C57BL/6JCya-Ncapd2em1flox/Cya
Common Name:
Ncapd2-flox
Product ID:
S-CKO-14137
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Ncapd2-flox
Strain ID
CKOCMP-68298-Ncapd2-B6J-VA
Gene Name
Product ID
S-CKO-14137
Gene Alias
2810406C15Rik; 2810465G24Rik; CAP-D2; CNAP1; mKIAA0159
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
6
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Ncapd2em1flox/Cya mice (Catalog S-CKO-14137) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000043848
NCBI RefSeq
NM_146171
Target Region
Exon 7~9
Size of Effective Region
~1.6 kb
Detailed Document
Overview of Gene Research
Ncapd2, also known as Non-SMC condensin I complex subunit D2, is one of the three non-SMC subunits in condensin I. It plays a crucial role in chromosome condensation and segregation, and is involved in various biological processes [1,2,3,4,5,6,7,8,9].
In multiple cancers, Ncapd2 has been shown to act as a tumor promoter. In a colorectal cancer AOM/DSS-induced mice model, Ncapd2 knockout suppressed cancer development. Ncapd2 was found to inhibit autophagy via the Ca2+/CAMKK2/AMPK/mTORC1 pathway and PARP-1/SIRT1 axis, thus promoting colorectal cancer progression [1].
In breast cancer, knockdown of Ncapd2 restrained cancer progression by inhibiting proliferation and migration and enhancing apoptosis in vitro, and inhibited tumor growth in vivo. Ncapd2 promoted breast cancer progression through the ERK5 signaling pathway and the NCAPD2/E2F1/CDK1 axis [2].
In liver cancer, its overexpression led to cell cycle progression at the G2/M-phase transition, activation of the PI3K-Akt-mTOR/c-Myc signaling pathway and EMT progression [3].
In oral squamous cell carcinoma, knockdown of Ncapd2 inhibited cell proliferation, promoted apoptosis, and inhibited migration both in vitro and in vivo, and it was involved in the Wnt/β-catenin signaling pathway [4].
In lung adenocarcinoma, silencing Ncapd2 suppressed cell proliferation, migration, invasion, EMT, and cell cycle progression in vitro [6].
In Crohn's disease, NCAPD2 knockdown in a TNBS-induced mouse model inhibited intestinal inflammation. NCAPD2 was found to inhibit autophagy by promoting mTOR phosphorylation and down-regulating autophagy-related proteins, and also activated the NF-κB signaling pathway [7].
In conclusion, Ncapd2 is essential for chromosome-related functions. Its role as a tumor promoter and its influence on autophagy and inflammation in diseases like cancer and Crohn's disease have been revealed through gene knockout and other functional studies in mouse models. These findings highlight Ncapd2 as a potential therapeutic target in these disease areas.
References：
1. Jing, Zuolei, He, Xinyuan, Jia, Zhirong, Yang, Bolin, Liu, Ping. 2021. NCAPD2 inhibits autophagy by regulating Ca2+/CAMKK2/AMPK/mTORC1 pathway and PARP-1/SIRT1 axis to promote colorectal cancer. In Cancer letters, 520, 26-37. doi:10.1016/j.canlet.2021.06.029. https://pubmed.ncbi.nlm.nih.gov/34229059/
2. He, Jinsong, Gao, Rui, Yang, Jianbo, Zhou, Zihan, Wei, Wei. 2022. NCAPD2 promotes breast cancer progression through E2F1 transcriptional regulation of CDK1. In Cancer science, 114, 896-907. doi:10.1111/cas.15347. https://pubmed.ncbi.nlm.nih.gov/35348268/
3. Gu, Jiang-Xue, Huang, Ke, Zhao, Wei-Lin, Huang, Yu-Gang, Hu, Pei. 2024. NCAPD2 augments the tumorigenesis and progression of human liver cancer via the PI3K‑Akt‑mTOR signaling pathway. In International journal of molecular medicine, 54, . doi:10.3892/ijmm.2024.5408. https://pubmed.ncbi.nlm.nih.gov/39092569/
4. Ma, Ping, Yu, Huajiao, Zhu, Mingda, Han, Zhengxue, Jin, Wulong. 2024. NCAPD2 promotes the malignant progression of oral squamous cell carcinoma via the Wnt/β-catenin pathway. In Cell cycle (Georgetown, Tex.), 23, 588-601. doi:10.1080/15384101.2024.2348918. https://pubmed.ncbi.nlm.nih.gov/38743408/
5. Li, Zihao, Zheng, Yuxuan, Wu, Zuotao, Wang, Yongyong, Chen, Mingwu. . NCAPD2 is a novel marker for the poor prognosis of lung adenocarcinoma and is associated with immune infiltration and tumor mutational burden. In Medicine, 102, e32686. doi:10.1097/MD.0000000000032686. https://pubmed.ncbi.nlm.nih.gov/36701707/
6. Wu, Peiling, Zhao, Lifang, Zhang, Hongyan, Liu, Xueqing, Jiang, Handong. 2024. NCAPD2 serves as a potential prognostic biomarker for lung adenocarcinoma and promotes cell proliferation, migration, invasion and cell cycle in vitro. In Oncology research, 32, 1439-1452. doi:10.32604/or.2024.047490. https://pubmed.ncbi.nlm.nih.gov/39220139/
7. Ge, Hao, Wang, Can, Zhao, Haoran, Liu, Ping, Yang, Bolin. . Targeting NCAPD2 as a Therapeutic Strategy for Crohn's Disease: Implications for Autophagy and Inflammation. In Inflammatory bowel diseases, 31, 178-188. doi:10.1093/ibd/izae211. https://pubmed.ncbi.nlm.nih.gov/39340820/
8. Dong, Xiaoying, Liu, Ting, Li, Zhizhao, Zhai, Yongzhen. 2023. Non-SMC condensin I complex subunit D2 (NCAPD2) reveals its prognostic and immunologic features in human cancers. In Aging, 15, 7237-7257. doi:10.18632/aging.204904. https://pubmed.ncbi.nlm.nih.gov/37498296/
9. Mai, Yuhua, Liao, Chuanjie, Wang, Shengyu, Qin, Yingfen, Deng, Ganlu. 2024. High glucose-induced NCAPD2 upregulation promotes malignant phenotypes and regulates EMT via the Wnt/β-catenin signaling pathway in HCC. In American journal of cancer research, 14, 1685-1711. doi:10.62347/HYNZ9211. https://pubmed.ncbi.nlm.nih.gov/38726276/
Quality Control Standard
Sperm Test
Pre-cryopreservation: Measurement of sperm concentration, determination of sperm viability.
Post-cryopreservation: A vial of cryopreserved sperms is selected for in-vitro fertilization from each batch.
Environmental Standards:SPF
Available Region:Global
Source:Cyagen