C57BL/6JCya-Bcl6bem1/Cya
Common Name
Bcl6b-KO
Product ID
S-KO-01201
Backgroud
C57BL/6JCya
Strain ID
KOCMP-12029-Bcl6b-B6J-VB
When using this mouse strain in a publication, please cite “Bcl6b-KO Mouse (Catalog S-KO-01201) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Basic Information
Strain Name
Bcl6b-KO
Strain ID
KOCMP-12029-Bcl6b-B6J-VB
Gene Name
Product ID
S-KO-01201
Gene Alias
Bazf
Background
C57BL/6JCya
NCBI ID
Modification
Conventional knockout
Chromosome
Chr 11
Phenotype
Datasheet
Application
--
Strain Description
Ensembl Number
ENSMUST00000000326
NCBI RefSeq
NM_007528
Target Region
Exon 2~5
Size of Effective Region
~2.0 kb
Overview of Gene Research
Bcl6b, also known as BAZF, ZBTB28, and ZNF62, operates as a sequence-specific transcriptional repressor in the nucleus. It plays crucial roles in multiple biological functions, including tumor suppression, immune response, stem cell self-renewal, and vascular angiogenesis [2]. It is involved in pathways such as the VEGF-Notch signaling balance, which is important for endothelial cell activation [1].
In animal models, Bcl6b-deficient endothelial cells showed Notch signal activation and attenuated cord formation by blocking the VEGF-VEGFR2 signaling pathway. Bcl6b-targeting small-interfering ribonucleic acid decreased choroidal neovascularization lesions and suppressed ocular edema in the neuroretina, indicating its role in ocular vascular diseases [1]. In mice, knockout of Bcl6b worsened gastric cancer and aggravated the inflammatory response, while re-activation of Bcl6b impeded inflammatory amplification and gastric cancer development [3]. Also, Bcl6b transgenic rats were less susceptible to hepatocellular damage, inflammation, and fibrosis [4].
In conclusion, Bcl6b is essential in regulating various biological processes and disease conditions. Gene knockout models, especially in mice, have revealed its significant roles in ocular vascular diseases, gastric cancer, and liver-related pathologies. These findings suggest that Bcl6b could be a potential therapeutic target for these diseases.
References:
1. Tanaka, Miruto, Nakamura, Shinsuke, Sakaue, Tomohisa, Higashiyama, Shigeki, Hara, Hideaki. 2023. BCL6B Contributes to Ocular Vascular Diseases via Notch Signal Silencing. In Arteriosclerosis, thrombosis, and vascular biology, 43, 927-942. doi:10.1161/ATVBAHA.123.318987. https://pubmed.ncbi.nlm.nih.gov/37078291/
2. Li, Zhonghao, Wu, Wei, Li, Qiushi, Xiao, Qingzhong, Yan, Yi. 2024. BCL6B-dependent suppression of ETV2 hampers endothelial cell differentiation. In Stem cell research & therapy, 15, 226. doi:10.1186/s13287-024-03832-y. https://pubmed.ncbi.nlm.nih.gov/39075623/
3. Cai, Wang-Yu, Lin, Ling-Yun, Wang, Lin, Chen, Mao-Li, Luo, Qi-Cong. 2019. Inhibition of Bcl6b promotes gastric cancer by amplifying inflammation in mice. In Cell communication and signaling : CCS, 17, 72. doi:10.1186/s12964-019-0387-6. https://pubmed.ncbi.nlm.nih.gov/31288844/
4. Wang, Weilin, Huang, Pengfei, Wu, Panyisha, Zhou, Lin, Zheng, Shusen. . BCL6B expression in hepatocellular carcinoma and its efficacy in the inhibition of liver damage and fibrogenesis. In Oncotarget, 6, 20252-65. doi:. https://pubmed.ncbi.nlm.nih.gov/25970780/
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
Contact Us
Connect with our experts for your custom animal model needs. Please fill out the form below to start a conversation or request a quote.
Cyagen values your privacy. We’d like to keep you informed about our latest offerings and insights. Your preferences:
You may unsubscribe from these communications at any time. See our Privacy Policy for details on opting out and data protection.
By clicking the button below, you consent to allow Cyagen to store and process the personal information submitted in this form to provide you the content requested.
