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C57BL/6JCya-Atad2em1/Cya
Common Name:
Atad2-KO
Product ID:
S-KO-18359
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Atad2-KO
Strain ID
KOCMP-70472-Atad2-B6J-VC
Gene Name
Atad2
Product ID
S-KO-18359
Gene Alias
2610509G12Rik
Background
C57BL/6JCya
NCBI ID
70472
Modification
Conventional knockout
Chromosome
15
Phenotype
MGI:1917722
Document
Click here to download >>
Application
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Note
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Atad2em1/Cya mice (Catalog S-KO-18359) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000038194
NCBI RefSeq
NM_027435
Target Region
Exon 10~28
Size of Effective Region
~24.7 kb
Detailed Document
Click here to download >>
Overview of Gene Research
ATAD2, an ATPase family AAA domain-containing protein 2, is a highly conserved bromodomain family protein. It functions mainly through its AAA ATPase and bromodomain, acting as an epigenetic decoder, transcription factor or co-activator. ATAD2 is involved in crucial cellular activities such as transcriptional regulation, DNA replication, and protein modification. It participates in multiple oncogenic signaling pathways, including Rb/E2F-cMyc, steroid hormone signaling, p53 and p38-MAPK-mediated apoptotic, AKT, hedgehog, HIF1α, and EMT pathways [1].

In human cancer cell lines and mouse embryonic stem cells, knockout (KO) of ATAD2 leads to an accumulation of the histone chaperone HIRA. ChIP-seq mapping in Atad2 KO mouse ES cells shows that HIRA and FACT are trapped on nucleosomes at the transcription start sites of active genes, resulting in abnormal nucleosome presence on TSS-associated nucleosome-free regions, highlighting its role in chromatin dynamics regulation [2]. In ovarian cancer, ATAD2 ablation caused mitotic arrest and decreased the ability of OC cells to pass through nocodazole-arrested mitosis. Disrupting the MYBL2-ATAD2 signaling by Nuclease technology-mediated ATAD2 ablation inhibited the in vivo growth of OC in a subcutaneous tumor xenograft mouse model [3]. In pancreatic cancer cells, ATAD2 silencing sensitizes cells to gemcitabine and radiation, enhancing the efficacy of their combination treatment [4].

In conclusion, ATAD2 is essential for normal chromatin dynamics and cellular activities. Through KO/CKO mouse models and cell-based functional studies, its role in promoting tumorigenesis, cancer progression, chemoresistance in various malignancies like ovarian, pancreatic, and colorectal cancers has been revealed. These findings suggest that targeting ATAD2 could be a potential strategy for cancer therapy.

References:
1. Nayak, Aditi, Dutta, Madhuri, Roychowdhury, Anasuya. 2021. Emerging oncogene ATAD2: Signaling cascades and therapeutic initiatives. In Life sciences, 276, 119322. doi:10.1016/j.lfs.2021.119322. https://pubmed.ncbi.nlm.nih.gov/33711386/
2. Wang, Tao, Perazza, Daniel, Boussouar, Fayçal, Verdel, André, Khochbin, Saadi. 2021. ATAD2 controls chromatin-bound HIRA turnover. In Life science alliance, 4, . doi:10.26508/lsa.202101151. https://pubmed.ncbi.nlm.nih.gov/34580178/
3. Liu, Qun, Liu, Heshu, Huang, Xuying, Miao, Jinwei, Liu, Jian. 2022. A targetable MYBL2-ATAD2 axis governs cell proliferation in ovarian cancer. In Cancer gene therapy, 30, 192-208. doi:10.1038/s41417-022-00538-2. https://pubmed.ncbi.nlm.nih.gov/36151333/
4. Dutta, Madhuri, Mohapatra, Debasish, Mohapatra, Amlan Priyadarshee, Senapati, Shantibhusan, Roychowdhury, Anasuya. 2022. ATAD2 suppression enhances the combinatorial effect of gemcitabine and radiation in pancreatic cancer cells. In Biochemical and biophysical research communications, 635, 179-186. doi:10.1016/j.bbrc.2022.10.021. https://pubmed.ncbi.nlm.nih.gov/36279679/
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
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