Cers6-KO 基因敲除小鼠

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产品名称

Cers6-KO 基因敲除小鼠

产品编号

S-KO-07299

品系全称

C57BL/6JCya-Cers6em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-241447-Cers6-B6J-VA

品系状态

使用本品系发表的文献需注明: Cers6-KO 基因敲除小鼠 mice (Strain S-KO-07299) were purchased from Cyagen.
交付类型
周龄
性别
基因型
数量

基本信息

基因研究概述

质控标准

基因
基因全称
ceramide synthase 6
基因别称
4732462C07Rik,Lass6,T1L
染色体号
Chr 2 (Mouse)
转录本 ID
NCBI: NM_001347161 | Ensembl: ENSMUST00000176018
修饰方式
全身性基因敲除
靶向范围
Exon 2
敲除长度
~0.1 kb
品系说明
该品系是基于策略设计时的数据库信息制作而成,建议您在购买前查询最新的数据库和相关文献,以获取最准确的表型信息。
表型提示
MGI:2442564Mice homozygous for a knockout allele exhibit hind limb clasping, habituation deficit and altered lipid homeostasis.
CERS6,也称为CerS6,是一种重要的基因,编码神经酰胺合成酶6(CerS6),这是一种参与神经酰胺生物合成的酶。神经酰胺是一类生物活性分子,参与细胞信号传导、细胞凋亡、细胞生长和分化等生物学过程。CERS6的异常表达与多种疾病的发生和发展有关,包括炎症性肠病、癌症、酒精性肝病等。

在炎症性肠病(如溃疡性结肠炎)中,FTO(脂肪质量与肥胖相关蛋白)的缺乏会导致CERS6的表达下调,进而导致神经酰胺合成减少和神经酰胺-1-磷酸(S1P)积累,进而加重炎症反应。因此,CERS6的表达下调在溃疡性结肠炎的发生和发展中起着重要作用[1]。

在癌症中,CERS6的表达上调与多种癌症的发生和发展有关,包括非小细胞肺癌、结直肠癌、胰腺癌、胃癌、甲状腺癌和乳腺癌。CERS6的表达上调与不良预后、肿瘤分期、淋巴结转移和生存率降低有关。CERS6在癌症中的功能机制包括促进细胞增殖、迁移、侵袭和抑制细胞凋亡。此外,CERS6还可以通过竞争性内源RNA(ceRNA)机制调控miRNA的表达,进而影响癌症的发生和发展[2,3,4,5,6,7,8]。

在酒精性肝病中,CERS6的表达上调与肝脂肪变性的发生和发展有关。CERS6的敲除可以改善酒精性肝病小鼠的葡萄糖稳态、减轻体重增加和肝脂肪变性。此外,CERS6的敲除还可以减少长链神经酰胺的积累,抑制脂肪滴的形成[9]。

综上所述,CERS6是一种重要的基因,参与神经酰胺的生物合成和多种疾病的发生和发展。CERS6的表达异常与炎症性肠病、癌症和酒精性肝病的发生和发展有关。CERS6的研究有助于深入理解神经酰胺的生物学功能和疾病发生机制,为疾病的治疗和预防提供新的思路和策略[1,2,3,4,5,6,7,8,9]。

参考文献:
1. Ma, Yanru, Zhang, Xinyu, Xuan, Baoqin, Chen, Haoyan, Hong, Jie. 2024. Disruption of CerS6-mediated sphingolipid metabolism by FTO deficiency aggravates ulcerative colitis. In Gut, 73, 268-281. doi:10.1136/gutjnl-2023-330009. https://pubmed.ncbi.nlm.nih.gov/37734910/
2. Rastad, Hadith, Samimisedeh, Parham, Alan, Mahin Seifi, Hashemnejad, Maryam, Alan, Mahnaz Seifi. 2022. The role of lncRNA CERS6-AS1 in cancer and its molecular mechanisms: A systematic review and meta-analysis. In Pathology, research and practice, 241, 154245. doi:10.1016/j.prp.2022.154245. https://pubmed.ncbi.nlm.nih.gov/36580796/
3. Suzuki, Motoshi, Cao, Ke, Kato, Seiichi, Tomida, Shuta, Takahashi, Takashi. 2020. CERS6 required for cell migration and metastasis in lung cancer. In Journal of cellular and molecular medicine, 24, 11949-11959. doi:10.1111/jcmm.15817. https://pubmed.ncbi.nlm.nih.gov/32902157/
4. Jeon, Sookyoung, Scorletti, Eleonora, Dempsey, Joseph, Bataller, Ramon, Carr, Rotonya M. 2023. Ceramide synthase 6 (CerS6) is upregulated in alcohol-associated liver disease and exhibits sex-based differences in the regulation of energy homeostasis and lipid droplet accumulation. In Molecular metabolism, 78, 101804. doi:10.1016/j.molmet.2023.101804. https://pubmed.ncbi.nlm.nih.gov/37714377/
5. Yan, Kun, Hu, Chunyan, Liu, Chen, Ma, Shuyun, Li, Long. 2022. LncRNA CERS6-AS1, sponging miR-6838-5p, promotes proliferation and invasion in cervical carcinoma cells by upregulating FOXP2. In Histology and histopathology, 38, 823-835. doi:10.14670/HH-18-555. https://pubmed.ncbi.nlm.nih.gov/36444938/
6. Yu, Juan, Chen, Xiaoguang, Li, Jing, Wang, Furang. 2023. CERS6 antisense RNA 1 promotes colon cancer via upregulating mitochondrial calcium uniporter. In European journal of clinical investigation, 53, e13951. doi:10.1111/eci.13951. https://pubmed.ncbi.nlm.nih.gov/36628448/
7. Xiong, Shiyi, Song, Han. . LncRNA CERS6-AS1 Is a Tumor Promoter in Cervical Cancer by Sponging miR-195-5p. In Annals of clinical and laboratory science, 53, 30-41. doi:. https://pubmed.ncbi.nlm.nih.gov/36889776/
8. Jindal, Udita, Mamgain, Mukesh, Nath, Uttam Kumar, Datta, Dipak, Jain, Neeraj. 2024. Targeting CERS6-AS1/FGFR1 axis as synthetic vulnerability to constrain stromal cells supported proliferation in Mantle cell lymphoma. In Leukemia, 38, 2196-2209. doi:10.1038/s41375-024-02344-1. https://pubmed.ncbi.nlm.nih.gov/39003397/
9. Gao, Kan-Fei, Zhao, Yu-Fang, Liao, Wu-Jun, Xu, Guo-Li, Zhang, Jian-Dong. 2022. CERS6-AS1 promotes cell proliferation and represses cell apoptosis in pancreatic cancer via miR-195-5p/WIPI2 axis. In The Kaohsiung journal of medical sciences, 38, 542-553. doi:10.1002/kjm2.12522. https://pubmed.ncbi.nlm.nih.gov/35199935/