoonHuei Josiah Chai YuiChong Li JieTay Karine Su ShanChen Zhiyong