Ask about this productRelated genes to: ATP2B3 antibody
- Gene:
- ATP2B3 NIH gene
- Name:
- ATPase plasma membrane Ca2+ transporting 3
- Previous symbol:
- SCAX1, CLA2
- Synonyms:
- PMCA3, CFAP39
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-10
- Date modifiied:
- 2016-02-10
Related products to: ATP2B3 antibody
Related articles to: ATP2B3 antibody
- Cancer cell characteristics are determined by gene expression, influenced by genomic, epigenetic, and transcriptional modifications. Genomic rearrangements and transcriptional splicing can result in the formation of fusion genes. BCR-ABL1 is an established fusion gene employed as a biomarker in leukemia. A single gene can amalgamate with several other genes and may impact cellular fate. Ethnicity-specific variants of fusion genes have been identified, such as the TMPRSS2-ERG variation observed in prostate malignancies among African-American, Caucasian, and Japanese populations in research studies. Next-generation sequencing has provided a new method for predicting genomic and transcriptomic changes. We aim to identify fusion genes in the Indian population using cancer samples to enhance diagnostic outcomes. This study performed a meta-analysis of tumor-specific RNA sequencing data for liver, tongue, and ovarian cancers, which are available online. It identified known fusion genes, including TRO-MAGED2, KRT14-S100A9, RNASE10-CD38, ACTN4-ACTN1, RGPD1-RANBP2, CTSC-RAB38, C15orf57-CBX3, AMBRA1-CKAP5, ATP2B3-ATP2B4, CNKSR3-IPCEF1, E2F4-RPL14, and MZT2A-MZT2B, along with 101 novel fusion genes. Novel fusion genes GABRP_SCGB3A2 and WWOX_FUT1 were identified in all three tumor tissues. GABRP acts as a tumor inducer, whereas SCGB3A2 functions as a tumor suppressor. WWOX2 serves as a tumor suppressor, whereas FUT1 functions as a promoter of malignancy. The interplay between tumor inducers and suppressors may serve as a survival mechanism for cancer cells, a subject that has received limited research attention. - Source: PubMed
Publication date: 2026/02/09
Yadav RahulKhan HafsaSingh PoonamKumar PramodKumar Singhal Dinesh - The Brazilian population represents a mosaic of genetic diversity resulting from admixture ancestries. Given reported disparities in primary aldosteronism (PA) genetics across ethnicities, we investigated the genetic spectrum of aldosterone-producing adenomas (APAs) and nodules (APNs) with classical histology in a Brazilian cohort. - Source: PubMed
Publication date: 2026/01/07
Guimaraes Augusto GGoldbaum Tatiana SLedesma Felipe LFreitas-Castro FelipeSantana Lucas SSobrinho Jose Antonio B LRossetti Lucas BOkubo JessicaKawahara Eduardo ZBortolotto Luiz ASrougi VictorTanno Fabio YNahas Williams CChambo Jose LPereira Maria Adelaide APio-Abreu AndreaSilva Giovanio VDrager Luciano FFragoso Maria Candida B VLatronico Ana ClaudiaMendonca Berenice BZerbini Maria Claudia NAlmeida Madson Q - Normal spermatogenesis in Mongolian horses depends on the mitotic division of spermatogonia, two successive meiotic divisions, and the morphological transformation of spermatids into mature spermatozoa. The gene is involved in the meiosis cycle and is required for normal chromosome association during meiosis. Previous studies have shown that alternative splicing of may promote spermatogenesis in Mongolian horses. In this paper, the regulatory effects of different alternative splicing events on Mongolian horse spermatogenesis are investigated. - Source: PubMed
Publication date: 2025/11/28
Song DailingWang GuoqingBaterin TerigeleWeng YajuanDugarjaviin ManglaiLi Bei - Genetic abnormalities in ion channels that regulate the depolarization of adrenal glomerular cell plasma membranes have been identified as a cause of primary aldosteronism (PA) due to aldosterone-producing adenoma (APA). This study aimed to evaluate somatic variants in the KCNJ5, CACNA1D, CLCN2, ATP1A1, ATP2B3, GNAQ, GNA11, and CTNNB1 genes, assess the genotype-phenotype correlation, and analyze the outcomes in patients with APA from a heterogenic ethnic population. - Source: PubMed
Publication date: 2025/11/06
Maeda Leonardo KMermejo Livia MFernandes-Rosa Fabio LMoreira Ayrton CAntonini Sonir Rde Margaret - Primary aldosteronism (PA) is composed of different aldosterone-producing lesions including aldosterone-producing adenoma (APA), aldosterone-producing micronodules (APM), aldosterone-producing nodules (APN) and aldosterone-producing diffuse hyperplasia (APDH), all of which could result in hypertensive status and electrolyte imbalances. These aldosterone-producing lesions above are frequently accompanied by somatic mutations, including those of KCNJ5, CACNA1D, ATP1A1, and ATP2B3. APA is a neoplasm which frequently harbors KCNJ5 somatic mutations in tumor cells, especially those arising in East Asian patients. Histologically, APAs with KCNJ5 and ATP2B3 mutations presented with more clear cells, whereas those with ATP1A1 and CACNA1D mutations with more compact cells. In addition, the expression levels of steroidogenic enzymes such as aldosterone synthase (CYP11B2) in APAs varied among those with different patterns of somatic mutations, suggesting a potential association between specific mutations and altered aldosterone synthesis in APAs. In contrast, CACNA1D mutation was the most frequent subtype in non-neoplastic lesions including APM and APN, suggesting the possible correlation of KCNJ5 mutation with neoplastic aldosterone-producing lesions. This review provides pivotal insights into the histopathological diversity of aldosterone-producing lesions in PA patients and emphasizes the significance of genetic mutations in constituting the histological landscape of the lesion in order to better understand the detailed pathogenesis of primary aldosteronism. - Source: PubMed
Publication date: 2024/10/15
Gao XinYamazaki YutoOno YoshikiyoSatoh FumitoshiLi FapingZhou HonglanSasano Hironobu