CHRNA2 antibody (FITC)
- Known as:
- CHRNA2 (anti-) (fluorecein)
- Catalog number:
- orb13786
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- CHRNA2 antibody (FITC)
Related genes to: CHRNA2 antibody (FITC)
- Gene:
- CHRNA2 NIH gene
- Name:
- cholinergic receptor nicotinic alpha 2 subunit
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 8p21.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-05-11
- Date modifiied:
- 2016-10-05
Related products to: CHRNA2 antibody (FITC)
Related articles to: CHRNA2 antibody (FITC)
- Inhibition in central auditory pathways declines in old age, which contributes to age-related auditory processing deficits. In auditory cortex, most inhibitory interneurons can be identified by one of three marker proteins: parvalbumin (PV), somatostatin (SOM), or vasoactive intestinal peptide (VIP). About 10% of interneurons contain the α2 nicotinic acetylcholine receptor (α2 cells), and most of these are layer 5 Martinotti cells (α2-MCs). We examined the distribution of these four interneuron subtypes in auditory cortex of FVB mice, from young adult through old age, and the extent to which α2 cells express the marker proteins. We also examined the effects of chronic nicotine exposure (CNE) at older ages, as a step toward potential therapeutic applications. We found that the numbers of cells expressing PV, SOM and VIP, and α2-MCs, all declined with age, but total α2 cells did not. We also found that most (86%) α2 cells in young adult mice co-expressed SOM, but the co-expression declined sharply with age. Notably, CNE for three months-starting at age 9, 15, or 21 months-increased the numbers of cells with PV and VIP at 12, 18, and 24 months, respectively, to levels seen in young adults. CNE increased SOM interneurons only at 12 months and had no effect on the number of α2 cells. An analysis of immunofluorescence intensity in 12-month-old mice suggested that the increase in cell counts after CNE resulted from increased expression of marker protein, rather than appearance of interneurons. Thus, CNE partly or fully reversed the age-related decline of interneuron-marker expression and may prove useful for treatment of age-related auditory processing deficits. - Source: PubMed
Publication date: 2026/09/09
Intskirveli IrakliLazar RonitHidalgo DiannaMetherate Raju - Epilepsy is a complex disorder with multiple provoking factors and etiologies. Certain genetic alterations in certain genes have been related to the development of various types of epilepsy. We performed a systematic review to evaluate associations between four nAChR alpha subunit genes (CHRNA2/3/5/6) and epilepsy subtypes. - Source: PubMed
Publication date: 2026/08/11
Daas AhmadAl-Zu'bi Laith MarwanDarweesh Aisheh FatehiKhrisat Rama AbdullahALsharafat Hadeel DakhalalahBarhoush Rahaf MalekAl-Zoubi Raed MAl-Batayneh KhalidAl Zoubi Mazhar Salim - Metamorphosis is a critical ontogenetic transition for marine bivalves, marking the shift from planktonic to benthic lifestyles, where successful transformation dictates survival. The razor clam Sinonovacula constricta is economically important; however, low larval metamorphosis rates remain a major bottleneck in seedling production. To elucidate the mechanisms governing this process, we performed a comparative transcriptome analysis of S. constricta larvae at pre- and post-metamorphosis stages using Illumina sequencing. A total of 3701 differentially expressed genes (DEGs) were identified, including 3254 up-regulated and 447 down-regulated genes. Functional annotation of the respective top 20 significantly up-regulated and down-regulated DEGs indicated their potential pivotal roles in signal transduction (e.g., up-regulated: CAV1, CHRNA2; down-regulated: APP, NOTCH1), cellular proliferation and differentiation (e.g., up-regulated: TUBA, EGF1; down-regulated: KIF23, TTC25), transcriptional and epigenetic regulation (e.g., up-regulated: NFIL3; down-regulated: OVO, HMX1), substance transport (e.g., up-regulated: LRP2, LRP1B; down-regulated: SLC51A, Slc33a1), substance metabolism (e.g., up-regulated: CPK3, CYP26A1; down-regulated: RDMT1, ADAC), immunomodulation (e.g., up-regulated: CPN2, CRISP2), and protein homeostasis (e.g., up-regulated: HSP27, NAS-27). Functional enrichment analysis further revealed that DEGs were significantly enriched in pathways related to signal transduction and developmental regulation (e.g., Ras, TNF), cell death and homeostasis (e.g., apoptosis), immune responses (e.g., Toll-like receptor), energy metabolism (e.g., lipid), cardiovascular related (e.g., Fluid shear stress), cell junction and architecture (e.g., Tight junction), and infectious disease (e.g., measles). These results suggest a synergistic interplay between signaling, apoptosis, immunity, and metabolism during S. constricta metamorphosis. This study advances our understanding of marine bivalve metamorphosis and offers candidate genes for further mechanistic studies. - Source: PubMed
Publication date: 2026/08/14
Zhou QiangKong FeiLi DechengRan ZhaoshouXu Jilin - Optimal function of beige adipocytes is essential for energy balance and metabolic homeostasis. We previously identified that cholinergic receptor nicotinic α2 subunit (CHRNA2) mediates a beige fat selective signaling in mice and humans. Here, we investigate the molecular composition of CHRNA2-containing nicotinic acetylcholine receptors (nAChRs) in beige adipocytes and its impact on whole-body metabolism. Expression levels of cholinergic receptor nicotinic β2 subunit (CHRNB2) and CHRNA2 positively correlate within murine and human beige adipocytes, and both nAChRs are regulated by a spectrum of beige fat regulators. CHRNB2 is essential for the response to nAChR agonists in beige adipocytes. CHRNB2 partial agonists, a family of drugs clinically used for smoking cessation, activate both murine and human beige adipocytes. Mice deficient in Chrnb2, with both whole-body knockout or adipocyte-specific deletion, exhibit compromised adaptive thermogenesis in subcutaneous fat and more aggravated metabolic dysfunction after challenge with high-fat-diet feeding compared with control mice, underscoring the importance of the nAChR signaling in maintaining energy balance. This cholinergic signaling declines in subcutaneous fat with aging. These findings indicate CHRNB2 forms a functional receptor with CHRNA2 in beige adipocytes and highlight their potential as therapeutic targets against metabolic disorders. - Source: PubMed
Liu ShanshanZhu KezhouZhang WenwenPan TongO'Brien MartinAbe IchitaroDale LilyPiejak JustinHoussein NadiaZhang BiyangFein MatthewKajimura ShingoYung RaymondXu X Z ShawnWu Jun - In CA1 pyramidal neurons (CA1-PYRs), plateau potentials control synaptic plasticity and the emergence of place cell identity. Here, we show that dendritic inhibition terminates plateaus in an all-or-none manner in CA1-PYRs recorded in acute hippocampal slices from mice of either sex. Plateaus were initially resistant to inhibition but became increasingly susceptible to termination as they progressed. Two subtypes of dendrite-targeting oriens-lacunosum moleculare (OLM) interneurons, accessed in transgenic mice based on the expression of the genes or (OLM and OLM, respectively), could terminate plateau potentials. OLM generated slower postsynaptic currents that terminated plateaus more effectively than OLM Voltage-gated Ca channels (VGCCs) were necessary for plateaus, which were prolonged by blocking small-conductance Ca-activated K channels (SK). A single-compartment model with these two conductances recapitulated core experimental findings and provided a mechanistic explanation for terminations. Plateaus arose from VGCCs maintained in the active state by sustained Ca influx, a positive feedback loop that was quasi-balanced by I Inhibition terminated plateaus by driving the membrane potential below a dynamic threshold to deactivate VGCCs and end the positive feedback loop. Similar all-or-none termination dynamics were observed for plateaus evoked under cholinergic modulation. Lastly, two-photon Ca imaging showed that plateaus evoke large dendritic Ca transients that were graded by terminations. Overall, our results demonstrate how the feedback inhibitory circuit interacts with intrinsic cellular mechanisms to regulate plateau potentials and shape dendritic Ca signals in CA1-PYRs. - Source: PubMed
Publication date: 2026/05/20
Vaasjo Lee OKotermanski Shawn EPatel TiyaShi Hengyue JMachold RobertChamberland Simon