C57BL/6JCya-Stk17bem1/Cya
Common Name:
Stk17b-KO
Product ID:
S-KO-19390
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
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Basic Information
Strain Name
Stk17b-KO
Strain ID
KOCMP-98267-Stk17b-B6J-VC
Gene Name
Product ID
S-KO-19390
Gene Alias
3110009A03Rik; Drak2
Background
C57BL/6JCya
NCBI ID
Modification
Conventional knockout
Chromosome
1
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Stk17bem1/Cya mice (Catalog S-KO-19390) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000027263
NCBI RefSeq
NM_133810
Target Region
Exon 4
Size of Effective Region
~1.2 kb
Detailed Document
Overview of Gene Research
Stk17b, also known as DRAK2, is a serine/threonine protein kinase belonging to the death-associated protein kinase family. It is involved in various biological processes such as setting the threshold for T-cell activation [4]. In the immune system, it is a downstream effector of protein kinase C (PKC), and in cerebellar Purkinje cells, it regulates dendritic development [5].
In cancer research, Stk17b has been shown to have diverse roles. In ovarian cancer, its high expression promotes cell proliferation, invasion, and migration by promoting the epithelial-mesenchymal transition (EMT) process [1]. In hepatocellular carcinoma, it promotes carcinogenesis and metastasis via the AKT/GSK-3β/Snail signaling pathway [3]. In glioma, it is regulated by the TP53TG1/miR-96-5p ceRNA pathway, and methionine deprivation inhibits glioma progression by affecting this pathway related to Stk17b [6]. In skin cutaneous melanoma, lower Stk17b expression is associated with poor overall and disease-specific survival, and it is related to immune infiltration [2].
In conclusion, Stk17b plays important roles in multiple biological processes and disease conditions, especially in cancer progression and immune-related functions. Studies on Stk17b contribute to understanding the mechanisms of cancer development and immune-related diseases, potentially providing new targets for treatment.
References:
1. Jiang, Liping, Zhou, Jinhua, Zhao, Shaojie, Wang, Xuzhen, Chen, Youguo. . STK17B promotes the progression of ovarian cancer. In Annals of translational medicine, 9, 475. doi:10.21037/atm-21-601. https://pubmed.ncbi.nlm.nih.gov/33850872/
2. Shi, Xueying, Zhou, Qi, Huang, Bingqian, Fang, Shifeng, Lin, Jingrong. 2022. Prognostic and immune-related value of STK17B in skin cutaneous melanoma. In PloS one, 17, e0263311. doi:10.1371/journal.pone.0263311. https://pubmed.ncbi.nlm.nih.gov/35171924/
3. Lan, Yaliang, Han, Jihua, Wang, Yan, Subash, Sharma, Liu, Lianxin. 2018. STK17B promotes carcinogenesis and metastasis via AKT/GSK-3β/Snail signaling in hepatocellular carcinoma. In Cell death & disease, 9, 236. doi:10.1038/s41419-018-0262-1. https://pubmed.ncbi.nlm.nih.gov/29445189/
4. Scheuplein, Felix, Renner, Florian, Campbell, John E, Dorsch, Marion, Bischoff, James R. 2024. Evaluation of STK17B as a cancer immunotherapy target utilizing highly potent and selective small molecule inhibitors. In Frontiers in immunology, 15, 1411395. doi:10.3389/fimmu.2024.1411395. https://pubmed.ncbi.nlm.nih.gov/39502695/
5. Wu, Qin-Wei, Kapfhammer, Josef P. 2021. Serine/threonine kinase 17b (STK17B) signalling regulates Purkinje cell dendritic development and is altered in multiple spinocerebellar ataxias. In The European journal of neuroscience, 54, 6673-6684. doi:10.1111/ejn.15465. https://pubmed.ncbi.nlm.nih.gov/34536317/
6. Li, Jiafeng, Liu, Ruijie, Hu, Hong, Wang, Kaikai, Liu, Huailei. 2024. Methionine deprivation inhibits glioma proliferation and EMT via the TP53TG1/miR-96-5p/STK17B ceRNA pathway. In NPJ precision oncology, 8, 270. doi:10.1038/s41698-024-00763-y. https://pubmed.ncbi.nlm.nih.gov/39572759/
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