C57BL/6JCya-Naa40em1flox/Cya
Common Name:
Naa40-flox
Product ID:
S-CKO-14978
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Naa40-flox
Strain ID
CKOCMP-70999-Naa40-B6J-VA
Gene Name
Product ID
S-CKO-14978
Gene Alias
4931433E08Rik; Nat11; NatD
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
19
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Naa40em1flox/Cya mice (Catalog S-CKO-14978) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000025675
NCBI RefSeq
NM_027643
Target Region
Exon 2~3
Size of Effective Region
~2.3 kb
Detailed Document
Overview of Gene Research
Naa40, or N-alpha-acetyltransferase 40, is a highly specific epigenetic enzyme. It catalyzes the transfer of an acetyl moiety to the alpha -amino group of serine 1 on histones H4 and H2A, thus playing a role in epigenetic regulation [1,3,6]. This histone N -terminal acetylation is involved in various cellular processes, including gene expression control, chromatin function, and is associated with conditions like cancer, metabolic disorders [2,7].
Depletion of Naa40 in murine hepatocytes leads to increased intracellular acetyl -CoA levels and enhanced lipid synthesis, as well as impaired insulin signalling [2]. In colorectal cancer (CRC) cells, Naa40 depletion inhibits cell proliferation and survival, increases sensitivity to 5 -Fluorouracil treatment, and delays the growth of xenograft tumors. It also reduces symmetric dimethylation of histone H4 by downregulating PRMT5, altering the expression of oncogenes and tumor suppressor genes [1]. In CRC, Naa40 controls key one -carbon metabolic genes, promotes resistance to antimetabolite chemotherapy, and its expression is associated with TYMS levels and 5 -FU response [3]. In osteosarcoma, Naa40 depletion reduces cell viability, migration, and invasion, and Naa40 contributes to tumor development by regulating AGR2 expression epigenetically [5]. In HCT116 and HT -29 colorectal cancer cells, Naa40 depletion enhances apoptosis via the mitochondrial caspase -9 -mediated apoptotic cascade in a p53 -independent manner [6].
In conclusion, Naa40 is crucial for maintaining normal cellular functions, especially in processes related to metabolism and cancer. Through gene knockout -like experiments in cells and animal models, its role in promoting cancer cell growth, metabolic regulation, and apoptosis inhibition has been revealed, making it a potential therapeutic target for cancers such as colorectal cancer, liver cancer, and osteosarcoma [1,3,4,5,6].
References:
1. Demetriadou, Christina, Pavlou, Demetria, Mpekris, Fotios, Papageorgis, Panagiotis, Kirmizis, Antonis. 2019. NAA40 contributes to colorectal cancer growth by controlling PRMT5 expression. In Cell death & disease, 10, 236. doi:10.1038/s41419-019-1487-3. https://pubmed.ncbi.nlm.nih.gov/30858358/
2. Charidemou, Evelina, Tsiarli, Maria A, Theophanous, Andria, Griffin, Julian L, Kirmizis, Antonis. 2022. Histone acetyltransferase NAA40 modulates acetyl-CoA levels and lipid synthesis. In BMC biology, 20, 22. doi:10.1186/s12915-021-01225-8. https://pubmed.ncbi.nlm.nih.gov/35057804/
3. Demetriadou, Christina, Raoukka, Anastasia, Charidemou, Evelina, Tessarz, Peter, Kirmizis, Antonis. 2021. Histone N-terminal acetyltransferase NAA40 links one-carbon metabolism to chemoresistance. In Oncogene, 41, 571-585. doi:10.1038/s41388-021-02113-9. https://pubmed.ncbi.nlm.nih.gov/34785778/
4. Koufaris, Costas, Kirmizis, Antonis. 2021. Identification of NAA40 as a Potential Prognostic Marker for Aggressive Liver Cancer Subtypes. In Frontiers in oncology, 11, 691950. doi:10.3389/fonc.2021.691950. https://pubmed.ncbi.nlm.nih.gov/34150665/
5. Wu, Hanhua, Xu, Hua, Man, Yunan, Huang, Linhai, He, Maolin. 2025. N-terminal histone acetyltransferase NAA40 modulates osteosarcoma progression by controlling AGR2 expression. In Biochemical and biophysical research communications, 754, 151491. doi:10.1016/j.bbrc.2025.151491. https://pubmed.ncbi.nlm.nih.gov/40020320/
6. Pavlou, Demetria, Kirmizis, Antonis. . Depletion of histone N-terminal-acetyltransferase Naa40 induces p53-independent apoptosis in colorectal cancer cells via the mitochondrial pathway. In Apoptosis : an international journal on programmed cell death, 21, 298-311. doi:10.1007/s10495-015-1207-0. https://pubmed.ncbi.nlm.nih.gov/26666750/
7. Constantinou, Mamantia, Klavaris, Ariel, Koufaris, Costas, Kirmizis, Antonis. 2023. Cellular effects of NAT-mediated histone N-terminal acetylation. In Journal of cell science, 136, . doi:10.1242/jcs.260801. https://pubmed.ncbi.nlm.nih.gov/37013828/
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