C57BL/6JCya-Rbpjem1flox/Cya
Common Name:
Rbpj-flox
Product ID:
S-CKO-18031
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Rbpj-flox
Strain ID
CKOCMP-19664-Rbpj-B6J-VB
Gene Name
Product ID
S-CKO-18031
Gene Alias
CBF1; Igkjrb; Igkrsbp; RBP-J; RBP-J kappa; RBP-Jkappa; RBPjk; Rbpsuh
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
5
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Rbpjem1flox/Cya mice (Catalog S-CKO-18031) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000037618
NCBI RefSeq
NM_009035
Target Region
Exon 4
Size of Effective Region
~1.8 kb
Detailed Document
Overview of Gene Research
Rbpj, also known as Recombination signal-binding protein for immunoglobulin kappa J region, is a crucial transcriptional regulator. It is the central player in the Notch signaling pathway. In the Notch cascade, it either forms an activator complex with the Notch intracellular domain (NICD) or a repressor complex with corepressors, and this balance is determined by the Notch receptor's activation state. Rbpj is vital for maintaining immune homeostasis and is involved in many biological processes [2,4].
In pancreatic cancer, conditional transgenic mouse models (Ptf1α-CreERT-driven) showed that RBPJ deficiency in adult pancreatic acinar cells doesn't affect their homeostasis but sensitizes them to KRAS-mediated pancreatic intraepithelial neoplasia initiation, promoting fibrotic stroma formation [1].
In epithelial ovarian cancer, deletion of Rbpj in endothelial cells of adult mice reduced monocyte-derived macrophage infiltration into the tumor microenvironment, affecting tumor-associated macrophage (TAM) education and EOC progression [3].
In brain arteriovenous malformation (bAVM) mouse models, deletion of endothelial Rbpj normalized Notch4-induced bAVM, and in an in vivo mouse model of Rbpj-mediated bAVM, Rbpj deficiency disrupted vascular remodeling via abnormal Apelin and Cdc42 activity [5,9].
In uveitis, targeted RBPJ knockdown in rats promoted M2 macrophage polarization through the mtROS-mediated Notch1-Jagged1-Hes1 signaling pathway, ameliorating uveitis [7].
In metabolic dysfunction-associated steatotic liver disease, Rbpj deficiency in mice blunted inflammatory macrophages and monocyte-derived KC differentiation, promoting protective Ly6Clo monocytes [8].
In T-cell fate regulation, targeting RBPJ enhanced functional and epigenetic reprogramming of Tex cells, improving antitumour effects [6].
In conclusion, Rbpj plays essential roles in multiple biological processes mainly through its function in the Notch signaling pathway. Gene knockout and conditional knockout mouse models have significantly contributed to understanding its role in diseases such as pancreatic cancer, epithelial ovarian cancer, bAVM, uveitis, metabolic-associated liver disease, and cancer immunotherapy. These studies provide insights into potential therapeutic strategies targeting Rbpj in these disease areas.
References:
1. Pan, Leiling, Mulaw, Medhanie A, Gout, Johann, Wagner, Martin, Oswald, Franz. 2023. RBPJ Deficiency Sensitizes Pancreatic Acinar Cells to KRAS-Mediated Pancreatic Intraepithelial Neoplasia Initiation. In Cellular and molecular gastroenterology and hepatology, 16, 783-807. doi:10.1016/j.jcmgh.2023.07.013. https://pubmed.ncbi.nlm.nih.gov/37543088/
2. Giaimo, Benedetto Daniele, Gagliani, Ellen K, Kovall, Rhett A, Borggrefe, Tilman. . Transcription Factor RBPJ as a Molecular Switch in Regulating the Notch Response. In Advances in experimental medicine and biology, 1287, 9-30. doi:10.1007/978-3-030-55031-8_2. https://pubmed.ncbi.nlm.nih.gov/33034023/
3. Alsina-Sanchis, Elisenda, Mülfarth, Ronja, Moll, Iris, Fischer, Andreas, Rodriguez-Vita, Juan. . Endothelial RBPJ Is Essential for the Education of Tumor-Associated Macrophages. In Cancer research, 82, 4414-4428. doi:10.1158/0008-5472.CAN-22-0076. https://pubmed.ncbi.nlm.nih.gov/36200806/
4. Chen, Shuaishuai, Zhao, Weibo, Du, Juping, Zhou, Yuanlin, Chen, Shiyong. 2024. The expression of RBPJ and its potential role in rheumatoid arthritis. In BMC genomics, 25, 899. doi:10.1186/s12864-024-10804-2. https://pubmed.ncbi.nlm.nih.gov/39350019/
5. Nielsen, Corinne M, Zhang, Xuetao, Raygor, Kunal, Bollen, Andrew W, Wang, Rong A. 2022. Endothelial Rbpj deletion normalizes Notch4-induced brain arteriovenous malformation in mice. In The Journal of experimental medicine, 220, . doi:10.1084/jem.20211390. https://pubmed.ncbi.nlm.nih.gov/36441145/
6. Zhou, Peipei, Shi, Hao, Huang, Hongling, Pruett-Miller, Shondra M, Chi, Hongbo. 2023. Single-cell CRISPR screens in vivo map T cell fate regulomes in cancer. In Nature, 624, 154-163. doi:10.1038/s41586-023-06733-x. https://pubmed.ncbi.nlm.nih.gov/37968405/
7. Qu, Ruyi, Peng, Yuan, Xu, Shuqin, Bi, Hongsheng, Guo, Dadong. 2024. RBPJ Knockdown Promotes M2 Macrophage Polarization Through Mitochondrial ROS-mediated Notch1-Jagged1-Hes1 Signaling Pathway in Uveitis. In Inflammation, 48, 133-150. doi:10.1007/s10753-024-02053-y. https://pubmed.ncbi.nlm.nih.gov/38761249/
8. Guo, Wei, Li, Ziyi, Anagnostopoulos, Gerasimos, Su, Bing, Ginhoux, Florent. 2024. Notch signaling regulates macrophage-mediated inflammation in metabolic dysfunction-associated steatotic liver disease. In Immunity, 57, 2310-2327.e6. doi:10.1016/j.immuni.2024.08.016. https://pubmed.ncbi.nlm.nih.gov/39317200/
9. Adhicary, Subhodip, Fanelli, Kayleigh, Nakisli, Sera, Pearce, Isaac, Nielsen, Corinne M. 2023. Rbpj Deficiency Disrupts Vascular Remodeling via Abnormal Apelin and Cdc42 (Cell Division Cycle 42) Activity in Brain Arteriovenous Malformation. In Stroke, 54, 1593-1605. doi:10.1161/STROKEAHA.122.041853. https://pubmed.ncbi.nlm.nih.gov/37051908/
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