C57BL/6NCya-Hdac9em1/Cya
Common Name:
Hdac9-KO
Product ID:
S-KO-15269
Background:
C57BL/6NCya
Product Type
Age
Genotype
Sex
Quantity
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Contact for Pricing
Basic Information
Strain Name
Hdac9-KO
Strain ID
KOCMP-79221-Hdac9-B6N-VA
Gene Name
Product ID
S-KO-15269
Gene Alias
D030072B18Rik; HD7B; HD9; HDRP; Hdac7b; Mitr; mKIAA0744
Background
C57BL/6NCya
NCBI ID
Modification
Conventional knockout
Chromosome
12
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6NCya-Hdac9em1/Cya mice (Catalog S-KO-15269) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000209750
NCBI RefSeq
XM_036157675
Target Region
Exon 3~5
Size of Effective Region
~3.7 kb
Detailed Document
Overview of Gene Research
HDAC9, a histone deacetylase enzyme belonging to the class IIa of HDACs, catalyzes histone deacetylation. It inhibits cell proliferation through DNA repair, cell cycle arrest, apoptosis induction, and genetic expression alteration. HDAC9 is involved in various biological processes and is associated with multiple pathways related to different diseases [4].
In atherosclerotic disease, a variant in the HDAC9 gene is a risk factor. Reducing HDAC9 protein in animal and cellular models is associated with reduced disease, suggesting that inhibiting HDAC9 may be a novel treatment approach [1]. In male mouse kidney fibrosis models, tubule-specific deletion or pharmacological inhibition of HDAC9 alleviates epithelial cell cycle arrest in G2/M, reducing profibrotic cytokine production and tubulointerstitial fibrosis [2]. In intervertebral disc degeneration (IVDD), HDAC9KO mice spontaneously develop age-related IVDD, while overexpression of HDAC9 in NP cells alleviates IVDD symptoms in a surgically-induced mouse model [3]. In vascular calcification models, both pharmacological inhibition and knockdown of HDAC9 attenuated calcification of human vascular smooth muscle cells, while overexpression exacerbated it [5]. In matrix Gla protein-deficient mice (a model of human vascular calcification), mice lacking HDAC9 had a 40% reduction in aortic calcification and improved survival [6]. In myocardial infarction models, HDAC9 knockout induced the activation of Nrf2 and protected the heart from injury [7]. In the chronic restraint stress mouse model of depression, knockdown or knockout of HDAC9 in hippocampal neurons alleviated depression-like phenotypes [8].
In conclusion, HDAC9 plays a significant role in multiple biological processes and is involved in various diseases such as atherosclerosis, kidney fibrosis, IVDD, vascular calcification, myocardial infarction, and depression. Gene knockout mouse models have been crucial in revealing its functions in these disease conditions, providing potential therapeutic targets for treatment.
References:
1. Markus, Hugh S. 2023. HDAC9 Inhibition as a Novel Treatment for Stroke. In Stroke, 54, 3182-3189. doi:10.1161/STROKEAHA.123.044862. https://pubmed.ncbi.nlm.nih.gov/37942644/
2. Zhang, Yang, Yang, Yujie, Yang, Fan, Liu, Min, Yi, Fan. 2023. HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis in male mice. In Nature communications, 14, 3007. doi:10.1038/s41467-023-38771-4. https://pubmed.ncbi.nlm.nih.gov/37230975/
3. Lei, Ming, Lin, Hui, Shi, Deyao, Liao, Zhiwei, Yang, Cao. 2023. Molecular mechanism and therapeutic potential of HDAC9 in intervertebral disc degeneration. In Cellular & molecular biology letters, 28, 104. doi:10.1186/s11658-023-00517-x. https://pubmed.ncbi.nlm.nih.gov/38093179/
4. Das, Totan, Khatun, Samima, Jha, Tarun, Gayen, Shovanlal. . HDAC9 as a Privileged Target: Reviewing its Role in Different Diseases and Structure-activity Relationships (SARs) of its Inhibitors. In Mini reviews in medicinal chemistry, 24, 767-784. doi:10.2174/0113895575267301230919165827. https://pubmed.ncbi.nlm.nih.gov/37818566/
5. Lan, Zirong, Chen, An, Li, Li, Lu, Lihe, Yan, Jianyun. 2022. Downregulation of HDAC9 by the ketone metabolite β-hydroxybutyrate suppresses vascular calcification. In The Journal of pathology, 258, 213-226. doi:10.1002/path.5992. https://pubmed.ncbi.nlm.nih.gov/35894849/
6. Malhotra, Rajeev, Mauer, Andreas C, Lino Cardenas, Christian L, Post, Wendy S, O'Donnell, Christopher J. 2019. HDAC9 is implicated in atherosclerotic aortic calcification and affects vascular smooth muscle cell phenotype. In Nature genetics, 51, 1580-1587. doi:10.1038/s41588-019-0514-8. https://pubmed.ncbi.nlm.nih.gov/31659325/
7. Liu, Fan, Di, Yali, Ma, Wei, Li, Xia, Ji, Zheng. . HDAC9 exacerbates myocardial infarction via inactivating Nrf2 pathways. In The Journal of pharmacy and pharmacology, 74, 565-572. doi:10.1093/jpp/rgab065. https://pubmed.ncbi.nlm.nih.gov/33963859/
8. Dai, Yunjian, Wei, Taofeng, Huang, Yuwen, Lin, Zheng, Dai, Haibin. 2023. Upregulation of HDAC9 in hippocampal neurons mediates depression-like behaviours by inhibiting ANXA2 degradation. In Cellular and molecular life sciences : CMLS, 80, 289. doi:10.1007/s00018-023-04945-y. https://pubmed.ncbi.nlm.nih.gov/37690046/
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