ACCN4
- Known as:
- ACCN4
- Catalog number:
- 000997A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACCN4
Related genes to: ACCN4
- Gene:
- ASIC4 NIH gene
- Name:
- acid sensing ion channel subunit family member 4
- Previous symbol:
- ACCN4
- Synonyms:
- BNAC4
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 2003-06-05
- Date modifiied:
- 2016-10-05
Related products to: ACCN4
Related articles to: ACCN4
- Although light broadly affects animal physiology, it remains unclear whether specific wavelengths directly reshape basal glucose and lipid metabolism in developing non-visual photoreceptive animals, and what specific molecular pathways mediate these effects. Here, using Caenorhabditis elegans (C. elegans), a model lacking visual organs but retaining conserved metabolic pathways, we systematically evaluated metabolic phenotypes following early-life (L1 to young adult) exposure to red, green, blue, and white light spectra. We identified that blue light (450-460 nm) most strongly drove triglyceride accumulation and free glucose elevation, with the L4-to-young adult transition being the most susceptible developmental window. Mechanistically, blue light induced oxidative stress and mitochondrial dysfunction; antioxidants limited glucose and lipid abnormalities and reshaped physiology, establishing a functional role for ROS. Integrated multi-omics revealed that elevated ROS upregulated the DEG/ENaC family channel acd-1 and promoted the accumulation of an oxidized lipid metabolite feature putatively annotated as 12(13)Ep-9-KODE (EKODE), which was functionally evaluated as a candidate downstream oxidized lipid mediator associated with ACD-1-dependent metabolic remodeling. Moreover, chemically induced oxidative stress similarly upregulated both acd-1 mRNA expression and the abundance of this EKODE-annotated oxidized-lipid feature. Notably, in mammalian cells, overexpression of the human homolog ASIC4 or exogenous EKODE supplementation recapitulated key metabolic features, including lipid-droplet accumulation, triglyceride elevation, and coordinated bioenergetic remodeling. Together, our findings support a ROS-dependent ACD-1-associated oxidized lipid regulatory module in C. elegans and reveal how early-life blue light and oxidative challenges influence metabolic homeostasis. - Source: PubMed
Publication date: 2026/09/18
Zhu YaoLiu XinruJiao YiQiu YaminLiu Chang - Analysis of body fluids obtained from crime scenes provides important information for directing criminal investigations. Generally, chemical and immunological techniques, along with molecular methods that utilize RNA, are used for body fluid identification. However, these methods have some limitations, such as handling difficulty, sample consumption, false-positive or -negative results, and sample instability. To address these problems, several researchers have utilized DNA methylation for body fluid identification, including microarrays, combined bisulfite restriction analysis, single-base extension, and pyrosequencing. Although these methods have the advantage of simultaneously analyzing multiple target sites at the same time, they require considerable time and cost. In this study, a methylation-specific PCR (MSP)-based method was used to simultaneously discriminate between three human body fluids (semen, saliva, and blood). We designed primers with different amplicon sizes for each specific CpG region in the three body fluids ( for semen, for saliva, and for blood). For the accurate analysis, methylation and unmethylation primers were used separately for different amplifications. This MSP-based method can discriminate body fluids in unknown samples, although caution is required when analyzing mixed or low-quantity DNA samples. Our multiplex MSP-based approach enables confirmation of human body fluids and may provide a potentially simpler workflow compatible with conventional capillary electrophoresis platforms compared with methods such as the SNaPshot assay. We anticipate that this multiplex PCR system will be helpful in criminal investigations. - Source: PubMed
Publication date: 2026/04/21
Yu Kyeong-MinAhn Eu-ReePark Myung JinPark Hyun-Chul - BACKGROUND: Immune evasion is a major cause of the poor efficacy of therapies for pancreatic ductal adenocarcinoma (PDAC). However, the underlying mechanism by which MHC-I downregulation leads to low infiltration of cytotoxic T lymphocytes in PDAC remains incompletely elucidated. This study aims to identify the molecules responsible for the low expression of MHC-I and potential novel therapeutic targets, thereby providing a theoretical foundation for reversing immune evasion in pancreatic cancer. METHODS: Bioinformatic analysis identified the acid-sensing ion channel (ASIC4) as a key factor associated with low cytotoxic T lymphocyte (CTL) infiltration in pancreatic ductal adenocarcinoma (PDAC). The correlation between ASIC4 expression and patient prognosis was analyzed via immunohistochemistry (IHC). To elucidate the molecular mechanism by which ASIC4 mediates immune evasion in PDAC, we comprehensively utilized Western blotting, co-immunoprecipitation, and immunofluorescence. An orthotopic PDAC mouse model was established to assess the impact of ASIC4 deletion on CD8⁺ T cell infiltration and tumor growth in vivo. RESULTS: The study found that in pancreatic ductal adenocarcinoma (PDAC), the expression of ASIC4 was significantly upregulated and negatively correlated with the low expression of Major Histocompatibility Complex class I (MHC-I), which was associated with poor patient prognosis. Notably, knocking down ASIC4 led to a significant increase in CD8+ T cell infiltration and slowed tumor growth in vivo. Mechanistic investigations revealed that ASIC4 knockdown restored total and surface levels of MHC-I by inhibiting its autophagic-lysosomal degradation. CONCLUSION: This study revealed that ASIC4 is highly expressed in PDAC, and its elevated expression is significantly associated with poor prognosis in pancreatic cancer patients. Further mechanistic investigations demonstrated that ASIC4 promotes the degradation of MHC-I via the lysosomal pathway. The subsequent reduction in MHC-I expression leads to decreased infiltration of cytotoxic T lymphocytes (CTLs), ultimately accelerating pancreatic cancer progression. Silencing ASIC1 restored MHC-I expression and enhanced the antitumor efficacy of CD8⁺ T cells. These findings identify ASIC4 as a potential therapeutic target and provide a theoretical foundation for reversing the immune-cold phenotype of PDAC and developing combined immunotherapy strategies. - Source: PubMed
Publication date: 2026/02/24
An QiAn ZhongwuBo WeiboYan ChaochunSun NanMa JianxinLi JianyeWang Wenjuan - Menopausal syndrome (MPS) is a symptom of physical and psychosomatic abnormalities that women may face around the time of menopause. Hot flashes are the main symptom. Paeonia lactiflora extract (PLE) is the active ingredient extracted from . It can be used to treat MPS, such as hot flashes. However, its pharmacologic mechanism is unclear. - Source: PubMed
Publication date: 2025/07/22
Cui WeilinSong TingtingGao DongmeiWang XiaoyuSun YaFu LiyuHan YichaoWang Jieqiong - Lower-grade glioma (LGG) is a molecularly heterogeneous tumor in which acidic microenvironments and immune interactions critically influence prognosis. Acid-sensing ion channels (ASICs), particularly ASIC1, remain understudied in glioma biology despite their pH-sensing roles. This study investigates ASIC1/ASIC4 in LGG prognosis, immune regulation, and molecular subtyping. - Source: PubMed
Publication date: 2025/07/25
Mao KeleiGuo AngyangLi YizeYang WendiXiong YiduoWang WeiYan Xiaodong