CACNA1G
- Known as:
- CACNA1G
- Catalog number:
- Y214356
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- CACNA1G
Related genes to: CACNA1G
- Gene:
- CACNA1G NIH gene
- Name:
- calcium voltage-gated channel subunit alpha1 G
- Previous symbol:
- -
- Synonyms:
- Cav3.1, NBR13
- Chromosome:
- 17q21.33
- Locus Type:
- gene with protein product
- Date approved:
- 1999-01-08
- Date modifiied:
- 2016-10-05
Related products to: CACNA1G
Related articles to: CACNA1G
- Inherited ion channel gene mutations cause network synchronization disorders, but their early impact on circuit development is less understood. Childhood absence epilepsy features cortical spike-wave discharges driven by thalamocortical rebound bursting. Loss-of-function mutations in P/Q-type calcium channels impair neurotransmitter release yet paradoxically increase thalamic excitability. In tottering mice, global P/Q deficiency elevates T-type calcium and big potassium (BK) channel transcripts in thalamic relay neurons, increasing excitability before seizure onset and coincident with the N-to-P/Q exocytosis switch. Selective P/Q deletion in cortical L6 pyramidal presynaptic input to thalamus reproduced the coordinate transcript elevation, indicating a transsynaptic mechanism. Unexpectedly, tottering, but not L6 mutants, showed increased thalamic neurogenesis and β-catenin/Lef1 upregulation, linking intrinsic thalamic P/Q channel function to early structural brain development. These findings reveal that subtle inherited changes in P/Q-mediated transmitter release and postsynaptic membrane calcium dynamics disrupt a previously unrecognized embryonic homeostatic pathway regulating growth, plasticity, and excitability in thalamocortical circuits. - Source: PubMed
Publication date: 2026/04/02
Thompson Samantha JMiao Qing-LongSonig AnikaNoebels Jeffrey - Cholinergic neurons exhibit distinct firing patterns underlying diverse physiological and pathological states, but the mechanisms governing their dynamic switching, particularly in negative emotional contexts, remain unclear. Here, we demonstrate that medial habenula cholinergic (MHb) neurons transition from tonic to burst firing during nicotine withdrawal, driving anxiety-like behaviors in mice. Integrating transcriptomics, electrophysiology, and genetic manipulation, we identified the RNA-binding protein pumilio 1 (Pum1) as a critical brake on this switch. Pum1 binds Cacna1g mRNA (encoding Cav3.1) at nucleotides 6,498-6,501, promoting its decay. MHb neurons comprise two subpopulations: burst-firing Pum1 and tonic-firing Pum1 neurons. Withdrawal downregulates Pum1, derepressing Cav3.1 to induce pathological bursting. Genetic or pharmacological suppression of Cav3.1, or Pum1 overexpression, rescues burst firing and anxiety-like behaviors. Our study unveils MHb neurons' burst firing as a causal driver of anxiety and reveals the Pum1-Cav3.1 axis as a master regulator of firing plasticity, offering a potential targeted therapeutic strategy for cholinergic dysfunction-related disorders. - Source: PubMed
Publication date: 2026/03/27
Zheng Zhi-WeiMin Peng-XiangLuo Yi-LingMao Xing-FengZhang Yi-XuanLiu Xiu-XiuLu MingXu Eugene YujunHan FengLu Ying-Mei - The biological basis for the male sex bias in autism spectrum disorder (ASD) is poorly understood. Differential exposure to sex hormones during neurodevelopment has been proposed as a potential modulator of risk. To test the hypothesis that early exposure to the principal biologically active estrogen, 17β-estradiol, confers a protective effect against mutations in ASD and neurodevelopmental disorder (NDD) genes, we conduct a dual-system multi-modal screen of 36 functionally diverse, large-effect ASD/NDD genes in human induced pluripotent stem cell and larval zebrafish models. We uncover estradiol-dependent effects across genes and modalities, revealing convergent and divergent gene-by-estradiol interactions at the transcriptomic, circuit, and behavioral levels. Estradiol broadly ameliorates ASD/NDD gene expression patterns across all knockouts examined and selectively dampens network hyperexcitability phenotypes in human neurons and zebrafish brains in a subset of ASD/NDD genes (, . Two genes, and , show comprehensive estradiol rescue of differential gene expression and network bursting activity in human neurons as well as sleep-wake and visual-startle phenotypes in larval zebrafish mutants. Moreover, estradiol rescues seizures and regional increases in brain activity in larval zebrafish mutants. Altogether, we describe novel roles of estradiol in modulating network hyperexcitability in the context of loss of function mutations of select ASD/NDD genes. - Source: PubMed
Publication date: 2026/02/18
Pruitt AprilYang LiangLee SeoyeonBalafkan NovinSeah CarinaDai YiDavidson ElizabethKhan SuhaSen AnnabelLiu JennyWood IsabelXu GangHuang XiayuanCarlson MarinaZhao DejianJamadagni PriyankaDossou GraceRetallick-Townsley KaylaLi XinyunDeans P J MichaelGarcia Meilin FernandezGao HuanyaoWang ZuohengHuckins Laura MHoffman Ellen JBrennand Kristen J - Growing evidence supports that epigenetic dysregulation through histone deacetylases (HDACs) plays a critical role in synaptic dysfunction and memory loss in Alzheimer’s disease (AD), and that HDACs have been highlighted as an attractive class of targets for AD therapy. Moreover, restoring Wnt/β-catenin signaling, which is greatly suppressed in AD brains, is a promising therapeutic strategy. CI-994 is an orally active class I HDAC inhibitor that has undergone several phase II/III clinical trials on cancer treatment. Importantly, CI-994 can cross the blood–brain barrier and is a cognitive enhancer. - Source: PubMed
Publication date: 2026/02/07
Lu WenyanKawatani KeijiRen YingxueNambara ToshihikoJia LinJeevaratnam SurenLee EunmiMartinez Paula RodriguezIzhar TahaWang NiRaulin Ana-CarolineWszolek Zbigniew KBu GuojunKanekiyo TakahisaLi Yonghe - In veterinary medicine, voltage-gated calcium channels (VGCCs) are key drug targets. Calcium channel blockers (CCBs) are the standard treatment for common feline diseases, such as systemic hypertension and hypertrophic cardiomyopathy. However, therapeutic strategies are limited due to the adverse effects of existing drugs like amlodipine, such as activation of the renin-angiotensin-aldosterone system. A critical lack of feline-specific data on the tissue distribution of VGCC subtypes fundamentally hinders the safe and effective application of CCBs in cats. This is because knowledge from other species is often not translatable due to the unique metabolic pathways in cats. - Source: PubMed
Publication date: 2025/11/30
Matsuura TakumiMorita ShoheiFukushima Ryuji