ANO2
- Known as:
- ANO2
- Catalog number:
- 001668A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANO2
Ask about this productRelated genes to: ANO2
- Gene:
- ANO2 NIH gene
- Name:
- anoctamin 2
- Previous symbol:
- C12orf3, TMEM16B
- Synonyms:
- -
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2000-08-24
- Date modifiied:
- 2016-10-04
Related products to: ANO2
Related articles to: ANO2
- Epstein-Barr virus (EBV) is a critical risk factor for multiple sclerosis (MS), but the pathogenic mechanisms remain elusive. To clarify its role in MS, we examined the sequence of EBV-related antibody responses over a broad period before the clinical onset of MS, from early childhood to middle age. A nested case-control study was performed by linking Swedish MS registries with biobanks to identify pre-symptomatic samples from individuals who later developed MS and matched controls. Leveraging these samples, we analysed the immune responses to EBV in and before the prodromal phase of MS. Antibodies against EBV (viral capsid antigen, VCA; EBV nuclear antigen 1, EBNA1; early antigen-diffuse, EA-D) and the putative autoantibody target Anoctamin 2 (ANO2) were quantified by immunoassay. Serum neurofilament light chain (S-NfL), a marker of axonal injury, was quantified by single-molecule array. Ratios of these markers were calculated within each matched case-control set, plotted against time to the clinical onset of MS, and analysed with Loess regression to visualise the temporal order of events on group level. Samples from 981 cases and 1278 controls were included. Median age at blood sampling was 22 years and 32% of the participants were children or adolescents. The median time from the blood sample to the clinical onset of MS was 9 years. On the group level, we observed the following sequence of events: Seroreactivity against lytic EBV antigens (VCA-IgG, VCA-IgM, EA-D) - characterizing primary EBV infection and reactivation - were significantly higher in cases than in controls more than 20 years before MS onset and onwards. Increased seroreactivity against the latent antigen EBNA1 was observed 15 years before onset, followed by increased ANO2 seroreactivity from 9 years and onwards. Finally, a significant elevation of S-NfL was observed from 7 years prior to MS onset. These findings demonstrate a more extensive lytic EBV infection in the decades before MS onset, consistent with the hypothesis that EBV is a driver of MS development. The sequence of increasing seroreactivity against EBNA1 and ANO2 was closely followed by biochemical signs of neuroaxonal injury, suggesting epitope spreading from EBNA1 before the subclinical onset of neuroaxonal damage. This sequence of events supports the hypothesis that EBV infection promotes autoreactive immune cells contributing to MS pathogenesis. - Source: PubMed
Publication date: 2026/08/22
Grut ViktorIngvarsson JensBiström MartinJons DanielMichels Birgitta EButt JuliaWaterboer TimBergström TomasNilsson StaffanThomas Olivia GOlsson TomasSundström Peter - Anoctamin 2 (ANO2, TMEM16B) is a calcium-activated chloride channel best known for its role in sensory neurons, yet its expression in multiple brain regions associated with dopamine-related signaling, including the prefrontal cortex, striatum, substantia nigra, ventral tegmental area, and cerebellum, suggests broader functions in central neural circuits. However, the contribution of ANO2 to dopamine-related neural function and behavior remains undefined. To address this question, we generated ANO2-deficient mice using CRISPR-Cas9-mediated gene editing and examined their behavioral and neurochemical phenotypes. ANO2 knockout mice exhibited age-dependent hyperactivity, impaired inhibitory behavioral control, altered aversive/risk-related responses, and selective motor coordination deficits, while spatial learning and memory were preserved. Neurochemically, ANO2 deficiency resulted in reduced tyrosine hydroxylase expression and phosphorylation, decreased dopamine levels despite unchanged dopamine transporter expression, region- and subtype-dependent dopamine receptor alterations, and reduced downstream signaling markers across cortico-striatal and cerebellar circuits. These changes suggest impaired dopamine biosynthesis and altered dopamine-related signaling rather than broad disruption of dopaminergic neuronal identity. Together, these findings identify ANO2 as a potential modulator of dopamine-related signaling and inhibitory behavioral control, expanding current understanding of calcium-activated chloride channel function in neural circuits relevant to behavioral domains implicated in neuropsychiatric disorders. - Source: PubMed
Publication date: 2026/08/19
Cho EunsilBae JooeunSong Jae GwangSeo JoeunKwon Seung-HaeHwang Eun MiSung Young HoonKim Hyung WookPark Jae-Yong - The gas phase reactivity of actinide monocations (Th, Pa, U, Np, Pu, Am, Cm and Cf) with O and CO was studied using inductively coupled plasma mass spectrometry (ICP-MS). Total reactions were observed for all actinides, except californium, for which only partial reactions occurred. Depending on the actinide, different reaction products are formed. AnO and AnO products are formed sequentially for Th, Pa, U, Np and Pu, whereas only AnO is formed for Am, Cm and Cf. Among all investigated actinides, Cf is the least reactive. The results are compared to experimental and calculated bond dissociation energies of the AnO and AnO products. The smallest bond dissociation energies are found for AmO, CmO and CfO, suggesting that these species are the least stable, as expected given their lack of formation. Among the actinide monoxides, the AmO and CfO species exhibit the lowest bond dissociation energy, consistent with their weaker reactivity toward O and CO compared with the other actinides. - Source: PubMed
Publication date: 2026/07/29
Goujet MathildeQuemet AlexandreGuillaumont Dominique - The aim of the work was to identify the features of associations of single nucleotide polymorphisms (SNPs) that determine the level of sex hormones in the body with simple endometrial hyperplasia without atypia (EnH) in women with different body mass index (BMI). Two groups of BMI-differing subjects (BMI < 25 [n = 766]: 196 EnH, 570 control and BMI ≥ 25 [n = 727]: 324 EnH, 403 control) with a total number of 1493 women were formed to conduct this study. Nine SNPs meaningful for the level of sex hormones (proven in genome-wide association studies [GWAS]) such as rs34670419 [G>T] , rs148982377 [T>C] , rs11031002 [T>A] , rs11031005 [T>C] , rs112295236 [C>G] , rs117145500 [A>C] , rs727428 [C>T] , rs1641549 [C>T] , rs117585797 [C>A] were considered by us. In general, in the studied sample (EnH/control, n = 1493), an association of interactions of rs148982377 [T>C] × BMI with EnH (OR = 1.11) was revealed. As a result of a comparative analysis, we found that rs148982377 [T>C] was associated with EnH in women with a BMI ≥ 25 (OR = 1.77) and was not linked with the disease in women with a BMI < 25. Both common protective factors for EnH were also identified in women with BMI ≥ 25 and BMI < 25 (rs11031002 [T>A] (OR = 0.43 and OR = 0.46 respectively) and rs11031005 [T>C] (OR = 0.46 and OR = 0.58 respectively)). At the same time, in the BMI ≥ 25 cohort, the risk effect of the TT*rs11031002-rs11031005 haplotype (OR = 3.27) was more pronounced, and the contribution of interlocus interactions of sex hormone genes with EnH formation was more significant (7 SNPs in 12 models) than in the BMI < 25 group (OR = 2.31 and 4 SNPs in 3 models). In conclusion, the presented work is exploratory and demonstrates differences in the nature of the association with EnH in women with different BMI of the testosterone-determining polymorphism: SNP rs148982377 [T>C] was associated with EnH in women with a BMI ≥ 25 and was not linked with the disease in women with a BMI < 25. - Source: PubMed
Publication date: 2026/06/02
Churnosov VladimirChurnosova MariaReshetnikov EvgenyAristova InnaTsoy KirillSorokina InnaPolonikov AlexeySolodilova MariaChurnosov MikhailPonomarenko Irina - Odorants in the inhaled air bind to odorant receptors embedded in cilia of olfactory receptor neurons, triggering the opening of the two ciliary olfactory transduction channels; first, a cationic heterotetrameric cAMP-gated channel, followed by an excitatory Ca2+-activated Cl- channel TMEM16B (also called anoctamin 2), which gives rise to a transduction current. While cholesterol is known to modulate ion channels, its effect on the olfactory channels, specifically TMEM16B, is unclear. We addressed how membrane cholesterol regulates these transduction channels. We heterologously expressed the main subunit of the olfactory cyclic nucleotide-gated (CNG) channel, CNGA2, and the Cl- channel TMEM16B and recorded their function in control, cholesterol-depleted, and cholesterol-enriched membranes. Maximal cAMP- or Ca2+-evoked currents were not altered by varying cholesterol levels. TMEM16B showed a progressive reduction in current upon repeated exposure to Ca2+ ("rundown"), which was accelerated in cholesterol-depleted membranes but decelerated in cholesterol-enriched patches when compared with control patches. Maximal cAMP-gated currents were stable over time, but their sensitivity was altered, with lower and higher cholesterol levels increasing and decreasing the channel's sensitivity, respectively. Cholesterol depletion of patches excised from mouse olfactory cilia containing native channels entirely abolished the TMEM16B current, while the maximal current of the native CNG channel remained unaltered. Reduced cholesterol did not change the sensitivity of the native CNG channel. Thus, while both olfactory transduction channels are sensitive to changes in membrane cholesterol in differing ways, the precise channel stoichiometry and the specific membrane environment also contribute to their function. - Source: PubMed
Publication date: 2026/06/23
Ponissery Saidu SamsudeenKross AlexanderDibattista MicheleGaus KatharinaReisert Johannes