Slc39a1-KO 基因敲除小鼠

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产品名称

Slc39a1-KO 基因敲除小鼠

产品编号

S-KO-09071

品系全称

C57BL/6JCya-Slc39a1em1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-30791-Slc39a1-B6J-VA

品系状态

使用本品系发表的文献需注明: Slc39a1-KO 基因敲除小鼠 mice (Strain S-KO-09071) 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
solute carrier family 39 (zinc transporter), member 1
基因别称
Zip1,Zirtl
染色体号
Chr 3 (Mouse)
转录本 ID
NCBI: NM_013901 | Ensembl: ENSMUST00000015467
修饰方式
全身性基因敲除
靶向范围
Exon 2~3
敲除长度
~2.2 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:1353474On a zinc-adequate diet, homozygous null mutant mice exhibit normal fertility and normal embryonic and postnatal development. E14 embryos of dams fed a zinc-deficient diet from day E8 have <3.3-fold the incidence of abnormalities seen in wild-type embryos of zinc-deprived wild-type mothers.
SLC39A1,也称为ZIP1,是溶质载体家族39成员1,是一种锌离子转运蛋白。锌是细胞中重要的微量元素,参与多种生物学过程,包括基因表达、蛋白质合成、细胞信号传导和DNA修复。SLC39A1通过转运锌离子进入细胞,维持细胞内锌稳态,从而影响这些生物学过程。

SLC39A1在多种癌症中发挥重要作用。研究表明,SLC39A1在肝细胞癌(HCC)中过表达,与较差的预后、TNM分期晚和病理分级高相关。SLC39A1过表达与多种肿瘤相关通路相关,如细胞周期和Wnt信号通路。SLC39A1敲低可以抑制HCC细胞的增殖、侵袭和迁移能力,并降低肿瘤进展相关蛋白和Wnt信号通路相关蛋白的表达。此外,SLC39A1过表达与HCC中的免疫抑制相关,表现为Th2细胞浸润增加和细胞毒性细胞浸润减少[1]。

SLC39A1的表达水平对HCC患者的预后具有重要影响。研究表明,早期HCC患者中SLC39A1表达降低与较差的总生存期和无复发生存期相关。低表达SLC39A1是早期HCC患者独立的预后因素。因此,SLC39A1可以作为HCC的潜在诊断和预后生物标志物[2]。

SLC39A1在骨代谢中也发挥重要作用。SLC39A1可以与SLC13A5协同作用,调节骨细胞中柠檬酸的摄取和沉积,从而影响骨的矿化。SLC39A1缺失会导致骨强度下降,牙齿发育异常。SLC39A1在雌激素缺乏引起的骨质疏松症中发挥重要作用,其表达降低与骨质疏松症的发病机制相关[3,4,6]。

SLC39A1的表达和功能受到多种因素的调控。研究表明,microRNA-133可以靶向SLC39A1的3'非翻译区,下调SLC39A1的表达,从而影响成骨细胞的分化和骨的矿化[4]。此外,SLC39A1还受到细胞内锌浓度的调控,在锌缺乏时,SLC39A1的表达和功能会受到影响[5,7]。

SLC39A1在多种肿瘤和骨代谢中发挥重要作用。SLC39A1的表达水平和功能受到多种因素的调控,包括microRNA和锌浓度。SLC39A1可以作为肿瘤和骨质疏松症的潜在诊断和预后生物标志物,并为疾病的治疗和预防提供新的思路和策略。

参考文献:
1. Ma, Xiaowu, Zhuang, Hongkai, Wang, Qingbin, Chen, Yajin, Shang, Changzhen. 2022. SLC39A1 Overexpression is Associated with Immune Infiltration in Hepatocellular Carcinoma and Promotes Its Malignant Progression. In Journal of hepatocellular carcinoma, 9, 83-98. doi:10.2147/JHC.S349966. https://pubmed.ncbi.nlm.nih.gov/35211427/
2. Zhang, Qinglin, Pan, Jiadong, An, Fangmei, Nie, He, Zhan, Qiang. . Decreased SLC39A1 (Solute carrier family 39 member 1) expression predicts unfavorable prognosis in patients with early-stage hepatocellular carcinoma. In Bioengineered, 12, 8147-8156. doi:10.1080/21655979.2021.1987131. https://pubmed.ncbi.nlm.nih.gov/34615436/
3. Tang, Peifu, Xiong, Qi, Ge, Wei, Zhang, Lihai. . The role of microRNAs in osteoclasts and osteoporosis. In RNA biology, 11, 1355-63. doi:10.1080/15476286.2014.996462. https://pubmed.ncbi.nlm.nih.gov/25692234/
4. Lv, Hao, Sun, Yujie, Zhang, Yuchen. 2015. MiR-133 is Involved in Estrogen Deficiency-Induced Osteoporosis through Modulating Osteogenic Differentiation of Mesenchymal Stem Cells. In Medical science monitor : international medical journal of experimental and clinical research, 21, 1527-34. doi:10.12659/MSM.894323. https://pubmed.ncbi.nlm.nih.gov/26013661/
5. Zhang, Xu-Dong, Liu, Zhong-Yuan, Luo, Kai, Huang, Shuai, Li, Ren-Feng. 2023. Clinical implications of RAB13 expression in pan-cancer based on multi-databases integrative analysis. In Scientific reports, 13, 16859. doi:10.1038/s41598-023-43699-2. https://pubmed.ncbi.nlm.nih.gov/37803063/
6. Dirckx, Naomi, Zhang, Qian, Chu, Emily Y, Schmidt-Rohr, Klaus, Clemens, Thomas L. 2022. A specialized metabolic pathway partitions citrate in hydroxyapatite to impact mineralization of bones and teeth. In Proceedings of the National Academy of Sciences of the United States of America, 119, e2212178119. doi:10.1073/pnas.2212178119. https://pubmed.ncbi.nlm.nih.gov/36322718/
7. Kambe, Taiho, Geiser, Jim, Lahner, Brett, Salt, David E, Andrews, Glen K. 2008. Slc39a1 to 3 (subfamily II) Zip genes in mice have unique cell-specific functions during adaptation to zinc deficiency. In American journal of physiology. Regulatory, integrative and comparative physiology, 294, R1474-81. doi:10.1152/ajpregu.00130.2008. https://pubmed.ncbi.nlm.nih.gov/18353881/