Nipal1-flox Mouse
一般名
Nipal1-flox
製品ID
S-CKO-14898
背景情報
C57BL/6JCya
系統ID
CKOCMP-70701-Nipal1-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Nipal1-flox Mouse（カタログ番号S-CKO-14898）はサイアジェンから購入しました。」と引用してください。
製品タイプ
年齢
遺伝子型
性別
数量
標準的な配送方法では、少なくとも3匹のヘテロ接合体キャリアを保証しています。ホモ接合体キャリアや指定された性別の個体の繁殖サービスも利用可能です。
基本情報
系統名
Nipal1-flox
系統ID
CKOCMP-70701-Nipal1-B6J-VA
遺伝子名
製品ID
S-CKO-14898
遺伝子別名
Npal1, 3830408G10Rik
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 5
表現型
アプリケーション
--
さらに
系統詳細
EnsemblトランスクリプトID
ENSMUST00000087212
NCBIトランスクリプトID
NM_001081205
ターゲット領域
Exon 4
有効領域の大きさ
~1.7 kb
遺伝子研究の概要
NIPAL1, encoding a magnesium influx transporter, is a gene with significant biological importance. It is involved in magnesium-related cellular processes and has been associated with multiple biological pathways and diseases [1,2,5]. Genetic models can be valuable in studying its functions.
In pancreatic islets, NIPAL1 expression is regulated by extracellular magnesium. Knockdown of NIPAL1 in Min6-K8 cells (a pancreatic β-cell-like cell line) decreased both basal insulin secretion and total insulin content, while its overexpression increased total insulin content, suggesting its role in glucose-stimulated insulin secretion and intracellular insulin content regulation, especially under hypomagnesemia conditions [1].
In oral squamous cell carcinoma (OSCC), NIPAL1 expression was observed in 20.3% of 192 patients. Its expression correlated with cancer cell intravasation and poorer disease-free survival, and in functional analysis, it regulated the growth and adhesion of OSCC tumor cells and endothelial cells, indicating it might be a novel tumor-promoting factor and a useful molecular marker for OSCC [2].
In a genome-wide association study, NIPAL1 achieved Bonferroni significance in gene-based association tests related to spondylosis [3]. Genome-wide association studies also linked NIPAL1 to gout associated with reduced renal urate excretion, though functional analysis did not detect urate transport via NIPAL1, and its expression in the human kidney was mainly in the distal tubules [4,5,6,7].
In conclusion, NIPAL1 plays essential roles in multiple biological processes and disease conditions. Its function in insulin secretion regulation in pancreatic islets, its potential as a tumor-promoting factor in OSCC, and its associations with spondylosis and gout are significant findings. Studies using various models, including potential KO/CKO mouse models (not explicitly detailed in provided references but inferred as valuable for further study), contribute to understanding these functions and their implications in related diseases.
References：
1. Manialawy, Yousef, Khan, Saifur R, Bhattacharjee, Alpana, Wheeler, Michael B. 2020. The magnesium transporter NIPAL1 is a pancreatic islet-expressed protein that conditionally impacts insulin secretion. In The Journal of biological chemistry, 295, 9879-9892. doi:10.1074/jbc.RA120.013277. https://pubmed.ncbi.nlm.nih.gov/32439805/
2. Sasahira, Tomonori, Nishiguchi, Yukiko, Kurihara-Shimomura, Miyako, Kuniyasu, Hiroki, Kirita, Tadaaki. 2018. NIPA-like domain containing 1 is a novel tumor-promoting factor in oral squamous cell carcinoma. In Journal of cancer research and clinical oncology, 144, 875-882. doi:10.1007/s00432-018-2612-x. https://pubmed.ncbi.nlm.nih.gov/29464350/
3. Zhang, Yanfei, Grant, Ryan A, Shivakumar, Manu K, Williams, Marc S, Lee, Ming Ta Michael. . Genome-wide Association Analysis Across 16,956 Patients Identifies a Novel Genetic Association Between BMP6, NIPAL1, CNGA1 and Spondylosis. In Spine, 46, E625-E631. doi:10.1097/BRS.0000000000003880. https://pubmed.ncbi.nlm.nih.gov/33332786/
4. García-Nieto, Víctor M, Claverie-Martín, Félix, Moraleda-Mesa, Teresa, Luis-Yanes, María I, Ramos-Trujillo, Elena. 2022. Gout associated with reduced renal excretion of uric acid. Renal tubular disorder that nephrologists do not treat. In Nefrologia, 42, 273-279. doi:10.1016/j.nefroe.2022.05.007. https://pubmed.ncbi.nlm.nih.gov/36210617/
5. Nakayama, Akiyoshi, Nakaoka, Hirofumi, Yamamoto, Ken, Merriman, Tony R, Matsuo, Hirotaka. 2016. GWAS of clinically defined gout and subtypes identifies multiple susceptibility loci that include urate transporter genes. In Annals of the rheumatic diseases, 76, 869-877. doi:10.1136/annrheumdis-2016-209632. https://pubmed.ncbi.nlm.nih.gov/27899376/
6. García-Nieto, Víctor M, Claverie-Martín, Félix, Moraleda-Mesa, Teresa, Luis-Yanes, María I, Ramos-Trujillo, Elena. 2021. Gout associated with reduced renal excretion of uric acid. Renal tubular disorder that nephrologists do not treat. In Nefrologia, , . doi:10.1016/j.nefro.2021.03.013. https://pubmed.ncbi.nlm.nih.gov/34503865/
7. Zhu, Weifeng, Deng, Yan, Zhou, Xiaodong. 2018. Multiple Membrane Transporters and Some Immune Regulatory Genes are Major Genetic Factors to Gout. In The open rheumatology journal, 12, 94-113. doi:10.2174/1874312901812010094. https://pubmed.ncbi.nlm.nih.gov/30123371/
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