Bdkrb1-flox Mouse
一般名
Bdkrb1-flox
製品ID
S-CKO-01407
背景情報
C57BL/6JCya
系統ID
CKOCMP-12061-Bdkrb1-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Bdkrb1-flox Mouse（カタログ番号S-CKO-01407）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
Bdkrb1-flox
系統ID
CKOCMP-12061-Bdkrb1-B6J-VA
遺伝子名
製品ID
S-CKO-01407
遺伝子別名
B1R, BKR1, B1BKR, Bdkrb, BRADYB1
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 12
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
ENSMUST00000041229
NCBIトランスクリプトID
NM_007539
ターゲット領域
Exon 1
有効領域の大きさ
~2.1 kb
遺伝子研究の概要
Bdkrb1, encoding the bradykinin B1 receptor, is involved in the kallikrein-kinin system. Bradykinin, by activating BDKRB1/B2, can prompt calcium influx. BDKRB1 is associated with multiple biological pathways such as the Ca2+-MEK1-ERK1/2-NF-κB pathway, and is important in inflammation, cell migration, and tissue remodeling [1,4,5,6]. Genetic models, like knockout mice, are valuable for studying its functions.
In glioblastoma cells, knocking-down BDKRB1 decreased aquaporin 4 (AQP4) mRNA expression and cell migration and invasion, indicating BDKRB1's role in promoting glioblastoma cell migration and invasion through regulating AQP4 expression via the Ca2+-MEK1-ERK1/2-NF-κB mechanism [1]. In Wolfram syndrome rat models, Bdkrb1 expression was drastically down-regulated at an early stage, suggesting its disturbance in the normal functioning of the renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system (KKS) [2]. Mice lacking Cd13 or Bdkrb1 were resistant to bleomycin-induced skin fibrosis and inflammation, highlighting BDKRB1's role in scleroderma fibrosis [3]. In a neuropathic pain model, an antagonist of BDKRB1 suppressed the over-expressed BDKRB1 levels and inhibited hyperpathia, while remimazolam alleviated neuropathic pain by inactivating BDKRB1 signalling [5]. In experimental autoimmune encephalomyelitis, Bdkrb1-deficient mice showed more severe disease with enhanced CNS-immune cell infiltration, suggesting Bdkrb1 limits encephalitogenic T lymphocyte recruitment to the CNS [6]. Kinin B1 receptor knockout mice had increased bone loss and more osteoclasts in a periodontitis model, indicating Bdkrb1's role in periodontitis pathogenesis [7].
In conclusion, Bdkrb1 plays essential roles in multiple biological processes and disease conditions. Model-based research, especially KO mouse models, has revealed its functions in cancer cell migration, neurodegenerative diseases, fibrosis, neuropathic pain, CNS inflammation, and periodontitis, providing potential therapeutic targets for these diseases.
References：
1. Sun, Ding-Ping, Lee, Yuan-Wen, Chen, Jui-Tai, Lin, Yung-Wei, Chen, Ruei-Ming. 2020. The Bradykinin-BDKRB1 Axis Regulates Aquaporin 4 Gene Expression and Consequential Migration and Invasion of Malignant Glioblastoma Cells via a Ca2+-MEK1-ERK1/2-NF-κB Mechanism. In Cancers, 12, . doi:10.3390/cancers12030667. https://pubmed.ncbi.nlm.nih.gov/32182968/
2. Punapart, Marite, Seppa, Kadri, Jagomäe, Toomas, Vasar, Eero, Plaas, Mario. 2021. The Expression of RAAS Key Receptors, Agtr2 and Bdkrb1, Is Downregulated at an Early Stage in a Rat Model of Wolfram Syndrome. In Genes, 12, . doi:10.3390/genes12111717. https://pubmed.ncbi.nlm.nih.gov/34828323/
3. Muraoka, Sei, Brodie, William D, Mattichak, Megan N, Fox, David A, Tsou, Pei-Suen. 2024. Targeting CD13/Aminopeptidase N as a Novel Therapeutic Approach for Scleroderma Fibrosis. In Arthritis & rheumatology (Hoboken, N.J.), 77, 80-91. doi:10.1002/art.42973. https://pubmed.ncbi.nlm.nih.gov/39175116/
4. Angers, Martin, Drouin, Régen, Bachvarova, Magdalena, Usheva, Anny, Bachvarov, Dimcho. . In vivo DNase I-mediated footprinting analysis along the human bradykinin B1 receptor (BDKRB1) gene promoter: evidence for cell-specific regulation. In The Biochemical journal, 389, 37-46. doi:. https://pubmed.ncbi.nlm.nih.gov/15705059/
5. Xie, Haiyu, Lu, Feng, Liu, Weilian, Wang, Lifeng, Zhong, Maolin. . Remimazolam alleviates neuropathic pain via regulating bradykinin receptor B1 and autophagy. In The Journal of pharmacy and pharmacology, 73, 1643-1651. doi:10.1093/jpp/rgab080. https://pubmed.ncbi.nlm.nih.gov/34061162/
6. Schulze-Topphoff, Ulf, Prat, Alexandre, Prozorovski, Timour, Aktas, Orhan, Zipp, Frauke. 2009. Activation of kinin receptor B1 limits encephalitogenic T lymphocyte recruitment to the central nervous system. In Nature medicine, 15, 788-93. doi:10.1038/nm.1980. https://pubmed.ncbi.nlm.nih.gov/19561616/
7. Gonçalves-Zillo, Thais Oliveira, Pugliese, Lívia Souza, Sales, Vicência Micheline Toledo, Monteiro, Ana Carolina, Pesquero, João Bosco. 2013. Increased bone loss and amount of osteoclasts in kinin B1 receptor knockout mice. In Journal of clinical periodontology, 40, 653-60. doi:10.1111/jcpe.12097. https://pubmed.ncbi.nlm.nih.gov/23534940/
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