ATP4B
- Known as:
- ATP4B
- Catalog number:
- 002182A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATP4B
Related genes to: ATP4B
- Gene:
- ATP4B NIH gene
- Name:
- ATPase H+/K+ transporting subunit beta
- Previous symbol:
- -
- Synonyms:
- ATP6B
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-26
- Date modifiied:
- 2018-04-23
Related products to: ATP4B
Related articles to: ATP4B
- Intrinsic resistance to anti-PD-1 immunotherapy remains a major obstacle in treating metastatic gastric cancer (GC), particularly in tumors harboring concurrent YAP hyperactivation and TP53 loss. Here, using a genetically engineered mouse model with conditional YAP hyperactivation and Tp53 deletion in gastric Atp4b cells (AYP), we show this "double-hit" alone suffices to recapitulate human refractory GC, including histopathological heterogeneity, multi-organ metastasis, and intrinsic PD-1 resistance. We identified BST2 as a direct YAP-TEAD transcriptional target. In human GC, BST2-high tumor correlates with poor anti-PD-1 response. Mechanistically, tumor cell-derived BST2 engages the inhibitory receptor PIRA2 on neutrophils and liver Kupffer cells, instructing an immunosuppressive, pro-metastatic phenotype that inhibits T cells antitumor response and confers PD-1 resistance. Therapeutically, dual BST2/PD-1 blockade in the AYP model suppresses primary tumor growth and eradicates established liver metastases. Thus, YAP activation, cooperating with TP53 loss, fuels metastatic GC and immunotherapy resistance via BST2 induction. - Source: PubMed
Publication date: 2026/09/21
Zhang WeihongWang ShilongWang MengYu RuixianYue JingwuShao LinZhang HuiZhu MengwenTian LuyangCheng ShutingQin WeiminTang YangHan YiWang WenjiaAn LiweiMeng YanJiao ShiZhou Zhaocai - Renal cell carcinoma (RCC) is characterized by profound inter- and intratumoral heterogeneity and extensive tumor microenvironment (TME) remodeling, yet the spatially resolved cellular programs and intercellular communication networks orchestrating malignant progression remain poorly defined. LMX1B, a LIM homeodomain transcription factor essential for kidney morphogenesis, has not been previously investigated in renal carcinogenesis. - Source: PubMed
Publication date: 2026/09/18
Liu YuSong LiangFeng YuankangZhang SongxinHan XuTan YouzhiLi NingyangWang YingjinSun ShaoliangGao JingweiZhang LongJia ZhankuiYang Jinjian - Kidney stone disease is a common metabolic disorder with high recurrence rates and an associated risk of chronic kidney disease, while proton pump inhibitors (PPIs) are widely used medications with potential links to renal complications. Previous observational studies have suggested an association between PPI use and kidney stones, but the causal relationship remains unclear. This study aimed to investigate the causal effect of PPIs on kidney stones using the Mendelian randomization (MR) analysis. - Source: PubMed
Publication date: 2026/03/18
Jiang YaohuiLin LedeCheng ChaoZhou Liang - Although the global incidence of gastric cancer (GC) has declined over the past 5 years, it remains the fourth leading cause of cancer-related mortality worldwide. Given the molecular heterogeneity of GC, survival outcomes can vary significantly among patients receiving the same treatment at the same stage. Therefore, this study aimed to develop and validate a robust prognostic model for GC that complements the current staging system, to ultimately facilitate better clinical decision-making. - Source: PubMed
Publication date: 2026/02/25
Li MusuSun YueZhang LiaoweiLu ZixuanWo HongmeiShao FangTang ShaowenZhao YangDai JunchengYi Honggang - The vertebrate stomach is responsible for the secretion of hydrochloric acid (HCl) and is the first site of protein digestion in the gut. The secretion of HCl occurs through the gastric proton pump, a hydrogen-potassium ATPase (HKA) composed of α and β subunits encoded by the ATP4A and ATP4B genes, respectively. In the past, the evidence for the role of the gastric acid secretion in nutrient digestion and absorption, growth and postprandial energy metabolism has been gathered using indirect methods such as diet modulation experiments, or the use of proton-pump inhibitors. These methods may introduce confounding factors and lead to erroneous conclusions. With the aim of directly observing the role of the gastric proton pump, we have generated a knockout model using targeted gene editing. Using atp4a-null Astyanax mexicanus, we examined the growth rate, nitrogen and energy metabolism, and nutrient assimilation in the presence and absence of gastric acidification. Our results show no effect of knockout on growth or appetite, but a significant reduction in post-prandial nitrogen excretion and oxygen consumption (specific dynamic action). Furthermore, atp4a-/- animals had significantly less body magnesium, calcium, phosphorus and protein, while having more lipid in their carcasses. Importantly, administration of proton-pump inhibitors suppressed growth in both experimental groups, indicating possible off-target effects of these drugs. This study is the first to directly examine the impact of gastric acidification on body composition, growth and metabolism and offers new and targeted evidence on the importance of stomach acidification for gut and digestion homeostasis. - Source: PubMed
Publication date: 2026/04/30
Ferreira Patrícia GomesFlávio HugoWilson Jonathan M