C57BL/6JCya-Nrip3em1/Cya
Common Name:
Nrip3-KO
Product ID:
S-KO-15186
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Nrip3-KO
Strain ID
KOCMP-78593-Nrip3-B6J-VA
Gene Name
Product ID
S-KO-15186
Gene Alias
A330103B05Rik; D7H11orf14; ICRFP703B1614Q5.2
Background
C57BL/6JCya
NCBI ID
Modification
Conventional knockout
Chromosome
7
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Nrip3em1/Cya mice (Catalog S-KO-15186) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000033331
NCBI RefSeq
NM_020610
Target Region
Exon 2~4
Size of Effective Region
~3.2 kb
Detailed Document
Overview of Gene Research
NRIP3, also known as nuclear receptor interacting protein 3, is a gene involved in multiple biological processes. It has been implicated in various signaling pathways, and its function appears to be significant in cancer-related processes. Genetic models, such as gene knockout mouse models, can potentially offer insights into its exact role in normal and diseased states.
In colorectal cancer (CRC), NRIP3 methylation was found in 50.6% of CRC samples, 32.2% of colorectal adenomatous polyps, and 2.7% of resected margin samples from CRC tissue. NRIP3 methylation was associated with late-onset, poor tumor differentiation, lymph node metastasis, and poor 5-year overall survival, and was an independent poor prognostic marker. NRIP3 inhibited cell proliferation, colony formation, invasion, and migration, while inducing G1/S arrest and suppressing CRC growth by inhibiting PI3K-AKT signaling both in vitro and in vivo. Additionally, NRIP3 methylation sensitized CRC cells to combined PI3K and ATR/ATM inhibitors [1].
In esophageal squamous cell carcinoma (ESCC), NRIP3 promoted tumor cell growth and resistance to chemoradiotherapy by increasing and binding to DDI1 and RTF2, and accelerating the removal of RTF2. Elevated NRIP3 was associated with poor clinical outcomes in ESCC patients receiving radiotherapy and/or cisplatin-based chemotherapy [2].
In MYCN-amplified neuroblastoma cells, depletion of L3MBTL2, which normally silences NRIP3, suppressed cell proliferation via cell-cycle arrest and gamma-H2A.X upregulation, and profoundly suppressed xenograft tumor formation [3].
In conclusion, NRIP3 appears to play a crucial role in cancer development and response to treatment. In CRC, its methylation status is related to prognosis and treatment sensitivity, while in ESCC, it promotes resistance to chemoradiotherapy. In neuroblastoma, its regulation by L3MBTL2 affects cell proliferation. These findings from model-based research, including in vivo studies, help understand the complex biological functions of NRIP3 in cancer-related processes.
References:
1. Zhang, Meiying, Li, Xiaoyun, Herman, James G, He, Kunlun, Guo, Mingzhou. 2024. Methylation of NRIP3 Is a Synthetic Lethal Marker for Combined PI3K and ATR/ATM Inhibitors in Colorectal Cancer. In Clinical and translational gastroenterology, 15, e00682. doi:10.14309/ctg.0000000000000682. https://pubmed.ncbi.nlm.nih.gov/38235705/
2. Suo, Daqin, Wang, Ling, Zeng, Tingting, Guan, Xin-Yuan, Li, Yan. 2020. NRIP3 upregulation confers resistance to chemoradiotherapy in ESCC via RTF2 removal by accelerating ubiquitination and degradation of RTF2. In Oncogenesis, 9, 75. doi:10.1038/s41389-020-00260-4. https://pubmed.ncbi.nlm.nih.gov/32839439/
3. Okada, Ryu, Takenobu, Hisanori, Satoh, Shunpei, Ohira, Miki, Kamijo, Takehiko. 2024. L3MBTL2 maintains MYCN-amplified neuroblastoma cell proliferation through silencing NRIP3 and BRME1 genes. In Genes to cells : devoted to molecular & cellular mechanisms, 29, 838-853. doi:10.1111/gtc.13148. https://pubmed.ncbi.nlm.nih.gov/39189159/
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