Flii-KO 基因敲除小鼠

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产品名称

Flii-KO 基因敲除小鼠

产品编号

S-KO-02081

品系全称

C57BL/6JCya-Fliiem1/Cya

品系背景

C57BL/6JCya

品系编号

KOCMP-14248-Flii-B6J-VA

品系状态

使用本品系发表的文献需注明: Flii-KO 基因敲除小鼠 mice (Strain S-KO-02081) 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
flightless I actin binding protein
基因别称
3632430F08Rik,Fliih
染色体号
Chr 11 (Mouse)
转录本 ID
NCBI: NM_022009.2 | Ensembl: ENSMUST00000002889
修饰方式
全身性基因敲除
靶向范围
Exon 2~7
敲除长度
~2974 bp
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:1342286Embryos homozygous for a knock-out allele are able to initiate uterine implantation but degenerate rapidly thereafter. Heterozygous mutant mice display enhanced wound healing with increased epithelial migration and improved wound contraction.
Flii,也称为Flightless-I,是一种重要的肌动蛋白结合蛋白。它参与多种生物学过程,包括细胞迁移、肌细胞分化、胚胎发育和伤口愈合。Flii蛋白在细胞内与肌动蛋白细丝相互作用,调节肌动蛋白细丝的长度和组织。Flii蛋白还与多种其他蛋白质相互作用,包括组织素-1 (TMOD1) 和YAP1,参与调节细胞粘附、肌原细胞分化和伤口愈合。

Flii基因在人类心脏疾病中发挥重要作用。研究发现,Flii基因的变异与心脏重塑和心肌病的发生有关。Flii基因的变异会导致肌动蛋白细丝缩短,进而影响心脏的收缩功能。此外,Flii基因的变异还与儿童心肌病的发生有关,它通过破坏心肌细胞粘附和肌原纤维组织来导致心肌病。Flii基因的变异还与皮肤疾病,如大疱性表皮松解症的发生有关。Flii基因的过表达会导致皮肤水疱形成,而降低Flii基因的表达可以减少水疱的严重程度并改善皮肤损伤的修复。

Flii基因的变异还与生长性状和基因表达有关。在牛中,Flii基因的变异与生长性状和基因表达有关,可以作为分子标记用于辅助选择育种。此外,Flii基因的变异还与脂肪储存有关。在果蝇中,Flii基因的变异会导致脂肪储存的增加,从而影响能量代谢和代谢性疾病的发生。

Flii基因的变异还与视网膜细胞的基因表达有关。Flii基因与组蛋白甲基转移酶MLL1协同调节芳烃受体介导的转录。Flii基因的变异还与肌原细胞分化有关。Flii基因的变异会抑制肌原细胞分化和肌管形成,从而影响肌肉的生长和发育。

综上所述,Flii基因是一种重要的肌动蛋白结合蛋白,参与多种生物学过程。Flii基因的变异与多种疾病的发生有关,包括心脏疾病、皮肤疾病和代谢性疾病。Flii基因的研究有助于深入理解肌动蛋白结合蛋白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][10]。

参考文献:
1. Kuwabara, Yasuhide, York, Allen J, Lin, Suh-Chin, Pirruccello, James P, Molkentin, Jeffery D. 2023. A human FLII gene variant alters sarcomeric actin thin filament length and predisposes to cardiomyopathy. In Proceedings of the National Academy of Sciences of the United States of America, 120, e2213696120. doi:10.1073/pnas.2213696120. https://pubmed.ncbi.nlm.nih.gov/37126682/
2. Liu, Mei, Liu, Min, Li, Bo, Bai, Yueyu, Chen, Hong. 2016. Polymorphisms of FLII implicate gene expressions and growth traits in Chinese cattle. In Molecular and cellular probes, 30, 266-272. doi:10.1016/j.mcp.2016.07.005. https://pubmed.ncbi.nlm.nih.gov/27453522/
3. Ruijmbeek, Claudine Wb, Housley, Filomena, Idrees, Hafiza, Verhagen, Judith Ma, Reischauer, Sven. 2023. Biallelic variants in FLII cause pediatric cardiomyopathy by disrupting cardiomyocyte cell adhesion and myofibril organization. In JCI insight, 8, . doi:10.1172/jci.insight.168247. https://pubmed.ncbi.nlm.nih.gov/37561591/
4. Seong, Bo Kyung A, Dharia, Neekesh V, Lin, Shan, Fischer, Eric S, Stegmaier, Kimberly. 2021. TRIM8 modulates the EWS/FLI oncoprotein to promote survival in Ewing sarcoma. In Cancer cell, 39, 1262-1278.e7. doi:10.1016/j.ccell.2021.07.003. https://pubmed.ncbi.nlm.nih.gov/34329586/
5. Kopecki, Zlatko, Arkell, Ruth M, Strudwick, Xanthe L, Murrell, Dedee F, Cowin, Allison J. 2011. Overexpression of the Flii gene increases dermal-epidermal blistering in an autoimmune ColVII mouse model of epidermolysis bullosa acquisita. In The Journal of pathology, 225, 401-13. doi:10.1002/path.2973. https://pubmed.ncbi.nlm.nih.gov/21984127/
6. Jeong, Kwang Won. 2021. FLII and MLL1 Cooperatively Regulate Aryl Hydrocarbon Receptor-Mediated Transcription in ARPE-19 Cells. In Current issues in molecular biology, 43, 1623-1631. doi:10.3390/cimb43030115. https://pubmed.ncbi.nlm.nih.gov/34698116/
7. Nguyen, Mai Thi, Ly, Quoc Kiet, Kim, Hyun-Jung, Lee, Wan. 2023. FLII Modulates the Myogenic Differentiation of Progenitor Cells via Actin Remodeling-Mediated YAP1 Regulation. In International journal of molecular sciences, 24, . doi:10.3390/ijms241814335. https://pubmed.ncbi.nlm.nih.gov/37762638/
8. Lyu, Xuehui, Cui, Yingzi, Kong, Yinfei, Li, Yan, Du, Peng. 2024. A transient transcriptional activation governs unpolarized-to-polarized morphogenesis during embryo implantation. In Molecular cell, 84, 2665-2681.e13. doi:10.1016/j.molcel.2024.06.005. https://pubmed.ncbi.nlm.nih.gov/38955180/
9. Thomsen, Nicole, Chappell, Anna, Ali, Radiya G, Cowin, Allison J, Arkell, Ruth M. 2011. Mouse strains for the ubiquitous or conditional overexpression of the Flii gene. In Genesis (New York, N.Y. : 2000), 49, 681-8. doi:10.1002/dvg.20735. https://pubmed.ncbi.nlm.nih.gov/21786402/
10. Park, Jung-Eun, Lee, Eun Ji, Kim, Jung Kwan, Choi, Jang Hyun, Kang, Min-Ji. 2018. Flightless-I Controls Fat Storage in Drosophila. In Molecules and cells, 41, 603-611. doi:10.14348/molcells.2018.0120. https://pubmed.ncbi.nlm.nih.gov/29890821/