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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- 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 - Double seronegative myasthenia gravis (dSnMG) is defined as myasthenia gravis (MG) without detectable antibodies to acetylcholine receptor (AChR) and muscle-specific kinase (MuSK). Absence of a disease-specific biomarker and clinical heterogeneity can significantly complicate diagnostic pathway. This study aimed to identify cases misdiagnosed as dSnMG. - Source: PubMed
Publication date: 2026/03/19
Ivanovic VukanPeric StojanBriggs CaitlinMarjanovic AnaPesovic JovanBasta IvanaJansson JohanRandhawa SimratRajic SonjaGokhale Sankalp - Barth syndrome (BTHS) is a rare X-linked mitochondrial disorder caused by mutations in the TAFAZZIN gene, which disrupts cardiolipin (CL) remodelling and mitochondrial function. While cardiac manifestations of BTHS are well characterized in male patients, the mechanisms underlying skeletal muscle weakness and fatigability are poorly understood. - Source: PubMed
Matias CatalinaSnider Paige LSierra Potchanant Elizabeth AHuot Joshua RRaghav RahulChin Michael TConway Simon JBrault Jeffrey J - In vitro experiments have contributed to numerous fields of knowledge, including fish skeletal muscle. Despite improved strategies, in vitro assays still show discrepancies with in vivo systems, especially for non-model organisms. In this sense, we characterized the transcriptional profile of pacu (Piaractus mesopotamicus) muscle cells in vitro and in vivo. Processes related to proliferation, glycolytic metabolism, and extracellular matrix were enriched in vitro, while energy production, muscle contraction, and amino acid processing were enriched in vivo. Through qPCR, the genes fn1a (fibronectin 1a), hk1 (hexokinase 1), and ctnnb1 (catenin beta 1), respectively related to extracellular matrix, glycolytic metabolism, and cell proliferation and differentiation, were highly expressed in vitro. The genes ckma (creatine kinase, muscle a), acat1 (acetyl-CoA acetyltransferase 1), mdh2 (malate dehydrogenase 2), and pkmb (pyruvate kinase M1/2b), respectively associated with ATP production, fatty acid oxidation, oxidative and glycolytic metabolism, and the genes musk (muscle, skeletal, receptor tyrosine kinase), chrna1 (cholinergic receptor, nicotinic, alpha 1) and clu (clusterin), involved in cell signaling, were highly expressed in vivo. Overall, our results indicate that the main limitation of in vitro muscle cell model is the maintenance of an embryonic-like molecular state, whereas in vivo muscle displays a mature transcriptional profile, providing a molecular basis to guide future strategies for improving fish muscle cell culture systems and supporting advances in sustainable aquaculture and in vitro meat production. - Source: PubMed
Publication date: 2026/03/10
Zanella Bruna Tereza ThomaziniPerez Érika StefaniDos Santos Barbosa Mirely FrancineValente Jéssica SilvinoDuran Bruno Oliveira SilvaDal-Pai-Silva Maeli - Disuse-induced muscle atrophy commonly occurs following illness, injury, or falls and becomes increasingly frequent with ageing. Whether skeletal muscle retains a "memory" of repeated disuse remains unknown. We investigated repeated lower-limb immobilization in young adults and a refined aged rat model, integrating physiological, multi-omic, immunohistochemical, biochemical, and primary human muscle stem cell (MuSC) analyses. To enable robust age comparisons, we integrated previously published young rat data with newly generated aged rat data. In young human muscle, repeated disuse elicited attenuated transcriptional perturbations in oxidative and mitochondrial pathways, suggestive of a protective molecular memory, despite similar atrophy to initial disuse. In contrast, aged muscle exhibited a detrimental memory, characterized by greater atrophy, exaggerated suppression of aerobic metabolism genes despite recovery after initial disuse, NAD and mitochondrial DNA depletion, and activation of proteasomal, extracellular-matrix, and DNA-damage pathways. Whereas young rats recovered muscle mass after initial disuse, aged rats failed to do so. Across species, repeated disuse induced DNA hypermethylation and downregulation of aerobic metabolism and mitochondrial gene networks. NR4A1 and NR4A3 were among the strongest disuse-suppressed genes; NR4A1 acquired recovery-phase hypermethylation that maintained its transcriptional repression, while NR4A3 was the most downregulated gene after initial atrophy and remained persistently suppressed into recovery. Acetylcholine receptor subunit genes (CHRNA1, CHRND) were epigenetically primed, demonstrating hypomethylation and strong upregulation after disuse, and further amplification after repeated atrophy, while CHRNG was selectively induced after repeated atrophy only. NMRK2, an NAD biosynthesis gene, was the most downregulated gene across both atrophy periods, and supplementation with its substrate, nicotinamide riboside (NR), improved myotube size in MuSCs derived post-atrophy. Overall, repeated disuse atrophy imprints a molecular memory in skeletal muscle shaping transcriptional resilience in young adults and exaggerated susceptibility in aged muscle. - Source: PubMed
Publication date: 2026/02/25
Turner Daniel CRaastad TrulsUllrich MaxChristiansen Stian FSutherland HazelBoot JamesWozniak EvaMein CharlesDalbram EmilieTreebak Jonas TOwens Daniel JHughes David CBodine Sue CJarvis Jonathan CSharples Adam P