Polyclonal Rabbit RYR2 Antibody
- Known as:
- Polyclonal Rabbit RYR2 Antibody
- Catalog number:
- abx000677
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- Polyclonal Rabbit RYR2 Antibody
Related genes to: Polyclonal Rabbit RYR2 Antibody
- Gene:
- RYR2 NIH gene
- Name:
- ryanodine receptor 2
- Previous symbol:
- ARVD2
- Synonyms:
- ARVC2, VTSIP
- Chromosome:
- 1q43
- Locus Type:
- gene with protein product
- Date approved:
- 1989-12-07
- Date modifiied:
- 2019-04-23
Related products to: Polyclonal Rabbit RYR2 Antibody
Related articles to: Polyclonal Rabbit RYR2 Antibody
- Aberrant calcium signaling, particularly the ryanodine receptor (RYR) signaling, is linked to cancer development. Currently, little is known about the status of RYR in colorectal cancer (CRC), and the correlation of RYR with CRC phenotypes remains unclear. We analyzed genetic alterations in RYRs using data from 587 patients with CRC in the TCGA database. Mutations were spread across RYR channels without identified hotspot mutations. RYR2 exhibited the highest mutation frequency (59%), with mutually exclusive mutations between RYR2 and RYR1/RYR3. RYR2 revealed significantly elevated transcription in CRC tissues, while RYR1 and RYR3 revealed decreased transcription. Patients with RYR mutations had higher tumor mutational burden (TMB). Stage-related differences in RYR1 and RYR2 transcription were detected. Although age was correlated with RYR1 mutation status, no significant differences in age or BMI were found between patients with low and high RYR transcription. Age, clinical stage, and tumor location were identified as prognostic factors, with age, clinical stage, and location being independent risk factors. In conclusion, RYRs exhibited variable mutational and transcriptional profiles in CRC, with RYR2 revealing unique patterns. Age, clinical stage, and tumor location represent independent risk factors in CRC with RYR mutations. - Source: PubMed
Publication date: 2026/04/23
Hu JiangpingPeng MinxuanOu QiZhou Yi - - Source: PubMed
Publication date: 2026/04/24
- Calcium (Ca²⁺) signalling is essential for cardiomyocyte function, regulating excitation-contraction coupling and excitation-transcription coupling, and contributing to mitochondrial energy production (excitation-bioenergetics coupling). In this Review, we explore the role of Ca²⁺ microdomains, which compartmentalize Ca²⁺ signalling to ensure efficient cardiac function. We first describe the organization of these microdomains, followed by their functional importance, pathological alterations in heart failure and potential therapeutic strategies targeting key Ca²⁺-signalling mechanisms. The dyad, a crucial excitation-contraction coupling microdomain, brings L-type Ca²⁺ channels and ryanodine receptor Ca²⁺-release channels (RYR2) into close proximity, facilitating Ca²⁺-induced Ca²⁺ release for cardiomyocyte contraction. In heart failure, dyadic remodelling and altered Ca²⁺ handling contribute to cardiac contractile dysfunction and arrhythmogenesis. Emerging research shows that dyads are dynamic, rapidly adapting to modulators such as β-adrenergic signalling, offering new therapeutic targets. Under stress conditions, dyadic proteins can translocate to the nucleus to regulate gene expression. In addition to excitation-contraction coupling, which operates on a beat-to-beat basis, Ca²⁺ has additional roles in cardiomyocytes. Nuclear Ca²⁺ regulates the expression of genes related to hypertrophy, including those encoding Ca²⁺ channels and transporters. Disruptions in these microdomains drive pathological remodelling in heart failure and arrhythmias. Understanding Ca²⁺ microdomains is crucial for developing targeted interventions to restore cardiac function while minimizing pro-arrhythmic risks. - Source: PubMed
Publication date: 2026/04/22
Benitah Jean-PierrePereira LaetitiaPerrier RomainMercadier Jean-JacquesSabourin JessicaGómez Ana María - RNA therapeutics hold strong potential for treating genetic disease, yet progress is often limited by delivery, stability, and safety concerns. Here, we profile respiratory safety and cellular uptake of an inhaled siRNA targeting the cardiac RyR2 gene, which is responsible for catecholaminergic polymorphic ventricular tachycardia (CPVT), delivered via inhalation with calcium phosphate nanoparticles (CaP NPs). Barrier integrity, cytotoxicity, siRNA uptake, and immune activation, were assessed using a human 3D normal bronchial epithelial model (NHBE) under Air-Liquid Interphase (ALI) and dendritic cells (DCs), tested in monoculture and in co-culture. Barrier function, measured by transepithelial electrical resistance (TEER), remained stable after 48 h of exposure to 400 nM siRNA RyR2, scramble control, or CaP NPs, indicating preserved epithelial performance. Confocal imaging showed efficient internalization of Cy5-labeled siRNA in both mono- and co-cultures. Cytokine profiling revealed IL-8 release across all conditions in NHBE and NHBE + DC models, with IL-6 and TNF-α limited to immune-competent co-cultures; IFN-γ was below the limit of detection. No cytotoxicity was observed. Together, these data demonstrate that CaP NP-mediated delivery achieves robust siRNA uptake without compromising airway barrier integrity, while eliciting only modest, context-dependent immune responses (primarily IL-8 and TNF-α in the presence of DCs). This work supports the respiratory safety and translational potential of inhaled RyR2-targeting siRNA for CPVT. - Source: PubMed
Publication date: 2026/04/15
Bettinsoli ValeriaErlacher MagdalenaGalbiati ValentinaMarinovich MarinaCorsini EmanuelaWilflingseder Doris - Ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT) are rare causes of pediatric out-of-hospital cardiac arrest (OHCA), especially in toddlers. Within VT, catecholaminergic polymorphic ventricular tachycardia (CPVT) is an uncommon but potentially fatal channelopathy that may present as collapse during emotional or physical stress. - Source: PubMed
Publication date: 2026/04/13
Disla Cuevas AbiezerTran ChantelChung SunHeeDaya Mohamud