ATP2A2
- Known as:
- ATP2A2
- Catalog number:
- 002172A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATP2A2
Related genes to: ATP2A2
- 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
Related products to: ATP2A2
Related articles to: ATP2A2
- Diabetes mellitus (DM) is a chronic metabolic disease characterized by hyperglycemia, and the diaphragm-the primary respiratory muscle-is adversely affected by this diabetic process. The aim of this study is to investigate the effects of zinc sulfate (ZnSO) treatment on diaphragm muscle contractile dynamics, calcium homeostasis, apoptosis, and fibrosis in an 18-month-old female Type 2 diabetic rat model. Thirty-two 18-month-old female Wistar rats were randomly divided into four groups: Control (CON), CON + ZnSO, Diabetes Mellitus (DM), and DM + ZnSO. The DM model was induced by a high-fat diet and administration of 30 mg/kg streptozotocin (STZ); after the disease was confirmed, ZnSO was administered intraperitoneally at a daily dose of 10 mg/kg to the treatment groups. The mechanical functions of the diaphragm muscle were evaluated using a post-rest potentiation protocol in an isolated organ bath; qPCR analyses (, , ) were performed to investigate cellular apoptosis, fibrosis, and calcium regulation. Compared with the CON group, the DM group exhibited a severe ~90% reduction in diaphragmatic contraction force (CF) and a ~97% decline in maximal contraction/relaxation velocities (±dF/dt) ( < 0.0001), which strongly correlated with a 30% suppression of gene expression ( < 0.01). Concomitantly, apoptotic (~2.6-fold) and profibrotic (~3.1-fold) mRNA levels were significantly elevated ( < 0.0001). In the DM + ZnSO group, daily zinc treatment (10 mg/kg/day, i.p. for 6 weeks, initiated 4 weeks after diabetes confirmation) did not reverse the elevated and expressions ( > 0.05). However, expression was fully preserved back to control levels ( < 0.05 vs. DM), leading to a substantial ~3-fold improvement in CF and velocities ( < 0.05 to < 0.0001 vs. DM). On the other hand, the healthy CON + ZnSO group exhibited a physiological slowing of contractility (~53% decrease in CF), without histological damage, likely due to a competitive antagonism between excess divalent zinc (Zn) and calcium (Ca) on myofilaments. Although zinc cannot reverse the structural apoptotic and fibrotic remodeling in the aged diabetic diaphragm, it successfully rescues functional contractility by preserving transcriptional expression. - Source: PubMed
Publication date: 2026/08/26
Unal OmerAkgun-Unal Nilufer - How cancers regulate endoplasmic reticulum (ER) pH and minimize ER stress remains unclear. Here we show that in breast cancer, these processes are governed by the anion channel GPR89. While normally localized to the Golgi, we find GPR89 is also present in the ER of tumor cells, where it collaborates with vacuolar H⁺ ATPase to regulate pH, and reduces ER stress via IRE1α-HSP47-XBP1s, ATF6 and ATP2A2 pathways. This ER localization of GPR89 drives a tumor-specific dependency, rendering breast cancer cells, but not normal tissues, dependent on this anion channel. Structural modeling and mutagenesis identify five key amino acids essential for GPR89's ER pH regulatory function and tumor cell survival. Consistent with its cancer-specific functions, GPR89 cooperates with Myc to accelerate mammary tumorigenesis. These findings uncover how breast cancers adapt to oncogenic stress by co-opting Golgi mechanisms of pH regulation to support ER homeostasis and survival. - Source: PubMed
Publication date: 2026/08/24
Ferro RiccardoCarroll AlexandraMendes-Pereira Ana MReen VirinderVlachogiannis GeorgeUceda-Castro RebecaKrastev DragomirAmodeo ValeriaPettitt StephenD'Uonno NadjaMavrommati IoannaNavarro BlancaHitchen LukeTrendell JenniferStojiljkovic AnaPrince CynthiaJanghra NarinderRoxanis IoannisGazinska PatrycjaLarcombe-Young DanielMarlow RebeccaAnnunziato StefanoJonkers JosKanitkar Tejashree RajaramXu AmadeusPatel NirmeshLiv NalanAlexander JohnQuist JelmarPardo MercedesRoumeliotis Theodoros IChoudhary Jyoti SWeekes DanielMarra PierfrancescoLoizou Joanna INatrajan RachaelGrigoriadis AnitaMadhusudhan Mallur SrivatsanHaider SyedLord Christopher JTutt Andrew - - Source: PubMed
Publication date: 2026/08/17
Bowling Holly MOberlin David M - - Source: PubMed
Publication date: 2026/09/09
Bai Jia Qi AdamAbubaker FarahMerchant InaayaGeng Ryan S QSood SiddharthaYeung JensenMufti Asfandyar - Copper oxide nanoparticles (CuONPs) are widely employed in industrial and biomedical applications; however, their long-term exposure induces severe cardiac impairments. Spiraeoside (SPD) is a naturally occurring flavonoid with diverse biological properties. The current study was designed to investigate the cardioprotective effects of SPD against CuONPs-induced cardiotoxicity. Thirty-two rats were randomly allocated into four groups: control, CuONPs (100 mg/ kg), CuONPs (100 mg/kg) + SPD (200 mg/ kg), and SPD (200 mg/kg) alone treated group. Our findings showed that CuONPs exposure substantially reduced the expression of ATP2A2, RYR2, CACNA1C, and GSK3B while upregulating CAMK2D, AXIN2, WNT3A, and CTNNB1. Moreover, CuONPs intoxication induced severe oxidative imbalance as evidenced by high levels of ROS and MDA while reducing the activities of GST, GSR, CAT, HO-1, SOD and GPx. Besides, CuONPs administration increased the levels of Troponin-I, LDH, Troponin-T, CRP, BNP, NT-proBNP, CPK, and CK-MB. Severe echocardiographic alterations were found after CuONPs exposure as indicated by significant reduction in heart rate, high EDV and ESV, as well as ventricular dilation. Similarly, CuONPs induced marked upregulation of pro-inflammatory markers including COX-2, IL-6, IL-1β and TNF-α. A significant upregulation of Bax, Caspase-3, and Caspase-9 while a marked reduction in the levels of Bcl-2 was found following the exposure of CuONPs. Histopathological analysis showed severe structural myocardial damage in response to CuONPs intoxication. Nonetheless, SPD notably protected cardiac tissues via regulating calcium-dependent signaling pathways, inflammatory and apoptotic responses, echocardiographic parameters, oxidative stress, and histopathological alterations. Collectively, these findings suggest that SPD is a promising natural bioactive molecule against cardiac injury caused by nanoparticles. All preclinical studies, such as pharmacokinetic, toxicological, and dose optimization investigation, are still needed to assess the potential clinical applicability. - Source: PubMed
Publication date: 2026/08/28
Arshad RameeshaMehreen ArifaJamil SalimHassan Hesham MHalawani Ibrahim FAlsharif Khalaf FAlzahrani Khalid J