LASS5 antibody - N-terminal region (ARP37810_P050)
- Known as:
- LASS5 (anti-) - N-terminal region (ARP37810_P050)
- Catalog number:
- arp37810_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- LASS5 antibody - N-terminal region (ARP37810_P050)
Related genes to: LASS5 antibody - N-terminal region (ARP37810_P050)
- Gene:
- CERS5 NIH gene
- Name:
- ceramide synthase 5
- Previous symbol:
- LASS5
- Synonyms:
- Trh4, MGC45411, FLJ25304
- Chromosome:
- 12q13.12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-11
- Date modifiied:
- 2015-08-27
Related products to: LASS5 antibody - N-terminal region (ARP37810_P050)
Related articles to: LASS5 antibody - N-terminal region (ARP37810_P050)
- Ceramide synthases (CerS) are key enzymes in sphingolipid metabolism that regulate fundamental cellular processes, including apoptosis, cell growth, and homeostasis. Among the six known mammalian isoforms (CerS1-CerS6), CerS5 has been particularly well studied for its involvement in the synthesis of the sphingolipid C16-ceramide. However, its expression, localization, and functional significance of CerS5 in the retina remain unclear. In the present study, we investigated the presence, distribution, and functional role of CerS5 in mouse retina using CerS5 knockout (KO) mice. We performed quantitative polymerase chain reaction, X-gal staining, and immunohistochemistry to analyze the expression and localization. Electroretinography (ERG) was employed to assess the impact of CerS5 deficiency on retinal function. Our results demonstrated that CerS5 is localized to the inner nuclear layer and ganglion cell layer, co-localizing with horizontal cells and specific subsets of amacrine and ganglion cells. The retina of CerS5 KO mice showed a reduction in overall thickness, with significant thinning observed in all retinal layers except the photoreceptor, whereas the outer plexiform layer showed increased thickness. Despite these structural alterations, ERG recordings revealed no significant changes in retinal function. These findings suggest that CerS5 contributes to the maintenance of retinal structural integrity, particularly through its presence in specific retinal cell types, whereas its loss does not markedly impair retinal function in adult mice. The observed structural alterations highlight its potential role in retinal physiology and possible implications for retinal pathophysiology, warranting further investigation into compensatory mechanisms by other ceramide synthase isoforms. - Source: PubMed
Song Soo-JinKoo Jae-HyunKim Hee-YeonPark Joo-WonPaik Sun-SookKim In-BeomShin Jung-A - Myopia is one of the most common eye diseases affecting children and adolescents, with its etiology often attributed to a combination of genetic and environmental factors. This study utilized single-cell RNA sequencing (scRNA-seq) technology to investigate gene expression differences between guinea pigs with spontaneous high myopia (SHM) and those with normal vision. - Source: PubMed
Publication date: 2026/07/02
Bao BoLiu JinpengXie YunxiaoXi RuofanSun YuecongYan JingzheXin JizhaoYang ZhaohuiYin XueweiGuo DadongBi Hongsheng - The TGF-β/Smad signaling pathway plays a central role in the pathogenesis of idiopathic pulmonary fibrosis (IPF) and is modulated by sphingolipid metabolism. Ceramide, a key intermediate in this pathway, is synthesized in various acyl-CoA chain lengths by ceramide synthases (CerS). However, the specific role of ceramide synthase 5 (CerS5) in pulmonary fibrosis remains unclear. Therefore, this study aimed to elucidate the role of CerS5 in fibrotic responses using human lung fibroblasts (HFL1), IPF-derived myofibroblasts (IPF-MyoFs), and a bleomycin-induced mouse model of pulmonary fibrosis. CerS5 knockdown attenuated TGF-β1-induced expression of α-smooth muscle actin (αSMA), collagen I, fibronectin, and phosphorylated Smad2/3 in both HFL1 cells and IPF-MyoFs. It also suppressed TGF-β1-induced nuclear translocation of Smad2/3. Notably, CerS5 knockdown reduced protein levels of Smad3 and Smad4 even in the absence of TGF-β1 stimulation. Smad4 knockdown replicated the effects of CerS5 knockdown by decreasing TGF-β1-induced expression of fibrotic markers, phosphorylated Smad2/3, and total Smad3 levels. In vivo, CerS5 knockout significantly reduced bleomycin-induced lung fibrosis and Smad3/4 expression. These findings suggest that CerS5 regulates fibrotic responses via modulation of Smad4 and the TGF-β1/Smad signaling pathway. Targeting CerS5 may therefore represent a promising therapeutic strategy for the treatment of IPF. - Source: PubMed
Publication date: 2026/06/02
Zhou YuanLi XinyiHirose HanaKadowaki RyoKohama TakafumiHiraki MotoyaKobayashi RyosukeHorii TakuroHatada IzuhoKasuya YoshitoshiNakamura Hiroyuki - A comprehensive bioinformatics analysis of the expression of sphingosine-related genes and prognosis of patients with head and neck squamous cell carcinoma (HNSCC) was performed using TCGA data and TIMER. A keyword search using sphingosine identified 29 genes, 10 of which were associated with patient survival. The expression of CERS2, CERS5, PLPP3, SGPP1, and S1PR4 significantly differed between tumors and normal tissue. A protein-protein interaction analysis revealed a dense network of these genes. Survival rates decreased in patients with the high expression of CERS2, CERS5, and SGPP1, and increased in those with the high expression of PLPP3 and S1PR4. An examination of the relationship between the expression of these five genes and classical clinical risk factors revealed that the high expression of CESR5 negatively correlated with survival for all classical clinical risk factors, while that of S1PR4 positively correlated with survival. The TIMER analysis showed that CERS5 and S1PS4 expression on tumor-infiltrating immune cells from HNSCC patients was associated with survival. Collectively, these results indicate the potential of CERS5 as a marker of a poor prognosis, and the contribution of S1PR4 to a favorable prognosis through its expression on immune cells. Therefore, the expression of sphingosine-related genes on tumor cells and infiltrating immune cells is important for the prognosis of HNSCC patients. - Source: PubMed
Publication date: 2026/05/21
Hamada MasakazuYura YoshiakiUzawa Narikazu - Coffin-Siris syndrome (CSS) is predominantly attributed to variants in ARID1B gene, however, the molecular pathways connecting ARID1B to myelination and neural development are not well elucidated. - Source: PubMed
Publication date: 2026/04/10
Yang XingkunGan ZhongzhiZhou YasiZhang MingmingWu ShuijuanHe FeiShen ZongruiMa ShunfeiSu XiXiong Fu