Rgma-flox Mouse
一般名
Rgma-flox
製品ID
S-CKO-18084
背景情報
C57BL/6JCya
系統ID
CKOCMP-244058-Rgma-B6J-VB
状況
このマウス系統を論文で使用する場合は、「Rgma-flox Mouse（カタログ番号S-CKO-18084）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
Rgma-flox
系統ID
CKOCMP-244058-Rgma-B6J-VB
遺伝子名
製品ID
S-CKO-18084
遺伝子別名
C230063O06
遺伝子別名
C57BL/6JCya
遺伝子正式名称
repulsive guidance molecule family member A
NCBI ID
修正
Conditional knockout
染色体
Chr 7
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
ENSMUST00000094312
NCBIトランスクリプトID
NM_177740
ターゲット領域
Exon 3
有効領域の大きさ
~1.0 kb
遺伝子研究の概要
Rgma, or Repulsive guidance molecule A, is a glycosylphosphatidylinositol-linked glycoprotein. It was originally identified as a neuronal growth cone-collapsing factor and has multiple functions, including regulating axon guidance, neuronal differentiation, survival, and immune regulation. It exerts its functions mainly through binding to its receptor neogenin, thus playing a significant role in the development and pathology of the central nervous system (CNS) [1,3,4].
In disease-related research, knockdown of Rgma in mouse models has shown promising results. In mSOD1 mice (a model for amyotrophic lateral sclerosis, ALS), treatment with humanized anti-Rgma monoclonal antibody ameliorated clinical symptoms by reducing mutant SOD1 protein accumulation in motor neurons via inhibiting actin depolymerization [1]. In a mouse model of ischemia-reperfusion (I/R), knockdown of Rgma shifted neuronal energy metabolism towards oxidative phosphorylation and the pentose phosphate pathway, protecting mice from I/R injury [2]. In a neuromyelitis optica (NMO) rat model, treatment with Rgma-mAb suppressed neutrophil infiltration, decreased the expression of neutrophil chemoattractants, and ameliorated astrocytopathy and neuropathic pain [3]. In ApoE-/-mice, knockdown of Rgma inhibited the dedifferentiation of oxidized LDL-induced vascular smooth muscle cells (VSMCs), their proliferation and migration, and reduced neointima thickness [5]. In an experimental autoimmune encephalomyelitis (EAE) mouse model (related to multiple sclerosis), knockdown of Rgma strengthened the integrity of the blood-brain barrier (BBB) [6].
In conclusion, Rgma is a multifunctional molecule involved in various biological processes. Studies using gene-knockout or antibody-based loss-of-function models in different animal models have revealed its significant role in diseases such as ALS, I/R injury, NMO, atherosclerosis-related conditions, and multiple sclerosis. These findings suggest that targeting Rgma could potentially be a therapeutic strategy for these diseases.
References：
1. Shimizu, Mikito, Shiraishi, Naoyuki, Tada, Satoru, Okuno, Tatsusada, Mochizuki, Hideki. 2023. RGMa collapses the neuronal actin barrier against disease-implicated protein and exacerbates ALS. In Science advances, 9, eadg3193. doi:10.1126/sciadv.adg3193. https://pubmed.ncbi.nlm.nih.gov/37992159/
2. Wang, Zijie, Zhang, Shaoru, Cheng, Ruiqi, Jiang, Anan, Qin, Xinyue. 2024. Knockdown of RGMA improves ischemic stroke via Reprogramming of Neuronal Metabolism. In Free radical biology & medicine, 218, 41-56. doi:10.1016/j.freeradbiomed.2024.03.020. https://pubmed.ncbi.nlm.nih.gov/38556067/
3. Iwamoto, Shosuke, Itokazu, Takahide, Sasaki, Atsushi, Fujihara, Kazuo, Yamashita, Toshihide. 2022. RGMa Signal in Macrophages Induces Neutrophil-Related Astrocytopathy in NMO. In Annals of neurology, 91, 532-547. doi:10.1002/ana.26327. https://pubmed.ncbi.nlm.nih.gov/35167145/
4. Fujita, Yuki, Yamashita, Toshihide. 2017. The roles of RGMa-neogenin signaling in inflammation and angiogenesis. In Inflammation and regeneration, 37, 6. doi:10.1186/s41232-017-0037-6. https://pubmed.ncbi.nlm.nih.gov/29259705/
5. Yuan, Xiaofan, Xiao, Hongmei, Hu, Qingzhe, Shen, Guanru, Qin, Xinyue. 2022. RGMa promotes dedifferentiation of vascular smooth muscle cells into a macrophage-like phenotype in vivo and in vitro. In Journal of lipid research, 63, 100276. doi:10.1016/j.jlr.2022.100276. https://pubmed.ncbi.nlm.nih.gov/36089003/
6. Zhang, Lei, Tang, Shi, Ma, Yue, Feng, Jinzhou, Qin, Xinyue. 2022. RGMa Participates in the Blood-Brain Barrier Dysfunction Through BMP/BMPR/YAP Signaling in Multiple Sclerosis. In Frontiers in immunology, 13, 861486. doi:10.3389/fimmu.2022.861486. https://pubmed.ncbi.nlm.nih.gov/35664003/
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