Calcrl-flox Mouse
一般名
Calcrl-flox
製品ID
S-CKO-11816
背景情報
C57BL/6JCya
系統ID
CKOCMP-54598-Calcrl-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Calcrl-flox Mouse（カタログ番号S-CKO-11816）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
Calcrl-flox
系統ID
CKOCMP-54598-Calcrl-B6J-VA
遺伝子名
製品ID
S-CKO-11816
遺伝子別名
CRLR
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 2
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
ENSMUST00000074262
NCBIトランスクリプトID
NM_018782
ターゲット領域
Exon 6
有効領域の大きさ
~1.9 kb
遺伝子研究の概要
CALCRL, short for calcitonin receptor-like receptor, is a G-protein-coupled neuropeptide receptor. It is involved in various biological processes, and its associated pathways include cyclic AMP (cAMP) signaling pathway, which is activated when it forms a receptor complex with RAMP1 in response to ligands like calcitonin gene-related peptide (CGRP) [1,3,5,6]. It is of great biological importance in processes such as immune response, hematopoiesis, and drug-tolerance in cancer cells. Genetic models, like KO or CKO mouse models, are valuable for studying its functions.
In the spleen, nociceptors release CGRP which acts on B cells through the CALCRL-RAMP1 complex via the cAMP pathway, promoting germinal center response and humoral immunity [1]. In acute myeloid leukemia (AML), CALCRL is expressed in relapse-initiating drug-tolerant cells. Knockdown of CALCRL impairs leukemic growth, decreases the frequency of leukemia-initiating cells, and sensitizes cells to cytarabine [2]. In tendon-bone healing, overexpression of Calcrl in mice improves osteogenic differentiation, type H vessel and nerve fiber intensity at the tendon-bone interface, as well as gait and biomechanical performance [3]. In AML/ETO + AML patients, lower CALCRL expression is associated with longer survival, and its expression decreases after chemotherapy-induced remission [4]. In AML cells, overexpression of CALCRL confers resistance to daunorubicin through up-regulation of the XRCC5/TYK2/JAK1 pathway [7]. In glioma, interfering with CALCRL expression in U87 cells (a glioma cell line) inhibits proliferation, promotes apoptosis, and is related to prognosis, especially in low-grade gliomas [8].
In conclusion, CALCRL plays essential roles in multiple biological processes. Through model-based research, its significance in immune regulation, cancer drug-resistance, and tissue repair has been revealed. In particular, in diseases like AML and glioma, studies using KO/CKO mouse models could potentially provide insights into novel therapeutic strategies targeting CALCRL.
References：
1. Wu, Min, Song, Guangping, Li, Jianing, Zhang, Yucheng, Li, Huiyan. 2024. Innervation of nociceptor neurons in the spleen promotes germinal center responses and humoral immunity. In Cell, 187, 2935-2951.e19. doi:10.1016/j.cell.2024.04.027. https://pubmed.ncbi.nlm.nih.gov/38772371/
2. Larrue, Clément, Guiraud, Nathan, Mouchel, Pierre-Luc, Récher, Christian, Sarry, Jean-Emmanuel. 2021. Adrenomedullin-CALCRL axis controls relapse-initiating drug tolerant acute myeloid leukemia cells. In Nature communications, 12, 422. doi:10.1038/s41467-020-20717-9. https://pubmed.ncbi.nlm.nih.gov/33462236/
3. Zhao, Xibang, Wu, Guanfu, Zhang, Jing, Yu, Ziyi, Wang, Jiali. 2024. Activation of CGRP receptor-mediated signaling promotes tendon-bone healing. In Science advances, 10, eadg7380. doi:10.1126/sciadv.adg7380. https://pubmed.ncbi.nlm.nih.gov/38457499/
4. Wang, Rongrong, Li, Miao, Bai, Yujia, Jiao, Yang, Qi, Xiaofei. 2022. CALCRL Gene is a Suitable Prognostic Factor in AML/ETO+ AML Patients. In Journal of oncology, 2022, 3024360. doi:10.1155/2022/3024360. https://pubmed.ncbi.nlm.nih.gov/35342399/
5. Hou, Yu, Sun, Linyu, LaFleur, Martin W, Sharpe, Arlene H, Kuchroo, Vijay K. 2024. Neuropeptide signalling orchestrates T cell differentiation. In Nature, 635, 444-452. doi:10.1038/s41586-024-08049-w. https://pubmed.ncbi.nlm.nih.gov/39415015/
6. Gao, Xin, Zhang, Dachuan, Xu, Chunliang, Caron, Kathleen M, Frenette, Paul S. 2020. Nociceptive nerves regulate haematopoietic stem cell mobilization. In Nature, 589, 591-596. doi:10.1038/s41586-020-03057-y. https://pubmed.ncbi.nlm.nih.gov/33361809/
7. Tang, Shanhao, Li, Shuangyue, Shi, Xiaowei, Wu, An, Ouyang, Guifang. 2023. CALCRL induces resistance to daunorubicin in acute myeloid leukemia cells through upregulation of XRCC5/TYK2/JAK1 pathway. In Anti-cancer drugs, 35, 163-176. doi:10.1097/CAD.0000000000001547. https://pubmed.ncbi.nlm.nih.gov/37948318/
8. Gu, Shengcai, Shu, Lei, Zhou, Lv, Gao, Peng, Cheng, Hongwei. . Interfering with CALCRL expression inhibits glioma proliferation, promotes apoptosis, and predicts prognosis in low-grade gliomas. In Annals of translational medicine, 10, 1277. doi:10.21037/atm-22-5154. https://pubmed.ncbi.nlm.nih.gov/36618798/
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