Ask about this productRelated genes to: ATP2B4 antibody
- Gene:
- ATP2B4 NIH gene
- Name:
- ATPase plasma membrane Ca2+ transporting 4
- Previous symbol:
- ATP2B2, MXRA1
- Synonyms:
- PMCA4
- Chromosome:
- 1q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-10-05
- Date modifiied:
- 2016-02-10
Related products to: ATP2B4 antibody
Related articles to: ATP2B4 antibody
- To describe the available research on genetic determinants with special emphasis on the developmental dysplasia of the hip (DDH), in Saudi Arabia and Gulf nations, with reference to the genetic variants, family trend, and environmental factors. - Source: PubMed
Publication date: 2026/08/06
Alrashdi Naif ZAlmansour Ahmed MJamal Azfar - Age-related hearing loss and balance decline are prevalent features of organismal aging, yet how the cochlea and vestibular organs converge on shared cellular liabilities remains insufficiently resolved. In particular, whether mitochondrial ultrastructural injury and mitochondrial quality-control programs co-vary with synaptic vulnerability and sensory functional decline across these systems within an age-resolved framework has not been clearly delineated. Here, we compared cochlear and vestibular aging in SAMP8 mice of different ages using integrated functional assays, region-resolved quantification of hair cells and CtBP2/GluA2 synapses, cochlear NF200+ fiber area fraction, transmission electron microscopy, and targeted qPCR of mitophagy/autophagy-lysosome genes. The results show that ABR thresholds rose progressively across 5.6-32 kHz. VsEP exhibited age-dependent threshold shifts and prolonged P-wave latency. Relative to the magnitude of synaptic and functional changes, cochlear hair-cell numbers were broadly preserved, although regional OHC loss was observed in middle-to-basal turns, whereas vestibular macular hair-cell density declined with age. Ultrastructurally, the proportion of pathological mitochondria increased with age, featuring electron-lucent matrix, disrupted cristae organization, and rounded/swollen profiles. What's more, guided by an adult-versus-aged transcriptomic screen nominating the Ca extrusion gene Atp2b4, we derived z-scored molecular indices, including a flux-burden signature (z(p62)-z(Lc3b)) and a TFEB-lysosome module. Descriptive coupling across age-group means indicated that mitochondrial pathology burden aligned closely with high-frequency ABR loss and basal synaptic uncoupling, and tracked the flux-burden signature more consistently than the TFEB-lysosome module. Together, these findings support age-aligned associations among mitochondrial ultrastructural injury, molecular remodeling, synaptic vulnerability, and progressive sensory decline across cochlear and vestibular systems. - Source: PubMed
Xie JingyiZhang XujiaTian JinyiYan YuluShi KePan YongqiZhang YanniChen ZichenSun JianbinLv HuiChen JingguoRen XiaoyongKamogashira TeruZhang XiaotongGao Ying - Transcription factors are modulated by a precisely coordinated set of conditions, including cell context, target sequences and their accessibility, and co-factor recruitment. Disruption to any of these conditions can dramatically affect transcription factor activity, but quantitatively characterizing the consequences of individual mutations-either in the transcription factors themselves or in their target sequences-has remained a technical challenge. Zambo et al. present an innovation on their native holdup assay that measures DNA-protein binding activity under physiologic or near-physiologic conditions and use mutant GATA1-ATP2B4 binding as an illustrative example. This technique holds promise for uncovering the molecular mechanisms underlying genetically-driven diseases. - Source: PubMed
Publication date: 2026/06/01
Takasaki Kaoru - The intrinsic radio-resistance of pancreatic cancer cells significantly hinders therapeutic efficacy. However, the precise molecular mechanisms underlying this resistance remain inadequately understood and warrant further investigation. Here, using the high-throughput metabolic CRISPR library screening and RNA sequencing, we identified an ATPase Plasma Membrane Ca Transporting 4 (ATP2B4) as a novel molecular contributor to radiotherapy resistance in pancreatic cancer both in vitro and in vivo. Functionally, micrococcal nuclease assay, drug rescue assays, along with overexpression and silencing experiments, revealed that knockout of ATP2B4 induced chromatin decompaction through the downregulation of histone H1.0, thereby exacerbating DNA damage and increasing RT-induced cell apoptosis. Mechanistically, TurboID-based mass spectrometry and immunoprecipitation (IP) demonstrated that ATP2B4 stabilized ELAVL1, maintaining its function, which further regulated the mRNA stability of histone H1.0. Taken together, our findings identified ATP2B4 as a key regulator of chromatin compaction and DNA damage response, positioning it as a potential biomarker for predicting RT outcomes and a promising therapeutic target for overcoming RTR. - Source: PubMed
Publication date: 2026/05/25
Luo YuyuJiang WeiLiu YanfangLi QinghuaChen YuanfeiLin ShiwanTsai Hsiang-IZhang LirongWang DongqingLiao XiangZhu Haitao - BACKGROUND: Prostate cancer (PCa) clinical management is challenged by tumor heterogeneity, driving the need for robust prognostic biomarkers, with altered glutamine metabolism emerging as a promising target. This investigation aimed to construct a metabolism-based prognostic signature for PCa and translate it into a targeted nanotherapeutic strategy. METHODS: Transcriptomic data from The Cancer Genome Atlas (TCGA) were analyzed to identify dysregulated glutamine metabolism genes and construct a prognostic model via univariate Cox, LASSO, and multivariate Cox regression with validation in an independent cohort. The model’s characteristics were assessed through tumor microenvironment (TME), tumor mutation burden (TMB), and consensus clustering analyses. The pivotal gene of the model was selected to functionally validate in vitro through proliferation, clonogenicity, migration, and invasion assays. To exploit this vulnerability, a CB/CDDP@lipo nanoplatform was engineered to co-deliver cisplatin and glutaminase inhibitor CB-839, with evaluation in PCa models in vitro and in vivo. RESULTS: A novel five-gene prognostic signature (ASNS, ATP2B4, GLYATL1, SLC6A20, SLC7A9) was established and stratified PCa patients into high- and low-risk groups based on progression-free interval (PFI). High-risk patients exhibited an immunosuppressive TME, higher TMB and TP53 mutations, and activation of proliferation-related pathways. Functional validation identified ASNS as a key oncogenic driver, enhancing PCa tumor cell proliferation, migration, and invasion. Therapeutically, CB/CDDP@lipo nanoplatform demonstrated potent synergistic cytotoxicity by depleting glutathione (GSH) and amplifying oxidative stress. This dual-action mechanism triggered significant apoptosis and tumor suppression with a favorable safety profile. CONCLUSIONS: Our study establishes a glutamine metabolism-based prognostic signature, pinpointing ASNS as a key driver. The resulting CB/CDDP@lipo nanoplatform offers a promising chemo-metabolic strategy for enhanced PCa treatment. - Source: PubMed
Publication date: 2026/04/18
Li WenyaGe WeiyingNi WenjieZhang HaoGuo YangyangXie YuxinZhou ZhenLi YimingZheng ZheLi JianminZhao Yang