ACER1
- Known as:
- ACER1
- Catalog number:
- 001004A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ACER1
Ask about this productRelated genes to: ACER1
- Gene:
- ACER1 NIH gene
- Name:
- alkaline ceramidase 1
- Previous symbol:
- ASAH3
- Synonyms:
- -
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-29
- Date modifiied:
- 2015-09-21
Related products to: ACER1
Related articles to: ACER1
- SKH-1 hairless mice were used as the in vivo model in this study to evaluate the efficacy of oral snail extract powder (SEP) on skin hydration and barrier enhancement. The skin serves as a primary barrier against external stimuli and plays a critical role in maintaining water homeostasis. Optimal skin hydration is essential for preserving barrier integrity and preventing dermatological conditions such as xerosis and atopic dermatitis. Although edible snail has demonstrated moisturizing effects when applied topically, its efficacy following oral administration has not been sufficiently characterized. In this study, we evaluated the moisturizing efficacy and safety of orally administered edible snail extract powder in SKH-1 hairless mice. Animals were divided into a control group and three treatment groups receiving 20, 40, or 80 mg/kg B.W. of SEP daily for 13 weeks. Skin hydration and transepidermal water loss (TEWL) were measured periodically throughout the experiment. To investigate the underlying mechanisms, we analyzed the mRNA expression of genes related to hydration and barrier function, quantified skin hyaluronic acid (HA) levels via ELISA, and performed immunohistochemical staining. Oral SEP administration increased skin hydration and decreased TEWL, suggesting improved barrier function. Gene expression analyses revealed upregulation of Has1-3, Col1a1, Col3a1, Tgf-β1, Flg, and Cers2, along with downregulation of Hyal1 and Acer1. These effects were supported by higher hyaluronic acid content and confirmed by altered protein expression of HAS2, HYAL1, and TGF-β1. No significant changes were observed in body weight, food intake, or organ weights, and no adverse effects were observed at tested doses, supporting the safety of oral SEP administration. Overall, these findings suggest that orally administered SEP improves skin hydration and strengthens barrier integrity by regulating both molecular and tissue-level pathways, highlighting its potential as a functional food ingredient for skin health. - Source: PubMed
Publication date: 2025/10/16
Lee ChaerinBaek SeoyoungLim WonchulLim Tae-Gyu - Psoriasis is an inflammatory disorder characterized by scaly erythematous plaques and significant comorbidities. Recent studies have suggested that impaired mitophagy, the cellular mechanism for removing dysfunctional mitochondria, may contribute to the pathogenesis of psoriasis. - Source: PubMed
Publication date: 2025/07/01
Yu ShanshanLong FangyuanYan HuiXu YongfangLi JunHao Zhimin - In atopic dermatitis (AD), epidermal disease hallmarks are driven by a complex cutaneous inflammatory milieu that varies between patients. How these variable inflammatory signals affect cellular and molecular epidermal AD phenotypes is difficult to study in vivo. - Source: PubMed
Publication date: 2025/05/21
Meesters Luca DRoubroeks Janou A YGerritsen ArankaVelthuijs NielsKlijnhout Jaimy ALaberthonnière Camillevan Vlijmen-Willems Ivonne MHübenthal MatthiasRodijk-Olthuis DianaPeters Rens H WRikken GijsSzymczak SilkeFyhrquist NannaAlenius HarriWeidinger StephanSmits Jos P HMhlanga MusaZhou HuiqingNiehues Hannavan den Bogaard Ellen H - Given the absence of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (Her-2) in triple-negative breast cancer (TNBC) cells, the efficacy of targeted therapies is limited. In this study, we uncovered that triptolide (TP) effectively suppresses the migration and invasiveness of MDA-MB-231 cells by activating autophagic pathways. Western blotting analysis revealed that TP significantly reduced the expression levels of p62 protein, while simultaneously markedly increasing the expression levels of LC3B-II, BNIP3, BNIP3L, ATG5, and ULK1 proteins, strongly suggesting an enhancement of autophagic activity in the cells. Based on PCR array screening, we identified the ACER1 gene as exhibiting notable expression alterations post-TP treatment. Overexpression of ACER1 gene enhanced the TP-induced apoptosis in MDA-MB-231 cells and augmented the regulation of autophagy-related proteins p62 and LC3B-II, leading to an increase in autophagosome numbers and a marked reduction in cellular migration and invasiveness. Conversely, ACER1 gene knockdown reversed these effects. In vivo experiments demonstrated that TP effectively inhibits the growth of MDA-MB-231 xenograft tumors, concurrently upregulating ACER1 and LC3B-II expression in tumor tissues, while p62 protein levels were notably decreased. Hematoxylin and eosin (H&E) staining results indicated no evident toxicity in liver and kidney tissues of BALB/c mice at a TP dose of 0.4 mg/kg. This study, for the first time, elucidates a novel mechanism by which TP inhibits TNBC through an autophagic process mediated by ACER1. - Source: PubMed
Publication date: 2025/01/27
Huang LingyueXue RuiZhu MingfeiXu SiyuanLuo YuqinQin ChulingYang ChangJia LuluTang KeTan Qinyou - Skin disorders occur more frequently with sodium-dependent glucose cotransporter type 2 (SGLT2) inhibitors than with other antidiabetic drugs. We conducted basic research using ipragliflozin, with the aim of identifying new measures to prevent skin disorders caused by SGLT2 inhibitors. - Source: PubMed
Publication date: 2024/12/22
Ikarashi NobutomoTabata KeitoShinozaki YuiKon RisakoSakai HiroyasuHosoe Tomoo