Ask about this productRelated genes to: CACNB2 Blocking Peptide
- Gene:
- CACNB2 NIH gene
- Name:
- calcium voltage-gated channel auxiliary subunit beta 2
- Previous symbol:
- MYSB, CACNLB2
- Synonyms:
- -
- Chromosome:
- 10p12
- Locus Type:
- gene with protein product
- Date approved:
- 1992-03-27
- Date modifiied:
- 2019-04-23
Related products to: CACNB2 Blocking Peptide
Related articles to: CACNB2 Blocking Peptide
- Prenatal alcohol exposure (PAE) can result in fetal alcohol spectrum disorder (FASD), a permanent, heterogeneous condition characterized by severe neurodevelopmental impairments with or without microcephaly, characteristic facial dysmorphology, and congenital anomalies. Clinical and pre-clinical studies suggest that genetic factors, in the mother or fetus, influence the phenotypic outcomes following PAE. The objectives of this study were to evaluate the prevalence and types of DNA copy number variants (CNVs) in children (0-18 years) diagnosed with FASD and to identify genes known to be associated with neurodevelopmental disorders. - Source: PubMed
Byrnes SuzyCollins FelicityElliott Elizabeth - The purpose of this study is to clarify the role of LINC01094 in acute cerebral infarction (ACI) and to explore its potential molecular mechanisms. A total of 121 patients with ACI and 133 healthy controls were enrolled in this study. The expression levels of LINC01094, miR-499a-5p, and inflammatory markers (CRP, IL-6) were measured using RT-qPCR. The levels of MDA, SOD, and ROS were measured using commercial assay kits. The diagnostic value of LINC01094 for ACI was evaluated using ROC curve analysis. CCK-8 assay and flow cytometry were utilized to measure cell viability and apoptosis. The subcellular localization of LINC01094 in SH-SY5Y cells was determined. The predicted targeting relationship between LINC01094 and miR-499a-5p was validated using dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays. Serum LINC01094 expression was significantly elevated in ACI patients and demonstrated diagnostic value for ACI. miR-499a-5p expression was markedly reduced in both ACI patients and in vitro/in vivo models, showing a significant negative correlation with LINC01094 expression in patients. Downregulation LINC01094 mitigated OGD/R-induced damage in SH-SY5Y cells and cerebral injury in MCAO rats, while inhibition miR-499a-5p reversed this protective effect. Furthermore, CACNB2 was confirmed as a direct target of miR-499a-5p. LINC01094 participates in the pathological process of ACI injury by competitively binding to and inhibiting the activity of miR-499a-5p. These findings suggest that LINC01094 may serve as a potential therapeutic target for ACI treatment. - Source: PubMed
Publication date: 2026/06/06
Dong JingFeng YilinGuo Mengnan - Hypertension during pregnancy is a major cause of maternal and neonatal morbidity and mortality, yet the efficacy and safety of antihypertensive treatments in this setting remain uncertain. We evaluated the effects of antihypertensive drug targets on adverse pregnancy-related outcomes using genetic variants to instrument target perturbation. - Source: PubMed
Publication date: 2026/05/20
Borges Maria CarolinaUrquijo HelenaYang Qianvan der Graaf AdriaanMcBride NancyHaug Eirin BeateSoares Ana GoncalvesClayton Gemma CBond Tom AAl Arab MarwaHorn JulieThomas LaurentBhatta LaxmiÅsvold Bjørn OlavMagnus Maria CEvans David MBurden ChristyBirchenall KatherineBrumpton BenGaunt Tom RHart Emma CKutalik ZoltanLawlor Deborah A - To elucidate the genetic architecture of blood pressure (BP) and heart rate (HR) during early life and assess their potential relevance to adult health outcomes. - Source: PubMed
Publication date: 2026/04/27
Xie TianAni AlirezaVaez AhmadNolte Ilja MSu ShaoyongIshikuro MamiWang SiqiZhang WenboSoares Ana GoncalvesMotazedi EhsanCalas LucindaRonkainen JustiinaPedersen Casper-Emil TLu XuelingStinson Sara EFelix Janine FStankevic EvelinaWang Carol AThiering ElisabethFernández DietmarCalvo-Serra BeatrizStathopoulou Maria GFore RubyKumar AshishTuhkanen JohannaBilbao Jose RamonIbarluzea JesusIsaacs AaronFonvig Cilius EsmannRivadeneira FernandoLund Morten Asp VonsildHolm Louise Aasvan der Most Peter JRiese HarriëtteNarita AkiraTamiya GenFlexeder ClaudiaWiersma RikstjeArgoty-Pantoja Anna DVinding RebeccaHansen Tine WillumKümler ThomasEstarlich MarisaBustamante MarionaYuan Wen LunBoland-Augé AnneDeleuze Jean-FrançoisPetrelis Alexandros MRifas-Shiman SherylKajantie EeroFernandez-Jimenez NoraSanta-Marina LoretoArts Ilja C WLahti JariStrandberg TimoKull IngerBergström AnnaHivert Marie-FranceBønnelykke KlausKuriyama ShinichiBeilin Lawrence JMori Trevor AHartman Catharina AGrarup NielsThijs CarelRäikkönen KatriMelén ErikOken EmilyVisvikis-Siest SophieGützkow Kristine BGrazuleviciene ReginaHeude BarbaraChatzi LedaVrijheid MartineStandl MarieVrijkotte TanjaPennell Craig EOldehinkel Albertine JHansen TorbenJaddoe Vincent W VHolm Jens-ChristianSebert SylvainTimpson Nicholas JObara TakuWang XiaolingLawlor Deborah ACorpeleijn EvaAhluwalia Tarunveer SSnieder Harold - Coronary artery disease (CAD) causes irreversible myocardial dysfunction and progressive heart failure due to loss of contractile function and limited endogenous regenerative capacity. Current therapeutic strategies fail to restore lost myocardium or regenerate damaged cardiac tissue. Identifying dysregulated contractility-related genes may reveal actionable targets for stem cell engineering, iPSC-derived cardiomyocyte design, and tissue regeneration aimed at restoring myocardial contractility and function. - Source: PubMed
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