ATP2A2 ELISA kit
- Known as:
- ATP2A2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-ATP2A2-Mu
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- ATP2A2 ELISA kit
Related genes to: ATP2A2 ELISA kit
- Gene:
- ATP2A2 NIH gene
- Name:
- ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2
- Previous symbol:
- ATP2B, DAR
- Synonyms:
- SERCA2
- Chromosome:
- 12q24.11
- Locus Type:
- gene with protein product
- Date approved:
- 1990-09-10
- Date modifiied:
- 2016-02-10
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- The calcium ion (Ca) is a fundamental intracellular messenger involved in the transduction of diverse receptor signaling pathways. Transient increases in cytoplasmic Ca concentration ([Ca]) regulate many cellular functions, including the contraction of vascular smooth muscle cells (VSMCs), which are active components of the blood vessels. A key protein in intracellular Ca handling is the sarco/endoplasmic reticulum (SR/ER) Ca ATPase, or SERCA pump. This transmembrane protein belongs to the P-type ATPase family and uses energy from ATP hydrolysis to transport Ca from the cytoplasm into intracellular reservoirs within the SR of VSMCs. By lowering [Ca], SERCA activity promotes vasorelaxation. In mammals, three genes, ATP2A1, ATP2A2, and ATP2A3, encode at least twelve SERCA pump isoforms. Alternative mRNA splicing is the primary mechanism for generating most isoforms, leading to tissue-specific expression patterns. In VSMCs from the aorta and mesenteric arteries, the expression of SERCA2a, SERCA2b, and, more recently, SERCA3 has been reported. This chapter will review the structure, mechanism of action, and physiological role of the SERCA pump in the intracellular Ca handling of VSMCs, as well as its alterations in metabolic syndrome. - Source: PubMed
Publication date: 2026/05/12
Arriero-Carrillo Cristian JRueda Angélica - Darier disease (DD) is an inherited acantholytic disorder with autosomal dominant inheritance, having a mutation in ATP2A2 gene on chromosome 12. DD usually presents with hyperkeratotic papules and subsequently coalesce to form a plaque over seborrheic areas on the trunk, intertriginous areas, face, and scalp. Histologically, acantholysis and dyskeratosis characterize the disease. Herein, we report a case of a 59-year-old male patient with DD with the segmental presentation following blaschko lines. - Source: PubMed
Publication date: 2025/04/30
Aravind Prasanna MYogindher Singh RKaruna ManobalanLavanya M - Periodontitis is characterized by persistent immune-inflammatory responses and progressive alveolar bone loss, with macrophage polarization playing a pivotal role in shaping the local inflammatory microenvironment. Targeted immunopharmacological modulation of macrophage function, therefore, represents a promising strategy for controlling inflammation-associated tissue damage. Polydopamine (PDA), a multifunctional biomaterial with reported anti-inflammatory activity, has attracted increasing interest; however, the mechanisms underlying its immunomodulatory effects remain incompletely understood. In this study, we demonstrate that polydopamine nanoparticles (PDA NPs) effectively suppress lipopolysaccharide (LPS)-induced pro-inflammatory (M1) macrophage polarization while promoting an M2-like phenotype. Mechanistically, PDA NPs upregulate sarco/endoplasmic reticulum Ca-ATPase 2 (SERCA2), enhance Ca reuptake into the endoplasmic reticulum, and remodel intracellular calcium dynamics, thereby attenuating protein kinase R-like endoplasmic reticulum kinase (PERK)-mediated signaling and alleviating endoplasmic reticulum stress . Pharmacological inhibition of SERCA activity markedly reduces the regulatory effects of PDA NPs on calcium remodeling and macrophage polarization, indicating that SERCA2-associated calcium signaling contributes to PDA-induced immunomodulation. Functionally, PDA NPs-reprogrammed macrophages remodel the inflammatory paracrine environment and indirectly enhance the osteogenic differentiation of human periodontal ligament stem cells under inflammatory conditions in vitro. Collectively, these findings suggest that SERCA2-mediated calcium remodeling represents a potential immunopharmacological mechanism linking PDA nanoparticles to macrophage reprogramming. Moreover, the findings underscore the potential of PDA nanoparticles to simultaneously modulate inflammation and support osteogenesis in periodontal disease. - Source: PubMed
Publication date: 2026/04/26
Yang HongyiRan GaoyingChen YunbingLi XinpingZhang LifangGuo ZehongZeng Shuguang - The sarco(endo)plasmic reticulum calcium (Ca2+)-ATPase 2 (SERCA2) is a crucial regulator of cardiac muscle function that is sensitive to changes in the cellular environment, such as increased oxidative stress. This can be observed in heat stress experiments, where the thermal inactivation of SERCA is linked to an increased production of reactive oxygen species. Previous studies have shown that regulatory proteins, including phospholamban (PLN) and heat shock protein 70 (Hsp70), can physically bind to SERCA2, preserving its function in the face of heat stress. Furthermore, we have demonstrated that the inhibition of glycogen synthase kinase 3β (GSK3β) can alter the protein levels of PLN and HSP70 in cardiac tissues obtained from male mice; however, its potential downstream effects on the thermal inactivation of SERCA have not yet been investigated. In the present study, we examined the potential effects of GSK3β inhibition through six weeks of low-dose lithium chloride supplementation (LiCl, 10 mg/kg body mass/day via drinking water) on the thermal inactivation of left ventricle SERCA2 obtained from male C57BL/6J mice. Our results show that LiCl supplementation increased inhibitory serine 9 phosphorylation on GSK3β while also significantly raising SERCA2 content and the SERCA2:PLN ratio. There were no changes to Hsp70 with LiCl supplementation. Although LiCl decreased baseline maximal SERCA activity, the decline in activity in response to heat stress was less compared with control. In conclusion, GSK3β inhibition with LiCl is associated with protection of SERCA from thermal inactivation in the heart, and future studies should explore the underlying cellular mechanisms. - Source: PubMed
Hamstra Sophie IGeromella Mia SKlentrou PanagiotaTiidus Peter MMacPherson Rebecca E KFajardo Val A - The rising prevalence of opioid use during pregnancy poses serious public health concerns. The placenta is a critical organ during gestation, and opioid exposure can disrupt its function and fetal development. However, the molecular mechanisms through which opioids such as oxycodone affect feto-placental development remain poorly understood. This study aimed to investigate the effects of chronic in-utero oxycodone exposure on the composition and signaling functions of placenta-derived small extracellular vesicles (PSEVs) using a rat model. Extracellular vesicles (EVs) were isolated from placental tissue and characterized through nanoparticle tracking analysis, transmission electron microscopy, western blotting, and label-free quantitative proteomics. Bioinformatic enrichment analyses were conducted to evaluate changes in EVs biophysical properties and protein cargo. Chronic oxycodone exposure significantly altered PSEV characteristics, including particle size distribution and proteomic composition. Among the 456 identified EV proteins, 107 proteins were significantly dysregulated. We found key downregulatory proteins including Atp2a2, Lmna, Tgfb3, Agt, and Sgce, which are crucial for myocardial calcium cycling, nuclear integrity, extracellular matrix remodeling, and blood pressure regulation. These findings indicate disruptions in fetal cardiac programming, particularly hypertrophic and dilated cardiomyopathy pathways. Additionally, enrichment analyses revealed notable perturbations in metabolic processes (e.g., citrate cycle, fatty acid degradation, N-glycan biosynthesis), along with upregulation of vesicle transport and neurodevelopment-related proteins, indicating broader systemic effects on fetal development. While these proteomic findings are robust, further independent validation (e.g., via targeted assays or Western blotting) will be necessary to confirm individual protein-level changes. These results highlight PSEVs as sensitive molecular indicators linking maternal oxycodone use to disrupted fetal cardiovascular, metabolic, and neurodevelopmental pathways. This study provides a novel systems-level framework for understanding opioid-induced placental signaling alterations and lays the groundwork for developing EV-based diagnostic biomarkers and targeted interventions. - Source: PubMed
Publication date: 2026/02/10
Foroughi-Nezhad AminMoore DaliaSchaal Victoria LHediyal Tousif AhmedStone ElizabethKolli SreeAthota PranaviShukri OmarYelamanchili Sowmya VPendyala Gurudutt