Ask about this productRelated genes to: UNC50 Blocking Peptide
- Gene:
- UNC50 NIH gene
- Name:
- unc-50 inner nuclear membrane RNA binding protein
- Previous symbol:
- -
- Synonyms:
- URP, UNCL, GMH1
- Chromosome:
- 2q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-21
- Date modifiied:
- 2016-10-05
Related products to: UNC50 Blocking Peptide
Related articles to: UNC50 Blocking Peptide
- WAC is an autism-associated gene involved in neurodevelopment. However, the effects of reduced WAC function on behavior and synaptic regulation in vivo remain unclear. Taking cues from the previous studies on the wac gene and the C. elegans model of ASD, we elucidated the effects of wac gene deletion on food-leaving behavior, a known parameter linked to ASD associated genes along with the cholinergic pathway. -deficient worms exhibited curtailed food-leaving behavior. Notably, observed phenotype was similar to that exhibited by nematodes with mutation in ASD related gene, neuroligin. In addition, -deficient worms showed impaired growth, reduced pharyngeal pumping, and lifespan. To examine potential synaptic mechanisms, we analyzed expression of genes related to cholinergic signaling across all developmental stages (L1-L4) through young adult (YA). Stage-specific transcriptional changes were observed, with increased expression of and at L1, at L3, and , and at L4. The transcriptomic alteration was most prominent at YA stage, exhibiting upregulation of , and . To identify specific suppressor of upmodulated Ach signaling, RNAi of the upregulated genes was performed. was identified as a specific suppressor of elevated Ach signaling. encodes a high-affinity choline transporter responsible for choline uptake in the pre-synapse. These studies identify the molecular mechanisms pertaining to up-modulation of cholinergic signaling in mutant worms. - Source: PubMed
Publication date: 2026/04/21
Kim Da-WoonBoonpraman NapissaraKuhn Nathan CSammi Shreesh Raj - Insect nicotinic acetylcholine receptors (nAChRs) serve as primary targets for neonicotinoid insecticides. Western flower thrips (Frankliniella occidentalis) is a major agricultural pest that has developed increasing resistance to neonicotinoids, for which there is a lack of functional studies on the impacts of resistance-associated mutations (e.g., the R81T mutation in the β1 subunit in other insects). Therefore, establishing heterologous expression systems is essential to characterize nAChR pharmacology and resistance in this species. - Source: PubMed
Publication date: 2026/01/09
Huang HuixiuWen HuiqiWu HuihuiYang JingfangZhang KunWu Shaoying - Recent studies have suggested that the tick expresses nAChR subtypes which are activated by acetylcholine. Here, we investigated the potential of the Iricα6 subunit to form a functional receptor when expressed in oocytes. Electrophysiological recordings using a two-electrode voltage clamp suggested that the Iricα6 subunit can form a functional homomeric receptor when expressed alone or with chaperone proteins such as RIC-3, UNC-50 and UNC-74. We also found that Iricα6 is a non-selective cation channel. ACh-induced currents were blocked by the nicotinic antagonists methyllicaconitine and dihydro-β-erythroidine. In addition, the nicotinic antagonists α-bungarotoxin and mecamylamine elicited agonist-like responses, with EC values of 3.48 nM and 12.60 nM, respectively. These data indicated that Iricα6 homomeric receptors could have different pharmacological properties compared to homomeric receptors expressed in other species. - Source: PubMed
Publication date: 2025/12/03
Cartereau AlisonBoussaine KhalidTaillebois EmilianeThany Steeve H - Ambient air pollution aggravates cardiovascular-kidney-metabolic (CKM) disorders and sarcopenia, yet the shared genetic and epigenetic mechanisms that underlie their frequent co-occurrence remain poorly understood. - Source: PubMed
Publication date: 2025/11/19
Wei ShuxuShu ZhouwuLi XinyiZhong SuiqinXiao LingShen RonghuaiLu XiaojiaHe LingbinZhang YoutiQuan YanHuang Xianxi - Congenital myasthenic syndromes (CMS) are a heterogeneous group of disorders characterized by compromised neuromuscular signal transmission due to pathogenic germline variants in genes expressed at the neuromuscular junction (NMJ). A total of 40 genes have been reported in CMS (AGRN, ALG14, ALG2, CHAT, CHD8, CHRNA1, CHRNB1, CHRND, CHRNE, CHRNG, COL13A1, COLQ, DES, DOK7, DPAGT1, GFPT1, GMPPB, LAMA5, LAMB2, LRP4, MACF1, MUSK, MYO9A, PLEC, PREPL, PTPN11, PURA, RAPSN, RPH3A, SCN4A, SLC18A3, SLC25A1, SLC5A7, SNAP25, SYT2, TEFM, TOR1AIP1, UNC13A, UNC50 and VAMP1). The 40 genes are putatively classified into 13 subtypes by pathomechanical, clinical, and therapeutic features. A unique feature shared by recently identified genes is that CMS is concomitantly recognized in other mostly severer diseases. For example, four recently identified genes exhibit the following phenotypes: PURA-CMS, developmental delay; TEFM-CMS, mitochondrial disease; PTPN11-CMS, Noonan syndrome/Leopard syndrome; and DES-CMS, desmin myopathy. Conversely, these diseases are not always associated with CMS, although genetic and/or environmental factors that determine the involvement of the NMJ remain to be identified. In this review, particular emphasis will be placed on five recently identified genes (MACF1, TEFM, PTPN11, DES and UNC50). - Source: PubMed
Publication date: 2025/06/18
Ohno KinjiIto MikakoOhkawara Bisei