Lep-flox Mouse
一般名
Lep-flox
製品ID
S-CKO-03377
背景情報
C57BL/6JCya
系統ID
CKOCMP-16846-Lep-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Lep-flox Mouse（カタログ番号S-CKO-03377）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
Lep-flox
系統ID
CKOCMP-16846-Lep-B6J-VA
遺伝子名
製品ID
S-CKO-03377
遺伝子別名
ob, obese
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 6
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
ENSMUST00000069789
NCBIトランスクリプトID
NM_008493
ターゲット領域
Exon 3
有効領域の大きさ
~3.8 kb
遺伝子研究の概要
Lep, which encodes leptin, is a crucial gene. Leptin is a hormone mainly produced by adipose tissue and is a key regulator of energy balance, acting on the hypothalamus to regulate appetite and metabolism. It is also involved in multiple biological processes such as inflammation, fibrosis, and cell growth [1,2,5].
Lep seems to have a dual-edged role in wound healing. It exerts pro-inflammatory and profibrotic effects, but can also regulate hair follicle growth, making it a potential target for promoting scarless wound healing [1].
In breast cancer, LEP is downregulated in cancer tissues compared to normal tissues, and low LEP expression is associated with a poorer prognosis, suggesting it could be a potential biomarker and therapeutic target [2].
Regarding non-Hodgkin lymphoma, the LEP G2528A polymorphism may increase the risk, while the A19G polymorphism may decrease the risk, especially for follicular lymphoma [3]. Some LEP gene variants like rs7799039 may be associated with energy intake [4].
In bovine intramuscular preadipocytes, LEP inhibits adipogenesis through the AMPK signaling pathway [5].
In preeclampsia, miR-519d can downregulate LEP expression to inhibit the development of the disease [6].
In myeloid neoplasms, hypermethylation of the LEP promoter is an early event and is associated with a worse prognosis [7].
In the Ukrainian population, the LEPR gene polymorphism (rs1137101) may be related to the metabolic syndrome, and the presence of its alleles affects the level of leptin and other hormones [8].
In Prader-Willi syndrome, there are alterations in serum leptin and LEP/LEPR promoter methylation [9].
In conclusion, Lep is essential in regulating energy balance, and its dysregulation is associated with various diseases including wound-related fibrotic disorders, breast cancer, non-Hodgkin lymphoma, preeclampsia, myeloid neoplasms, the metabolic syndrome, and Prader-Willi syndrome. Studies on Lep, especially through genetic models, help understand the biological processes and mechanisms underlying these diseases, potentially providing new strategies for diagnosis and treatment.
References：
1. Zhang, Kai-Wen, Jia, Yuan, Li, Yue-Yue, Yuan, Zheng-Dong, Yuan, Feng-Lai. 2022. LEP and LEPR are possibly a double-edged sword for wound healing. In Journal of cellular physiology, 238, 355-365. doi:10.1002/jcp.30936. https://pubmed.ncbi.nlm.nih.gov/36571294/
2. Jin, Tong Yi, Saindane, Madhuri, Park, Kyoung Sik, Yang, Jung-Hyun, Yun, IkJin. . LEP as a potential biomarker in prognosis of breast cancer: Systemic review and meta analyses (PRISMA). In Medicine, 100, e26896. doi:10.1097/MD.0000000000026896. https://pubmed.ncbi.nlm.nih.gov/34414945/
3. Lin, Hai-Yan, Shi, Hui, Li, Chun-Yan, Liu, Peng-Cheng, Lou, Lie-ming. . LEP and LEPR polymorphisms in non-Hodgkin lymphoma risk: a systematic review and pooled analysis. In Journal of B.U.ON. : official journal of the Balkan Union of Oncology, 20, 261-8. doi:. https://pubmed.ncbi.nlm.nih.gov/25778326/
4. Kroll, Caroline, Mastroeni, Silmara S B S, Veugelers, Paul J, Mastroeni, Marco F. 2019. Associations of ADIPOQ and LEP Gene Variants with Energy Intake: A Systematic Review. In Nutrients, 11, . doi:10.3390/nu11040750. https://pubmed.ncbi.nlm.nih.gov/30935050/
5. Yu, Shengchen, Yu, Hengwei, Wang, Jianfang, Mei, Chugang, Zan, Linsen. . LEP inhibits intramuscular adipogenesis through the AMPK signaling pathway in vitro. In FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 38, e23836. doi:10.1096/fj.202400590RR. https://pubmed.ncbi.nlm.nih.gov/39044640/
6. Cai, Hairui, Li, Dongmei, Wu, Jun, Shi, Chunbo. 2021. miR-519d downregulates LEP expression to inhibit preeclampsia development. In Open medicine (Warsaw, Poland), 16, 1215-1227. doi:10.1515/med-2021-0244. https://pubmed.ncbi.nlm.nih.gov/34514168/
7. Kaastrup, Katja, Gillberg, Linn, Mikkelsen, Stine U, Hansen, Jakob W, Grønbæk, Kirsten. 2023. LEP promoter methylation in the initiation and progression of clonal cytopenia of undetermined significance and myelodysplastic syndrome. In Clinical epigenetics, 15, 91. doi:10.1186/s13148-023-01505-w. https://pubmed.ncbi.nlm.nih.gov/37237325/
8. Prodan, Andrii, Dzubanovsky, Ihor, Kamyshnyi, Oleksandr, Pidruchna, Svitlana, Voloshyn, Stanislava. 2023. GHRL, LEP, LEPR genes polymorphism and their association with the metabolic syndrome in the Ukrainian population. In Endocrine regulations, 57, 269-278. doi:10.2478/enr-2023-0030. https://pubmed.ncbi.nlm.nih.gov/38127688/
9. Wieting, Jelte, Jahn, Kirsten, Buchholz, Vanessa, Deest, Maximilian, Frieling, Helge. 2022. Alteration of serum leptin and LEP/LEPR promoter methylation in Prader-Willi syndrome. In Psychoneuroendocrinology, 143, 105857. doi:10.1016/j.psyneuen.2022.105857. https://pubmed.ncbi.nlm.nih.gov/35803048/
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