Polyclonal Rabbit CNGA2 Antibody
- Known as:
- Polyclonal Rabbit CNGA2 Antibody
- Catalog number:
- KA0810
- Product Quantity:
- 100ul
- Category:
- -
- Supplier:
- KareBay
- Gene target:
- Polyclonal Rabbit CNGA2 Antibody
Related genes to: Polyclonal Rabbit CNGA2 Antibody
- Gene:
- CNGA2 NIH gene
- Name:
- cyclic nucleotide gated channel alpha 2
- Previous symbol:
- CNCA1, CNCA
- Synonyms:
- CNG2, OCNC1, OCNCa, OCNCALPHA, OCNCalpha, FLJ46312
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1991-06-05
- Date modifiied:
- 2016-10-05
Related products to: Polyclonal Rabbit CNGA2 Antibody
Related articles to: Polyclonal Rabbit CNGA2 Antibody
- Quaternary stereocenters are prevalent in natural products and bioactive molecules, where they influence the molecular structure, conformation, and function by enhancing the fraction of sp character. The enantioselective construction of such structures via cross-coupling remains a long-standing challenge, owing to the steric demands of forging C(sp)-C(sp) bonds and the limited accessibility of suitable tertiary carbon coupling partners. Here, we report a palladium-catalyzed asymmetric decyanative allylation (ADA) platform of C(sp)-C(sp) cross-coupling that transforms stable and readily available tertiary nitriles into enantioenriched acyclic and cyclic compounds bearing quaternary centers. This process proceeds via the selective addition of in situ-formed allyl zinc reagent to the cyano group, followed by retro-Thorpe-type C-CN bond cleavage and asymmetric allylation, guided by newly developed chiral ligands. The method exhibits a broad substrate scope across three classes of tertiary nitriles─malononitriles, α-cyano indolinones, and α-cyano lactones─offering high yields and excellent enantioselectivities under mild conditions. This research establishes a conceptually distinct retrosynthetic paradigm, from prochiral or racemic quaternary carbons to enantioenriched quaternary centers, enabled by chemoselective C-C bond cleavage and stereoselective C-C bond formation. The synthetic utility of this strategy is demonstrated by the downstream synthesis of a monoamine reuptake inhibitor and a CNGA2 channel blocker as well as synthetic intermediates of natural products physovenine and physostigmine. - Source: PubMed
Publication date: 2025/10/29
Ding Gui-FengChen Zi-HaoDeng Jiang-LianZheng Yu-QingHu Xu-DongLiu Wen-Bo - Mammalian cyclic nucleotide-gated (CNG) channels play crucial roles in visual and olfactory signal transduction. In olfactory sensory neurons, the native CNG channel functions as a heterotetramer consisting of CNGA2, CNGA4, and CNGB1b subunits and is activated by cAMP. Calmodulin (CaM) modulates the activity of the olfactory CNG channel, enabling rapid adaptation to odorants. Here we present cryo-EM structures of the native human olfactory CNGA2/A4/B1b channel in both CaM-bound closed and cAMP-bound open states, elucidating the molecular basis of the 2:1:1 subunit stoichiometry in channel assembly and the asymmetrical channel gating upon cAMP activation. Combining structural and functional analyses with AlphaFold prediction, we define two distinct CaM binding sites (CaM1 and CaM2) on the N- and C-terminal regions of CNGB1b, respectively, shedding light on the molecular mechanism of Ca/CaM-mediated rapid inhibition of the native olfactory CNG channel. - Source: PubMed
Publication date: 2025/10/23
Xue JingGan NinghaiZeng WeizhongJiang Youxing - Patients with obstructive sleep apnea (OSA) experience chronic intermittent hypoxia (CIH). OSA patients and CIH-treated rodents exhibit overactive sympathetic nervous system and hypertension, mediated through hyperactive carotid body (CB) chemoreflex. Activation of olfactory receptor 78 (Olfr78) by hydrogen sulfide (H2S) is implicated in CB activation and sympathetic nerve responses to CIH, but the downstream signaling pathways remain unknown. Given that odorant receptor signaling is coupled to adenylyl cyclase 3 (Adcy3), we hypothesized that Adcy3-dependent cyclic adenosine monophosphate (cAMP) contributes to CB and sympathetic responses to CIH. Our findings show that CIH increases cAMP levels in the CB, a response absent in Adcy3, Cth (encoding CSE), and Olfr78 null mice. CBs from Cth and Olfr78 mutant mice lacked a persulfidation response to CIH, indicating that Adcy3 activation requires Olfr78 activation by H2S in CIH. CIH also enhanced glomus cell Ca2+ influx, an effect absent in Cnga2 (encoding cyclic nucleotide-gated channel alpha2 subunit) and Adcy3 mutants, suggesting that CIH-induced cAMP mediates enhanced Ca2+ responses through cyclic nucleotide-gated channels. Furthermore, Adcy3 null mice did not exhibit either CB activation or sympathetic activation by CIH. These results demonstrate that Adcy3-dependent cAMP is a downstream signaling pathway to H2S/Olfr78, mediating CIH-induced CB activation, sympathetic activity and hypertension. - Source: PubMed
Peng Ying-JieNanduri JayasriWang NingSu XiaoyuHildreth MatthewPrabhakar Nanduri R - An estimated 1 in 10 000 people are born without the ability to smell, a condition known as congenital anosmia, and about one third of those people have non-syndromic, or isolated congenital anosmia (ICA). Despite the significant impact of olfaction for our quality of life, the underlying causes of ICA remain largely unknown. Using whole exome sequencing (WES) in 10 families and 141 individuals with ICA, we identified a candidate list of 162 rare, segregating, deleterious variants in 158 genes. We confirmed the involvement of CNGA2, a previously implicated ICA gene that is an essential component of the olfactory transduction pathway. Furthermore, we found a loss-of-function variant in SREK1IP1 from the family gene candidate list, which was also observed in 5% of individuals in an additional non-family cohort with ICA. Although SREK1IP1 has not been previously associated with olfaction, its role in zinc ion binding suggests a potential influence on olfactory signaling. This study provides a more comprehensive understanding of the spectrum of genetic alterations and their etiology in ICA patients, which may improve the diagnosis, prognosis, and treatment of this disorder and lead to better understanding of the mechanisms governing basic olfactory function. - Source: PubMed
Publication date: 2023/12/26
Kamarck Marissa LTrimmer CaseyMurphy Nicolle RGregory Kristen MManoel DiogoLogan Darren WSaraiva Luis RMainland Joel D - Oxygen (O) sensing by the carotid body is critical for maintaining cardiorespiratory homeostasis during hypoxia. Hydrogen sulfide (HS) signaling is implicated in carotid body activation by low O. Here, we show that persulfidation of olfactory receptor 78 (Olfr78) by HS is an integral component of carotid body activation by hypoxia. Hypoxia and HS increased persulfidation in carotid body glomus cells and persulfidated cysteine in Olfr78 protein in heterologous system. mutants manifest impaired carotid body sensory nerve, glomus cell, and breathing responses to HS and hypoxia. Glomus cells are positive for G adenylate cyclase 3 (Adcy3) and cyclic nucleotide-gated channel alpha 2 (Cnga2), key molecules of odorant receptor signaling. or mutants exhibited impaired carotid body and glomus cell responses to HS and breathing responses to hypoxia. These results suggest that HS through redox modification of Olfr78 participates in carotid body activation by hypoxia to regulate breathing. - Source: PubMed
Publication date: 2023/07/05
Peng Ying-JieNanduri JayasriWang NingKumar Ganesh KBindokas VytautasPaul Bindu DChen XuanmaoFox Aaron PVignane ThibautFilipovic Milos RPrabhakar Nanduri R