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C57BL/6NCya-Hadhaem1/Cya
Common Name:
Hadha-KO
Product ID:
S-KO-19172
Background:
C57BL/6NCya
Product Type
Age
Genotype
Sex
Quantity
Price:
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Basic Information
Strain Name
Hadha-KO
Strain ID
KOCMP-97212-Hadha-B6N-VA
Gene Name
Hadha
Product ID
S-KO-19172
Gene Alias
Mtpa; TP-alpha
Background
C57BL/6NCya
NCBI ID
97212
Modification
Conventional knockout
Chromosome
5
Phenotype
MGI:2135593
Document
Click here to download >>
Application
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More
Rare Disease Data Center >>
Note
Note: When using this mouse strain in a publication, please cite “C57BL/6NCya-Hadhaem1/Cya mice (Catalog S-KO-19172) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000156859
NCBI RefSeq
NM_178878
Target Region
Exon 5
Size of Effective Region
~1.3 kb
Detailed Document
Click here to download >>
Overview of Gene Research
HADHA, also known as hydroxyacyl-CoA dehydrogenase trifunctional multienzyme complex subunit alpha, is a key mitochondrial β-oxidation enzyme. It is involved in fatty acid oxidation (FAO) pathway [3,4,8], which is crucial for energy production in cells. HADHA also plays a role in regulating metabolic processes such as ketone body production and is associated with multiple biological functions and disease-related pathways [1].

In various disease models, HADHA has shown significant impacts. In mice, liver-specific HADHA overexpression reversed hepatic gluconeogenesis, while knockdown augmented glucagon response, suggesting its role in diabetes-related metabolic regulation [1]. In hepatocellular carcinoma, miR-612 regulated invadopodia formation via HADHA-mediated lipid reprogramming, affecting cancer cell metastasis [2]. In ovarian cancer, HADHA overexpression was associated with poor survival, and its knockdown hindered cell growth and migration [5]. In glioma, high HADHA expression was linked to malignant progression, and knocking down HADHA decreased cell proliferation and migration [6]. In non-alcoholic fatty liver disease (NAFLD), HADHA alleviated hepatic steatosis and oxidative stress by inactivating the MKK3/MAPK pathway [7]. In regulatory T cells, Zfp335 controlled eTreg differentiation by regulating FAO through targeting HADHA, establishing immune tolerance [8]. In HTR-8/SVneo cells, HADHA inhibited cell migration and invasion by regulating the PI3K/AKT signaling pathway [9].

In conclusion, HADHA is essential for metabolic regulation through its role in fatty acid oxidation and ketone body production. Studies using gene knockout or knockdown models in mice and cell lines have revealed its significance in diseases such as diabetes, various cancers, NAFLD, and immune-related disorders. Understanding the function of HADHA provides potential targets for therapeutic interventions in these disease areas.

References:
1. Pan, An, Sun, Xiao-Meng, Huang, Feng-Qing, Liu, Qun, Qi, Lian-Wen. 2022. The mitochondrial β-oxidation enzyme HADHA restrains hepatic glucagon response by promoting β-hydroxybutyrate production. In Nature communications, 13, 386. doi:10.1038/s41467-022-28044-x. https://pubmed.ncbi.nlm.nih.gov/35046401/
2. Liu, Yang, Lu, Li-Li, Wen, Duo, Fan, Jia, Wu, Wei-Zhong. 2020. MiR-612 regulates invadopodia of hepatocellular carcinoma by HADHA-mediated lipid reprogramming. In Journal of hematology & oncology, 13, 12. doi:10.1186/s13045-019-0841-3. https://pubmed.ncbi.nlm.nih.gov/32033570/
3. Yang, Z, Wang, H, Xiao, J, Wang, X, Cao, Z. 2024. KDM6B-Mediated HADHA Demethylation/Lactylation Regulates Cementogenesis. In Journal of dental research, 104, 75-85. doi:10.1177/00220345241286460. https://pubmed.ncbi.nlm.nih.gov/39569625/
4. Qin, Chaoying, Gong, Shasha, Liang, Ting, Weintraub, Susan T, Bai, Yidong. 2024. HADHA Regulates Respiratory Complex Assembly and Couples FAO and OXPHOS. In Advanced science (Weinheim, Baden-Wurttemberg, Germany), 11, e2405147. doi:10.1002/advs.202405147. https://pubmed.ncbi.nlm.nih.gov/39488787/
5. Liu, Yinglan, Xiong, Ying. 2023. HADHA promotes ovarian cancer outgrowth via up-regulating CDK1. In Cancer cell international, 23, 283. doi:10.1186/s12935-023-03120-4. https://pubmed.ncbi.nlm.nih.gov/37986001/
6. Chen, Rudong, Chen, Hao, Hu, Changchen. 2024. HADHA promotes glioma progression by accelerating MDM2-mediated p53 ubiquitination. In Cancer gene therapy, 31, 1380-1389. doi:10.1038/s41417-024-00801-8. https://pubmed.ncbi.nlm.nih.gov/39039194/
7. Ding, Jiexia, Wu, Lili, Zhu, Guoxian, Luo, Pingping, Li, Youming. 2022. HADHA alleviates hepatic steatosis and oxidative stress in NAFLD via inactivation of the MKK3/MAPK pathway. In Molecular biology reports, 50, 961-970. doi:10.1007/s11033-022-07965-2. https://pubmed.ncbi.nlm.nih.gov/36376538/
8. Wang, Xin, Sun, Lina, Yang, Biao, Chen, WanJun, Zhang, Baojun. 2023. Zfp335 establishes eTreg lineage and neonatal immune tolerance by targeting Hadha-mediated fatty acid oxidation. In The Journal of clinical investigation, 133, . doi:10.1172/JCI166628. https://pubmed.ncbi.nlm.nih.gov/37843279/
9. Wu, Zhi-Hong, Wang, Yong-Heng, Liu, Tai-Hang, Li, Fang-Fang, Ding, Yu-Bin. . [HADHA Inhibits the Migration and Invasion of HTR-8/SVneo Cells by Regulating PI3K/AKT Signaling Pathway]. In Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 53, 805-814. doi:10.12182/20220960301. https://pubmed.ncbi.nlm.nih.gov/36224682/
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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