Ask about this productRelated genes to: SLC8A3 Blocking Peptide
- Gene:
- SLC8A3 NIH gene
- Name:
- solute carrier family 8 member A3
- Previous symbol:
- -
- Synonyms:
- NCX3
- Chromosome:
- 14q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-12-09
- Date modifiied:
- 2016-10-05
Related products to: SLC8A3 Blocking Peptide
Related articles to: SLC8A3 Blocking Peptide
- Carcass composition traits, such as lean meat percentage, bone percentage, and number of ribs, are critical factors determining meat production and profitability of pigs. Traditional slaughter measurements are time-consuming, labor-intensive and invasive and cannot be evaluated on selection candidates. However, computed tomography scanning, a non-invasive technique, enables in vivo measurement of these traits, facilitating rapid accumulation of extensive phenotypic data. Despite these advances, the genetic mechanisms underlying computed tomography-based carcass traits remain largely unexplored. - Source: PubMed
Publication date: 2025/12/17
Han HeYu PengfeiZhang ZhenyangWei RanZhao WeiHou XiaoliangWang JianlanHe YongqiFu YanWang ZhenPan YuchunWang QishanZhang Zhe - Cognitive dysfunction frequently arises from androgen deprivation therapy (ADT), a primary treatment for men with prostate cancer. ADT affects key cognitive functions like memory, learning, reasoning, and decision-making. Extant studies lack a systematic evaluation of biomarkers related to ADT's cognitive impact. To address this, we used nano-liquid chromatography tandem mass spectrometry (nLC-MS/MS) to identify biomarkers in specific brain regions of a mouse model. Sixteen-week-old BALB/c mice received enzalutamide, a nonsteroidal antiandrogen, at 50 mg/kg/day via oral gavage 5 days a week for 8 weeks to simulate the ADT protocol. Control mice received a comparable volume of the vehicle. Enzalutamide treatment resulted in modest weight gain along with behavioral changes, including attention deficits and reduced social activity. F-fluorodeoxyglucose positron emission tomography (F-FDG PET) showed altered glucose metabolism in the brain and peripheral tissues of treated mice. Histological analysis of brain sections revealed preserved neuron structure in control mice, whereas enzalutamide-treated mice showed decreased neuron density, signs of neuron damage, and astrocyte swelling. Proteomic analysis of the cortex, cerebellum, and hippocampus after euthanasia identified 29 proteins with altered expression linked to cognitive dysfunction in ADT-treated mice. Further validation showed significantly increased levels of Pum2, Mcur1, Slc39a14, Fbxo7, Myo10, Arl6ip1, Slc8a3, Mt1, and Mt3 in the blood plasma of treated mice compared to controls. These results suggest that blood could be a valuable source of biomarkers for ADT-induced cognitive dysfunction. Further studies are needed to assess their clinical applicability in monitoring cognitive decline in prostate cancer patients on ADT and in neurotypical aging. - Source: PubMed
Publication date: 2025/11/28
Singh VaibhavVerma ShivShankar EswarSwain DiyaWillard Belinda BChao Herta HLi Chiang-Shan RLee ZhenghongMacLennan Gregory TPonsky Lee EGupta Sanjay - The chorioallantoic membrane (CAM) is essential for ion transport, acid-base homeostasis, and respiratory gas exchange during chicken embryonic development. The temporal expression of ion transporter-related genes in CAM is still inadequately investigated. This study examined the developmental regulation of genes associated with the transport of calcium (Ca), sodium (Na), bicarbonate (HCO ), potassium (K), protons (H), and chloride (Cl) in the CAM at embryonic days (ED) 12, 15, and 18. Six hundred fertilized Cobb 500 broiler eggs were obtained from a local hatchery. After candling, on ED 10, a total of 236 eggs were selected for this experiment. All the eggs were incubated in an automated temperature regulation of 37.5°C, 55% relative humidity (RH), and egg rotation every 2 h. On days 12, 15, and 18 of the embryonic period, CAM tissues were collected (n = 6 per group), total RNA isolated, and target genes were analyzed using qPCR. At ED 12, chloride transporter genes ( and ) were significantly upregulated compared to ED 18 ( < 0.05). At ED 15, calcium transporters ( and ) were significantly upregulated compared to ED 12 and/or ED 18 ( < 0.05). Sodium transporters ( and ), bicarbonate transporters ( and ), potassium transporters (, and proton transporters ( and ) were also significantly upregulated at ED 15 compared to ED 12 ( < 0.05). At ED 18, sodium transporter ( and ) and proton transporter () were significantly upregulated compared to ED 12 and/or ED 15 ( < 0.05). The results indicate a synchronized, stage-dependent transcriptional activation of ion transporter genes in the CAM, especially at the mid-embryonic stage. - Source: PubMed
Publication date: 2025/08/28
Amaz Sadid AlPoudel SumanJha RajeshMishra Birendra - Over the last two decades, there has been an increasing interest in understanding the mechanisms underlying neurogenesis as potential neurorestorative strategy triggered by ischemic preconditioning (IPC). Among these mechanisms, neuronal calcium homeostasis plays a fundamental role in supporting neurogenesis. Since sodium/calcium exchangers NCX1 and NCX3 are key effectors of IPC-mediated neuroprotection, this study aimed to investigate their contribution to the activation and maintenance of endogenous neurogenesis induced by IPC. Specifically, in an adult rat model of ischemic preconditioning, we examined whether: (1) IPC+tMCAO modulates the neurogenesis through NCX1 and NCX3 activation in subventricular zone (SVZ) and in the ipsilateral striatum; (2) NCX1 and NCX3 silencing may modulate the expression of "immature" neurons expressing the transcriptional factor NeuroD1 in SVZ; (3) the effects of IPC+tMCAO on the two isoforms, NCX1 and NCX3, are mediated by the transcriptional factor NeuroD1 expressed by "immature" neurons; (4) NeuroD1 directly binds ncx promoter evaluated by luciferase assay. Our findings revealed that, in the SVZ, IPC+tMCAO enhances at the same time either the expression of the neurogenesis marker, NeuroD1, and the expression of NCX1 and NCX3. Furthermore, the silencing of both NCX1 or NCX3 not only abolished the protective effects of IPC+tMCAO, but also impaired neuroblast proliferation, as NeuroD1 upregulation was completely suppressed. More interestingly, NeuroD1 directly binds ncx1 promoter, thus increasing its expression. Collectively, these results demonstrated that the transcriptional factor NeuroD1 regulates IPC+tMCAO-induced neurogenesis in the subventricular zone and in striatum by activating sodium/calcium exchanger ncx1, but not ncx3, in ischemic rats. - Source: PubMed
Publication date: 2025/08/01
Cuomo OrnellaViscardi VivianaBrancaccio PaolaAnzilotti SerenellaGuida NatasciaLombardi GiovannaFormisano LuigiEsposito RodolfoVinciguerra AntonioCampanile MarioD 'Esposito LuciaAnnunziato LucioPignataro Giuseppe - Lung cancer is the most common cancer and the leading cause of cancer-related deaths. Developing therapies for lung cancer is challenging, and new targets are urgently required. TFIIB-related factor 2 (BRF2) plays a crucial role in the development and progression of various tumors. However, the potential role of BRF2 in lung squamous carcinoma (LUSC) is unclear. Therefore, the aim of this study was to elucidate the mechanism of BRF2 regulation in LUSC development. Flow cytometry, protein blotting, and in vivo experiments were performed to assess the function of BRF2 in LUSC. Transmission electron microscopy imaging and mitochondrial membrane potential (MMP) measurements were used to determine the effect of BRF2 on mitochondria in LUSC. The impact of the downstream molecule SLC8A3 was predicted using bioinformatics analysis, and the mechanism was investigated by analyzing quantitative reverse transcription-polymerase chain reaction and immunoprecipitation (IP) assays, which were confirmed through rescue experiments. BRF2 expression was upregulated in squamous carcinoma cells, which increased SLC8A3 protein expression, promoted mitochondrial autophagy, stabilized MMP, and reduced apoptosis. In addition, SLC8A3 overexpression inhibited PTEN-induced putative kinase 1 (PINK1) binding to TIMM23 to promote mitochondrial autophagy and stabilize the MMP, which counteracted BRF2 knockdown-induced apoptosis. BRF2 mediated SLC8A3 expression to reduce apoptosis in LUSC cells by maintaining mitochondrial homeostasis. These findings provide novel selective therapeutic targets and ideas for the treatment of LUSC. - Source: PubMed
Publication date: 2025/07/03
Yi ShenQi XingLuo FeiWang DingxinFeng ZitongMa LuyuanYu WenhaoWang CongTian HuiLu Ming