Ask about this productRelated genes to: CACNA1G Blocking Peptide
- 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 Blocking Peptide
Related articles to: CACNA1G Blocking Peptide
- The risk of atrial fibrillation (AF) is higher in endurance athletes. Pulmonary vein isolation (PVI) is effective in this group, implicating pulmonary vein (PV) remodelling, but underlying mechanisms are unclear. This study investigated if endurance training remodels PV sleeves and the PV-left atrial (LA) junction to promote PV triggers and a permissive peri-antral substrate for AF. - Source: PubMed
Publication date: 2026/05/25
Soattin LucaTopal LeilaTikhomirov RomanLagomarsino-Oneto DanieleAl-Othman SamiLee Angela W CSaluja SushantHornyik TiborHusti ZoltánPintér Jenő AntalMohammed Aiman Saleh ASmith MatthewFrancis Alice JMcKie MeganTorre EleonoraPolyák AlexandraFarkas AttilaBentzen Bo HjorthKeavney BernardNagy NorbertJost NorbertCasadei BarbaraMangoni Matteo EBoyett Mark RColman Michael ANiederer Steven AVarró AndrásMorris Gwilym MBaczkó IstvánD'Souza Alicia - RBM20 (RNA binding motif protein 20) is a cardiac splicing factor responsible for the splicing of several cardiac genes such as titin (), triadin (), ryanodine receptor 2 (), PDZ and LIM domain protein 1 (), and calcium/calmodulin-dependent protein kinase II (). Pathogenic variants in are a major cause of familial dilated cardiomyopathy, and lead to missplicing of RBM20 target genes. - Source: PubMed
Publication date: 2026/04/30
Pant PriyankaHuang YongGhouse ZakiyaBai FangKemmling ElenaKonrad LauraAlameldeen AhmedKistler RebeccaSeeger TimonGotthardt MichaelParikh Victoria Nvan den Hoogenhof Maarten M G - Dietary protein promotes satiety and weight loss, yet how appetite-regulating neurons sense dietary protein remains poorly understood. Here, we show that Cacna1g, which encodes the T-type voltage-gated calcium channel Cav3.1, is enriched in hypothalamic leucine-sensing neurons and mediates neuronal leucine sensing. Pharmacological inhibition of Cav3.1 blunts leucine-induced activation of pro-opiomelanocortin (POMC) neurons in cultured neurons and brain slices, thereby suppressing the anorectic response to hypothalamic leucine in vivo. Genetic deletion of Cacna1g in POMC neurons abolishes the appetite- and weight-suppressive effects of high-protein feeding. Mechanistically, leucine binds a hydrophobic pocket of Cav3.1 and lowers its threshold for voltage-dependent activation. Finally, pharmacological activation of mediobasal hypothalamic Cav3.1 promotes weight loss in diet-induced obese mice and potentiates responses to anorectic agents, including liraglutide. Together, these findings establish hypothalamic Cav3.1 as a neuronal leucine sensor and nominate it as a tractable target for anti-obesity therapy. - Source: PubMed
Publication date: 2026/04/22
Tsang Anthony HHeeley NicholasAlcaino ConstanzaHwang EunsangLam Brian YRahman TaufiqDarwish TamanaNuzzaci DanaeKay Richard GSarkar AmarWang RuiyanBasha NihalPunnoose AustinKirwan PeterMa MarcellaYeo Giles SMerkle Florian TGribble Fiona MReinmann FrankWilliams Kevin WBlouet Clémence - 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