C57BL/6JCya-Prdx3em1/Cya
Common Name
Prdx3-KO
Product ID
S-KO-01057
Backgroud
C57BL/6JCya
Strain ID
KOCMP-11757-Prdx3-B6J-VA
Status
When using this mouse strain in a publication, please cite “Prdx3-KO Mouse (Catalog S-KO-01057) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
The standard delivery applies for a guaranteed minimum of three heterozygous carriers. Breeding services for homozygous carriers and/or specified sex are available.
Basic Information
Strain Name
Prdx3-KO
Strain ID
KOCMP-11757-Prdx3-B6J-VA
Gene Name
Product ID
S-KO-01057
Gene Alias
Aop1, Ef2l, Mer5, Prx3, SP22, TDXM, D0Tohi1
Background
C57BL/6JCya
NCBI ID
Modification
Conventional knockout
Chromosome
Chr 19
Phenotype
Datasheet
Application
--
Strain Description
Ensembl Number
ENSMUST00000025961
NCBI RefSeq
NM_007452
Target Region
Exon 1~7
Size of Effective Region
~10.1 kb
Overview of Gene Research
Prdx3, peroxiredoxin 3, is a master regulator of mitochondrial oxidative stress, acting as an efficient hydrogen peroxide (H2O2) scavenger protecting cells from mitochondrial oxidative damage and apoptosis [2,3]. It is involved in multiple pathways such as mitochondrial reactive oxygen species (ROS)/TGF-β1/Smad2/3, and its dysregulation is associated with various diseases [2]. Genetic models like KO/CKO mouse models can provide insights into its function in vivo.
In mouse models of alcoholic and non-alcoholic fatty liver diseases, hyperoxidized Prdx3 was identified as a marker for ferroptosis, suggesting ferroptosis is responsible for hepatocyte death [1]. In liver fibrosis, AAV9-Prdx3 knockdown exacerbated hepatic fibrogenesis and HSC activation, while HSC-specific Prdx3 overexpression attenuated liver fibrosis, indicating Prdx3's role in regulating this process through the mitochondrial ROS/TGF-β1/Smad2/3 pathway [2]. In intestinal I/R injury mouse models, Prdx3 expression was decreased, and its overexpression attenuated H/R-induced mitochondrial oxidative damage and apoptosis. SIRT3-mediated deacetylation of Prdx3 was shown to be crucial in alleviating this injury [3].
In conclusion, Prdx3 plays essential roles in maintaining mitochondrial oxidative balance. Model-based research, especially KO/CKO mouse models, has revealed its significance in diseases like chronic liver diseases, liver fibrosis, and intestinal I/R injury, offering potential therapeutic targets for these conditions.
References:
1. Cui, Shaojie, Ghai, Anchal, Deng, Yaqin, Achilefu, Samuel, Ye, Jin. 2023. Identification of hyperoxidized PRDX3 as a ferroptosis marker reveals ferroptotic damage in chronic liver diseases. In Molecular cell, 83, 3931-3939.e5. doi:10.1016/j.molcel.2023.09.025. https://pubmed.ncbi.nlm.nih.gov/37863053/
2. Sun, Ruimin, Tian, Xinyao, Li, Yang, Zheng, Shusen, Yao, Jihong. 2022. The m6A reader YTHDF3-mediated PRDX3 translation alleviates liver fibrosis. In Redox biology, 54, 102378. doi:10.1016/j.redox.2022.102378. https://pubmed.ncbi.nlm.nih.gov/35779442/
3. Wang, Zhanyu, Sun, Ruimin, Wang, Guangzhi, Yao, Jihong, Tian, Xiaofeng. 2019. SIRT3-mediated deacetylation of PRDX3 alleviates mitochondrial oxidative damage and apoptosis induced by intestinal ischemia/reperfusion injury. In Redox biology, 28, 101343. doi:10.1016/j.redox.2019.101343. https://pubmed.ncbi.nlm.nih.gov/31655428/
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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