CHRNA1 antibody - N-terminal region (ARP34910_P050)
- Known as:
- CHRNA1 (anti-) - N-terminal region (ARP34910_P050)
- Catalog number:
- arp34910_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CHRNA1 antibody - N-terminal region (ARP34910_P050)
Related genes to: CHRNA1 antibody - N-terminal region (ARP34910_P050)
- 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
Related products to: CHRNA1 antibody - N-terminal region (ARP34910_P050)
Related articles to: CHRNA1 antibody - N-terminal region (ARP34910_P050)
- 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 - CircRNAs have been linked to the pathogenesis and progression of myasthenia gravis (MG), but research on this association remains limited. This study aims to provide a new perspective for understanding the molecular pathogenesis of MG. We obtained RNA-seq data from patients with acetylcholine receptor (AChR)-positive MG and healthy individuals from the Gene Expression Omnibus (GEO) database. A bioinformatics analysis was performed to identify differentially expressed circRNAs related to MG; the circRNA that was most consistently identified in most databases as a key factor involved in MG, hsa_circ_0065149, was chosen for further analysis. AChR localized at the postsynaptic membrane of the neuromuscular junction (NMJ) plays a pivotal role in mediating synaptic signal transmission. The CHRNA1 gene, which encodes the α1 subunit of AChR and is critical for its function-was subsequently selected as the target mRNA in our investigation, whereas our prediction pipeline identified miR-330-5p as the target. For functional assays, various constructs (e.g., hsa_circ_0065149-siRNA) were transfected as described in the Methods section. The qRT‒PCR results indicated that hsa_circ_0065149 knockdown significantly upregulated miR-330-5p and downregulated CHRNA1, while the inhibition of miR-330-5p significantly upregulated both hsa_circ_0065149 and CHRNA1. We also performed functional rescue experiments to confirm the regulatory hierarchical relationships among these factors. A dual-luciferase reporter assay confirmed that hsa_circ_0065149 and CHRNA1 are direct targets of miR-330-5p. These results suggest that hsa_circ_0065149 regulates MG by mediating the ceRNA network pathway, and we reasonably hypothesize that it may further contribute to the pathological process of MG by impairing signal transmission in the NMJ. - Source: PubMed
Publication date: 2026/05/22
Liu SiyuTian QinghuaLiu ZhaojunRen YingjieYu AoqingChen BiyingZhou TianyangLi XiangWang JianjianWang LihuaZhang Huixue