Nlrc3-flox Mouse
一般名
Nlrc3-flox
製品ID
S-CKO-09706
背景情報
C57BL/6JCya
系統ID
CKOCMP-268857-Nlrc3-B6J-VA
状況
このマウス系統を論文で使用する場合は、「Nlrc3-flox Mouse（カタログ番号S-CKO-09706）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
Nlrc3-flox
系統ID
CKOCMP-268857-Nlrc3-B6J-VA
遺伝子名
製品ID
S-CKO-09706
遺伝子別名
CLR16.2, mFLJ00348, D230007K08Rik
遺伝子別名
C57BL/6JCya
NCBI ID
修正
Conditional knockout
染色体
Chr 16
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
ENSMUST00000177551
NCBIトランスクリプトID
NM_001081280
ターゲット領域
Exon 2~3
有効領域の大きさ
~3.5 kb
遺伝子研究の概要
NLRC3, a member of the pattern recognition receptors nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) family, is an important regulator of innate immune system homeostasis [3,4]. It can inhibit excessive immune response in the body by influencing multiple signaling pathways, such as NF-κB, STING/TBK1, and inflammasome-related pathways. It also plays roles in cell fate regulation, like preventing proliferation, promoting apoptosis, and inhibiting pyroptosis [3].
NLRC3 deficiency promotes hypoxia-induced pulmonary hypertension development via the IKK/NF-κB p65/HIF-1α pathway. In hypoxia-induced mice models, NLRC3 knockout led to increased right ventricular systolic pressure, right ventricular hypertrophy and fibrosis. In vitro and in vivo, it promoted PASMCs proliferation, HUVECs apoptosis, migration and inflammation [1].
Myeloid-specific NLRC3 deletion in mice improved macrophage glycolysis and sepsis-induced immunosuppression, as NLRC3 was found to inhibit the binding of NF-κB p65 to NFAT5, controlling the expression of glycolytic genes and pro-inflammatory cytokines in immunosuppressive macrophages [2].
Nlrc3 knockout mice showed accelerated cutaneous wound healing, mainly due to its regulatory effects on p53 signaling. Nlrc3 was found to mediate the ubiquitination and degradation of p53 in an Hsp90-dependent manner [5].
After HTNV infection, Nlrc3-/-mice developed weight loss, renal hemorrhage, and tubule dilation, resembling human HFRS symptoms, with higher viral loads in serum, spleen, and kidney compared to wild-type mice [6].
In conclusion, NLRC3 plays a crucial role in regulating immune responses, cell proliferation, and apoptosis, and its dysregulation is associated with various diseases including pulmonary hypertension, sepsis, wound healing, and HTNV-induced renal diseases. The use of NLRC3 knockout mouse models has provided valuable insights into its functions in these disease-related biological processes, facilitating a better understanding of disease mechanisms and potential therapeutic targets.
References：
1. Maimaitiaili, Nuerbiyemu, Zeng, Yanxi, Ju, Peinan, Zhuoga, Deji, Yu, Qing. 2023. NLRC3 deficiency promotes hypoxia-induced pulmonary hypertension development via IKK/NF-κB p65/HIF-1α pathway. In Experimental cell research, 431, 113755. doi:10.1016/j.yexcr.2023.113755. https://pubmed.ncbi.nlm.nih.gov/37586455/
2. Xu, Jiqian, Gao, Chenggang, He, Yajun, Yao, Shanglong, Shang, You. 2022. NLRC3 expression in macrophage impairs glycolysis and host immune defense by modulating the NF-κB-NFAT5 complex during septic immunosuppression. In Molecular therapy : the journal of the American Society of Gene Therapy, 31, 154-173. doi:10.1016/j.ymthe.2022.08.023. https://pubmed.ncbi.nlm.nih.gov/36068919/
3. Sun, Deyi, Xu, Jiqian, Zhang, Wanying, He, Yajun, Shang, You. 2022. Negative regulator NLRC3: Its potential role and regulatory mechanism in immune response and immune-related diseases. In Frontiers in immunology, 13, 1012459. doi:10.3389/fimmu.2022.1012459. https://pubmed.ncbi.nlm.nih.gov/36341336/
4. Zhao, Yue, Li, Ruiting. 2022. Overview of the anti-inflammatory function of the innate immune sensor NLRC3. In Molecular immunology, 153, 36-41. doi:10.1016/j.molimm.2022.11.014. https://pubmed.ncbi.nlm.nih.gov/36403432/
5. Qin, Yuan, Wu, Kai, Zhang, Zheng, Lu, Liting, Lu, Xincheng. 2022. NLRC3 deficiency promotes cutaneous wound healing due to the inhibition of p53 signaling. In Biochimica et biophysica acta. Molecular basis of disease, 1868, 166518. doi:10.1016/j.bbadis.2022.166518. https://pubmed.ncbi.nlm.nih.gov/35963285/
6. Ma, Ruixue, Zhang, Xiaoxiao, Shu, Jiayi, Liu, Rongrong, Wu, Xingan. 2021. Nlrc3 Knockout Mice Showed Renal Pathological Changes After HTNV Infection. In Frontiers in immunology, 12, 692509. doi:10.3389/fimmu.2021.692509. https://pubmed.ncbi.nlm.nih.gov/34335602/
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