C57BL/6NCya-Ikbkeem1flox/Cya
Common Name:
Ikbke-flox
Product ID:
S-CKO-12131
Background:
C57BL/6NCya
Product Type
Age
Genotype
Sex
Quantity
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Basic Information
Strain Name
Ikbke-flox
Strain ID
CKOCMP-56489-Ikbke-B6N-VA
Gene Name
Product ID
S-CKO-12131
Gene Alias
IKK-E; IKK-i; IKKepsilon; Ikki
Background
C57BL/6NCya
NCBI ID
Modification
Conditional knockout
Chromosome
1
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6NCya-Ikbkeem1flox/Cya mice (Catalog S-CKO-12131) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000062108
NCBI RefSeq
NM_019777
Target Region
Exon 4~5
Size of Effective Region
~1.2 kb
Detailed Document
Overview of Gene Research
Ikbke, short for inhibitor of nuclear factor kappa-B kinase subunit epsilon, is a member of the nonclassical IKK family. It plays a crucial role in regulating inflammatory reactions, activation and proliferation of immune cells, and metabolic diseases. It is also involved in the cGAS/STING pathway which is related to antiviral immunity [2].
Depletion of Ikbke in various models has shown significant impacts. In mouse models, depletion of Ikbke decreased PyVMT-induced mouse mammary tumorigenesis and lung metastasis [3]. In glioblastoma, silencing Ikbke inhibited cell proliferation, invasion, and migration, and also affected angiogenesis by modulating VEGF expression [1,4]. In renal cell carcinoma, silencing Ikbke suppressed tumor progression and enhanced sunitinib sensitivity [5]. In pancreatic cancer mouse models, loss of Ikbke inhibited the initiation and progression of pancreatic tumors [6].
In conclusion, Ikbke is essential in multiple biological processes related to tumor development and antiviral immunity. The use of gene knockout (KO) or conditional knockout (CKO) mouse models has revealed its significant role in promoting tumor growth, invasion, metastasis, angiogenesis, and drug resistance in various cancers, highlighting its potential as a therapeutic target in oncology [1-7,9,10].
References：
1. Sun, Yan, Guo, Gaochao, Zhang, Yu, Nan, Yang, Huang, Qiang. 2024. IKBKE promotes the ZEB2-mediated EMT process by phosphorylating HMGA1a in glioblastoma. In Cellular signalling, 116, 111062. doi:10.1016/j.cellsig.2024.111062. https://pubmed.ncbi.nlm.nih.gov/38242271/
2. Reyahi, Azadeh, Studahl, Marie, Skouboe, Morten K, Eriksson, Kristina, Paludan, Søren R. 2023. An IKBKE variant conferring functional cGAS/STING pathway deficiency and susceptibility to recurrent HSV-2 meningitis. In JCI insight, 8, . doi:10.1172/jci.insight.173066. https://pubmed.ncbi.nlm.nih.gov/37937644/
3. Xie, Wei, Jiang, Qiwei, Wu, Xueji, Li, Jie, Guo, Jianping. 2022. IKBKE phosphorylates and stabilizes Snail to promote breast cancer invasion and metastasis. In Cell death and differentiation, 29, 1528-1540. doi:10.1038/s41418-022-00940-1. https://pubmed.ncbi.nlm.nih.gov/35066576/
4. Zhu, Lin, Guo, Gaochao, Jin, Yuwei, Hu, Aixia, Liu, Yang. 2023. IKBKE regulates angiogenesis by modulating VEGF expression and secretion in glioblastoma. In Tissue & cell, 84, 102180. doi:10.1016/j.tice.2023.102180. https://pubmed.ncbi.nlm.nih.gov/37573607/
5. Liu, Shiwei, Li, Junhong, Zhang, Junyu, Hong, Zhe, Dai, Bo. 2024. IKBKE regulates renal cell carcinoma progression and sunitinib resistance through the RRM2-AKT pathway. In International journal of biological sciences, 20, 6146-6161. doi:10.7150/ijbs.102666. https://pubmed.ncbi.nlm.nih.gov/39664571/
6. Rajurkar, Mihir, Dang, Kyvan, Fernandez-Barrena, Maite G, Lewis, Brian C, Mao, Junhao. 2017. IKBKE Is Required during KRAS-Induced Pancreatic Tumorigenesis. In Cancer research, 77, 320-329. doi:10.1158/0008-5472.CAN-15-1684. https://pubmed.ncbi.nlm.nih.gov/28069799/
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