CHRNA7 antibody - middle region (ARP35418_T100)
- Known as:
- CHRNA7 (anti-) - middle region (ARP35418_T100)
- Catalog number:
- arp35418_t100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CHRNA7 antibody - middle region (ARP35418_T100)
Related genes to: CHRNA7 antibody - middle region (ARP35418_T100)
- Gene:
- CHRFAM7A NIH gene
- Name:
- CHRNA7 (exons 5-10) and FAM7A (exons A-E) fusion
- Previous symbol:
- -
- Synonyms:
- D-10, CHRNA7-DR1
- Chromosome:
- 15q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-29
- Date modifiied:
- 2016-03-03
- Gene:
- CHRNA7 NIH gene
- Name:
- cholinergic receptor nicotinic alpha 7 subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 15q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-05-25
- Date modifiied:
- 2016-02-04
Related products to: CHRNA7 antibody - middle region (ARP35418_T100)
Related articles to: CHRNA7 antibody - middle region (ARP35418_T100)
- Nicotinic acetylcholine receptor of α7 type (α7-nAChR) is a ligand-gated ion channel composed of five identical α7 subunits. Secreted lymphocyte antigen-6 urokinase-type plasminogen activator receptor (Ly6/uPAR)-related protein-1 (SLURP-1) controls carcinoma progression by negative modulation of oncogenic α7-nAChR. In this study, we observed dramatic decrease of SLURP-1 plasma level in patients with metastatic melanoma. We suggested usage of recombinant analog of human SLURP-1 (rSLURP-1) to compensate this deficiency for metastatic melanoma treatment. rSLURP-1 did not affect viability of different patient-derived metastatic melanoma cells, but reduced migration of some of them. Metastatic melanoma cells of other lines were resistant to rSLURP-1. Antimigratory rSLURP-1 effect was mediated by α7-nAChR, whereas resistance to rSLURP-1 correlated with overexpression of human-specific gene, which encodes the α7 subunit with truncated N-terminal region (dupα7) able to form hybrid α7/dupα7-nAChR channels. Electrophysiological study in oocytes showed that rSLURP-1 inhibits α7/dupα7-nAChR weaker than α7-nAChR. In contrast, "Oncotag" peptide, which mimics the loop I of SLURP-1, inhibited α7/dupα7- and α7-nAChRs with similar efficiency. Oncotag suppressed metastatic melanoma cell migration independently on dupα7 expression. Computer modeling provided rationale for altered activities of rSLURP-1 and Oncotag on α7/dupα7-nAChR. The Cancer Genome Atlas Program (TCGA) database analysis revealed correlation between and gene expression and worse survival prognosis for patients with metastatic melanoma. Thus, ) low plasma SLURP-1 level may be a specific marker of metastatic melanoma development, ) metastatic melanoma progression can be controlled by α7-nAChR inhibition, and ) dupα7 overexpression is a new molecular mechanism of melanoma resistance to internal cholinergic control and new target for melanoma treatment. Metastatic melanoma is aggressive skin tumor often resistant to standard therapies. High α7-nAChR expression negatively correlates with survival of patients with metastatic melanoma, who are characterized by SLURP-1 drop in the plasma. Targeting α7-nAChR with recombinant SLURP-1 could significantly suppress metastatic melanoma cell migration; however, overexpression of human-specific dupα7 subunit forming hybrid α7/dupα7-nAChRs causes melanoma resistance to SLURP-1. This resistance can be overcome by the SLURP-1 mimicking peptide Oncotag, which exhibits activity against hybrid α7/dupα7-nAChRs. - Source: PubMed
Publication date: 2026/04/16
Kirichenko Artem VBychkov Maxim LKulbatskii Dmitry SShlepova Olga VShulepko Mikhail AGornostaeva Tamara YaOrekhov Philipp SParamonov Alexander SMikhaylova Irina NBurova Olga SMedyanik Igor AYashin Konstantin SWang HongshuangWang XiaohuiKirpichnikov Mikhail PShenkarev Zakhar OLyukmanova Ekaterina N - The clinical interest in mechanisms controlling the biosynthesis and release of the pro-inflammatory cytokine interleukin (IL)-1β is outstanding, as IL-1β is associated with life-threatening inflammatory diseases including hyperinflammation caused by extracellular ATP originating from damaged cells. Previously, we identified a cholinergic mechanism controlling ATP-dependent IL-1β release via metabotropic signaling of unconventional nicotinic acetylcholine receptors (nAChRs) containing subunits α7 and α9* (denoting homomeric or heteromeric α9) in monocytes. This study examines whether this mechanism is active in human macrophages (THP-1 cell-derived, peripheral blood mononuclear cell-derived, and peritoneal macrophages). - Source: PubMed
Publication date: 2025/10/27
Wolf Philipp M KHanke DominikSingh Vijay KKeller Hanno LEttischer Luca JTeppe LauraAmati Anca-LauraHecker AndreasHusain-Syed FaeqRohde MariusNuber Ulrike ABüttner KathrinMcIntosh J MichaelLiese JulianeMazurek SybilleGrau VeronikaRichter Katrin - Alzheimer’s disease (AD) is the most common neurodegenerative disorder, affecting over 32 million people globally. The variability in treatment response to AD medications is influenced by genetic factors, sex, comorbidities, and medication history. Pharmacogenomics, the study of how an individual’s genetic makeup influences drug response, offers a promising approach to understanding these differences. This systematic review investigated the role of genetic polymorphisms in affecting treatment outcomes in AD. Following PRISMA guidelines, we systematically searched PubMed, Scopus, Cochrane, and PharmGKB databases for studies on AD, pharmacogenomics, and treatment response. Ten researchers independently screened the articles, with two independent reviewers resolving conflicts. A total of 1126 records were identified, and after removing duplicates and screening, 58 studies met inclusion criteria. emerged as the most consistently studied gene, with ε2 and ε3 alleles generally associated with better responses to acetylcholinesterase inhibitors (AChEIs) and NMDA receptor antagonists, while ε4 carriage predicted poorer outcomes. The 10 allele, common in East Asian populations, was linked to enhanced donepezil response due to slower drug metabolism. Other genes, including , , , , , showed potential associations with treatment response, particularly with AChEIs, though results varied across populations and study designs. Polymorphisms in inflammatory, metabolic, and vascular genes such as ,, were also associated with cognitive outcomes, but findings were largely exploratory. In conclusion, and remain the most promising pharmacogenetic markers in AD, particularly for guiding donepezil therapy. However, evidence remains inconsistent due to varying study designs, populations, and clinical metrics. Additional genes show potential but require further validation. Larger, multiethnic studies with standardized treatment protocols and outcomes are needed to establish the clinical utility of pharmacogenomics in AD therapy. - Source: PubMed
Publication date: 2025/10/09
Climacosa Fresthel Monica MOrnos Eric David BGapaz Nicole Clarence Louise LGuantia Mary Gale RCruz Joana Marie CManalo Rafael Vincent MYu Melody LQureshi Almeera PCarampel Ajina CAsis Joannes Luke BReyes John Carlo BDacasin Aira BAnlacan Veeda Michelle M - The alpha 7 nicotinic acetylcholine (ACh) receptor (CHRNA7) is targeted by ACh, choline, and exogenous chemicals, including nicotine and insecticides. According to database searches, it is expressed by several cell types of the human ovary, including granulosa cells (GCs). This expression site was confirmed by immunohistochemistry in human and nonhuman primate ovaries. Cultured human GCs, derived from in vitro fertilization patients, express functional CHRNA7, indicated among others by acutely elevated intracellular Ca2+ levels upon addition of the selective CHRNA7 agonist PNU 282987. Heterogeneity in this acute response may be due, in part, to the varying expression of the human-specific channel variant CHRFAM7A, which acts as a negative regulator. CHRNA7 activation is reported to dampen inflammatory reactions in non-neuronal cells, and in cultured human GCs, as recently reported, inflammatory responses are induced by hypoxia (1% O2). Studies in GCs exposed to 1% O2 may mirror the physiological situation in the periovulatory human follicle, and we found that PNU 282987 significantly decreased the low O2-induced elevations of IL6, CXCL8, and IL1B. Proteomic studies identified further consequences in human GCs exposed to 1% O2. Thus, PNU 282987 increased abundances of 31 proteins and decreased abundances of six proteins. Of note, several collagens were among the decreased proteins, which might be novel ovarian biomarkers for GC luteinization and oocyte quality. Our results imply roles of endogenous CHRNA7 activators and possibly exogenous chemicals in limiting inflammatory responses and in the regulation of other human GC functions. This influence may depend on the relative abundance of CHRNA7 and translation of CHRFAM7A. - Source: PubMed
Seßenhausen PiaCaban Karolina MSchneider MichaelaEubler KatjaKreitmair NicoleSchneider JuliaDissen Gregory ABerg DieterBerg UlrikeStöckl Jan BKunz LarsFröhlich ThomasMayerhofer Artur - Prenatal nicotine exposure impairs fetal cortical grey matter volume, but the precise cellular mechanisms remain poorly understood. This study elucidates the role of nicotinic acetylcholine receptors (nAChRs) in progenitor cells and radial glia (RG) during human cortical development. We identify two nAChR subunits-CHRNA7 and the human-specific CHRFAM7A-expressed in SOX2+ progenitors and neurons, with CHRFAM7A particularly enriched along RG endfeet. nAChR activation in organotypic slices and dissociated cultures increases RG proliferation while decreasing neuronal differentiation, whereas nAChR knockdown reduces RG and increases neurons. Single-cell RNA sequencing reveals that nicotine exposure downregulates key genes in excitatory neurons (ENs), with CHRNA7 or CHRFAM7A selectively modulating these changes, suggesting an evolutionary divergence in regulatory pathways. Furthermore, we identify YAP1 as a critical downstream effector of nAChR signaling, and inhibiting YAP1 reverses nicotine-induced phenotypic alterations in oRG cells, highlighting its role in nicotine-induced neurodevelopmental pathophysiology. - Source: PubMed
Publication date: 2025/07/01
Mukhtar TanzilaSiebert Clara-VitaWang YuejunPebworth Mark-PhillipWhite Matthew LWu TianzhiHuang Tan IengZuo GuolongRoss JaydenBaltazar JenniferUpadhyay VarunShankar MerutZhou LiLombardi-Coronel IsabelMandala IshaanAdam Manal AWang ShaohuiBi QiuliHoekman Marco F MLi JingjingKriegstein Arnold R