C57BL/6NCya-Fhitem1flox/Cya
Common Name:
Fhit-flox
Product ID:
S-CKO-02423
Background:
C57BL/6NCya
Product Type
Age
Genotype
Sex
Quantity
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Basic Information
Strain Name
Fhit-flox
Strain ID
CKOCMP-14198-Fhit-B6N-VA
Gene Name
Product ID
S-CKO-02423
Gene Alias
Fra14A2
Background
C57BL/6NCya
NCBI ID
Modification
Conditional knockout
Chromosome
14
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6NCya-Fhitem1flox/Cya mice (Catalog S-CKO-02423) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000162278
NCBI RefSeq
NM_010210
Target Region
Exon 5
Size of Effective Region
~0.6 kb
Detailed Document
Overview of Gene Research
Fhit, the product of the fragile histidine triad (FHIT) gene, is an enzyme that hydrolyzes the dinucleotide Ap3A. The FHIT gene encloses the common chromosomal fragile site FRA3B and is associated with genomic instability, apoptosis, and DNA damage [1,2]. It has been hypothesized to act as a tumor suppressor gene, playing crucial roles in cancer-related biological processes [1].
Fhit knockout mice are predisposed to tumor development [4]. In breast cancer, when one Fhit allele was inactivated (Fhit(+/-)) in mice crossed with FVB/N mice carrying the rat HER2/neu proto-oncogene, all Fhit heterozygous mice developed mammary tumors, while 27% of mice with both Fhit alleles (Fhit(+/+)) remained tumor-free at twenty months, suggesting a protective role for FHIT in HER2-driven mammary tumors [5]. Also, loss of Fhit in cells leads to nucleotide imbalance, spontaneous replication stress, and DNA breaks, as Fhit increases thymidine kinase 1 (TK1) translation to balance deoxyribonucleotide triphosphates (dNTPs) for efficient DNA replication [3].
In conclusion, Fhit is a key factor in maintaining genome stability and has a significant tumor-suppressing role. Mouse models, especially Fhit knockout mice, have been instrumental in revealing its function in tumor development, particularly in breast cancer. Understanding Fhit's function provides insights into cancer biology and may potentially lead to new therapeutic strategies.
References:
1. Silveira Zavalhia, Lisiane, Weber Medeiros, Aline, Oliveira Silva, Andrew, Vial Roehe, Adriana. 2018. Do FHIT gene alterations play a role in human solid tumors? In Asia-Pacific journal of clinical oncology, 14, e214-e223. doi:10.1111/ajco.12868. https://pubmed.ncbi.nlm.nih.gov/29516675/
2. Simón-Carrasco, Lucía, Pietrini, Elena, López-Contreras, Andrés J. 2024. Integrated analysis of FHIT gene alterations in cancer. In Cell cycle (Georgetown, Tex.), 23, 92-113. doi:10.1080/15384101.2024.2304509. https://pubmed.ncbi.nlm.nih.gov/38234243/
3. Saldivar, Joshua C, Park, Dongju. 2018. Mechanisms shaping the mutational landscape of the FRA3B/FHIT-deficient cancer genome. In Genes, chromosomes & cancer, 58, 317-323. doi:10.1002/gcc.22684. https://pubmed.ncbi.nlm.nih.gov/30242938/
4. Pichiorri, Flavia, Palumbo, Tiziana, Suh, Sung-Suk, Huebner, Kay, Croce, Carlo M. . Fhit tumor suppressor: guardian of the preneoplastic genome. In Future oncology (London, England), 4, 815-24. doi:10.2217/14796694.4.6.815. https://pubmed.ncbi.nlm.nih.gov/19086848/
5. Bianchi, Francesca, Tagliabue, Elda, Ménard, Sylvie, Campiglio, Manuela. 2007. Fhit expression protects against HER2-driven breast tumor development: unraveling the molecular interconnections. In Cell cycle (Georgetown, Tex.), 6, 643-6. doi:. https://pubmed.ncbi.nlm.nih.gov/17374991/
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