Ask about this productRelated genes to: Ano6 Blocking Peptide
- Gene:
- ANO6 NIH gene
- Name:
- anoctamin 6
- Previous symbol:
- TMEM16F
- Synonyms:
- DKFZp313M0720
- Chromosome:
- 12q12
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-07
- Date modifiied:
- 2019-04-23
Related products to: Ano6 Blocking Peptide
Related articles to: Ano6 Blocking Peptide
- To investigate the effect of β-Sitosterol on interleukin (IL)-1β-induced chondrocyte injury and the related mechanism. - Source: PubMed
Publication date: 2026/06/03
Zhang LeKong XiaochuanHong GangZheng YinfengZang Lei - TMEM63B belongs to the OSCA/TMEM63 family of mechanosensitive ion channels. We recently identified it as a mechanosensitive lipid scramblase activated by changes in membrane physical properties. Cryo-EM analysis revealed that recombinant mouse TMEM63B (mTMEM63B) protein adopts either closed or open conformations depending on the detergent environment, and that the monoclonal antibody YN9303-24 stabilizes the open state; however, the antibody epitope and the mechanism of antibody-dependent conformational regulation remained unclear. Here, using chimeric constructs, C-terminal truncations, and internal deletions, we mapped the YN9303-24 epitope to the intracellular C-terminal tail and identified the AQV motif (residues 773-775) as the core binding determinant. Functional analyses revealed that this C-terminal region is essential for maintaining TMEM63B in an inactive state under resting conditions. Deletion of the adjacent LQD motif (Δ776-778) or substitution of Leu776 with alanine induced strong constitutive lipid scrambling, evidenced by phosphatidylserine externalization and enhanced incorporation of fluorescently labeled phosphatidylcholine, whereas substitutions at Gln777 or Asp778 had minimal effects. Structural analysis positioned the AQVLQD motif adjacent to conserved intracellular helices in the open conformation, with Leu776 located near several hydrophobic residues. Together, these findings identify an autoinhibitory role for the C-terminal tail region in maintaining TMEM63B in an inactive state, suggesting that interactions between this tail and intracellular helices regulate the activity of this mechanosensitive lipid scramblase. - Source: PubMed
Publication date: 2026/06/04
Nishimura MegumiMiyata YugoShiraki YuKuribayashi RisaNomura NorimichiNishizawa TomohiroSegawa Katsumori - Bovine mastitis causes significant economic losses in the dairy industry. Emerging evidence highlights the critical role of long non-coding RNAs (lncRNAs) in inflammation-associated epigenetic regulation through competing endogenous RNA (ceRNA) networks. In this study, we established a bovine mastitis model in three healthy primiparous Holstein cows by intramammary infection with . Infected and control mammary tissue samples were then collected for transcriptomic profiling, which identified 2005 differentially expressed lncRNAs. Among them, BMNCR was significantly upregulated in -infected mammary tissues and -stimulated BMECs. We evaluated the coding potential of BMNCR and confirmed its non-coding nature. Functional studies in BMECs demonstrated that knockdown of BMNCR suppressed proliferation, promoted apoptosis, and altered the expression of inflammatory factors, including IL-2, IL-6, IL-8, and IL-12. Mechanistically, BMNCR acted as a sponge for bta-miR-145, thereby leading to the derepression of . Silencing partly recapitulated the effects of BMNCR knockdown, impairing proliferation and increasing IL-8 expression. Collectively, these findings suggest that the BMNCR/miR-145/ axis is involved in the regulation of inflammatory responses and epithelial homeostasis during bovine mastitis, with BMNCR functioning as a protective regulator in this process. - Source: PubMed
Publication date: 2026/05/08
Zhao TianqiLu XubinChu ShuangfengChen YadanZhou JiayiZhao FengqiSun YujiaYang Zhangping - Pancreatic cancer is a highly aggressive malignancy with a 5-year relative survival rate of only 13%. Current treatment options have limited efficacy, and mRNA vaccines offer a new direction for its treatment. However, how to accurately identify antigen targets that possess tumor specificity, functional relevance, and immunogenicity remains the key bottleneck restricting the clinical translation of mRNA vaccines for pancreatic cancer. Recent clinical studies have advanced KRAS mutant vaccines and personalized neoantigen mRNA vaccines, yet most rely on single antigens or highly individualized designs, limiting scalability and broader clinical applicability. In this systematic review, we integrated evidence from public databases and experimental studies to identify and evaluate 16 potential pancreatic cancer mRNA vaccine antigens (ADAM9, WNT7A, TMOD3, MET, EFNB2, TPX2, AGPS, OSBPL9, KDM5A, NRAS, SCP-1, GAGE, RAB5A, ANO6, CHMP2B, and PAK2). All candidates were initially selected based on aberrant tumor expression and further prioritized using stratification strategies incorporating antigen-presenting cell infiltration, immune-related cell death pathways such as ferroptosis and pyroptosis, and functional relevance to tumor progression. ADAM9 and PAK2 showed high expression in pancreatic cancer and strong associations with tumor proliferation, invasion, and immune regulation. SCP-1 and GAGE, as cancer-testis antigens, exhibited high tumor specificity and immunogenic potential. In addition, KDM5A and ANO6 may enhance antitumor efficacy through modulation of ferroptosis or pyroptosis. Nevertheless, several candidates remain constrained by normal tissue expression or limited mechanistic evidence. This review provides a stratified framework for antigen prioritization and highlights key challenges in pancreatic cancer mRNA vaccine development, offering guidance for future multi-antigen vaccine design and translational immunotherapy. - Source: PubMed
Publication date: 2026/04/28
Xue YuzheYu JiaqiZhou HongkunChen WeiChen QiHu LingyuLuo RunzhouChen YingjingWang XiaoguangHe Xuesong - TMEM16F is a calcium-activated membrane protein that functions as both a non-selective ion channel and a phospholipid scramblase, linking intracellular Ca²⁺ signaling to dynamic regulation of plasma membrane lipid asymmetry. Recent studies have substantially advanced our understanding of TMEM16F structure and regulation, revealing pronounced conformational heterogeneity and allosteric mechanisms through which Ca²⁺, pH and membrane context coordinate its dual functions. Cell- and tissue-specific analyses indicate that TMEM16F-mediated membrane remodeling contributes to diverse physiological processes, including blood coagulation, cell-cell fusion, regulated cell death, immune responses, and neurodevelopment. Dysregulation of TMEM16F activity has been associated with a broad spectrum of pathological conditions, ranging from bleeding disorders and thromboinflammation to neurodegeneration, infection-associated tissue damage, and cancer. This review integrates recent structural, cellular and pathological insights to provide a comprehensive overview of TMEM16F biology, highlighting mechanisms underlying its dual functions and summarizing emerging evidence for its roles in health and disease. - Source: PubMed
Publication date: 2026/05/07
Chen LiQian Zhigang