C57BL/6JCya-Sod1em1flox/Cya
Common Name
Sod1-flox
Product ID
S-CKO-05168
Backgroud
C57BL/6JCya
Strain ID
CKOCMP-20655-Sod1-B6J-VA
When using this mouse strain in a publication, please cite “Sod1-flox Mouse (Catalog S-CKO-05168) were purchased from Cyagen.”
Product Type
Age
Genotype
Sex
Quantity
Basic Information
Strain Name
Sod1-flox
Strain ID
CKOCMP-20655-Sod1-B6J-VA
Gene Name
Product ID
S-CKO-05168
Gene Alias
B430204E11Rik, Cu/Zn-SOD, CuZnSOD, Ipo-1, Ipo1, SODC, Sod-1
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
Chr 16
Phenotype
Datasheet
Application
--
Strain Description
Ensembl Number
ENSMUST00000023707
NCBI RefSeq
NM_011434.2
Target Region
Exon 2
Size of Effective Region
~0.8 kb
Overview of Gene Research
Sod1, short for superoxide dismutase 1, is well-known for its ROS scavenging activity. It also plays additional roles in modulating metabolism, maintaining redox balance, and regulating transcription [2].
Mutations in the Sod1 gene are responsible for 15% of familial amyotrophic lateral sclerosis (ALS) cases, and Sod1 dysfunction may be involved in sporadic ALS as well [1]. In ALS, mutant Sod1 proteins misfold and aggregate, leading to mitochondrial dysfunction, which is an important pathogenic mechanism [4]. The mitochondrial accumulation of mutant Sod1 can lead to motor neuron pathology and death [4]. Also, the efficacy of Sod1 folding impacts neuronal loss in motor system neurodegenerative diseases [3].
In conclusion, Sod1 is crucial for multiple cellular functions such as ROS scavenging, metabolism modulation, etc. Its role in ALS, especially through mutant-induced misfolding, aggregation, and mitochondrial dysfunction, has been well-demonstrated. The study of Sod1, especially in the context of ALS, helps in understanding the disease mechanism and may lead to potential therapeutic strategies [1,2,3,4].
References：
1. Abati, Elena, Bresolin, Nereo, Comi, Giacomo, Corti, Stefania. 2020. Silence superoxide dismutase 1 (SOD1): a promising therapeutic target for amyotrophic lateral sclerosis (ALS). In Expert opinion on therapeutic targets, 24, 295-310. doi:10.1080/14728222.2020.1738390. https://pubmed.ncbi.nlm.nih.gov/32125907/
2. Banks, C J, Andersen, J L. 2019. Mechanisms of SOD1 regulation by post-translational modifications. In Redox biology, 26, 101270. doi:10.1016/j.redox.2019.101270. https://pubmed.ncbi.nlm.nih.gov/31344643/
3. Wright, Gareth S A. . Molecular and pharmacological chaperones for SOD1. In Biochemical Society transactions, 48, 1795-1806. doi:10.1042/BST20200318. https://pubmed.ncbi.nlm.nih.gov/32794552/
4. Tafuri, Francesco, Ronchi, Dario, Magri, Francesca, Comi, Giacomo P, Corti, Stefania. 2015. SOD1 misplacing and mitochondrial dysfunction in amyotrophic lateral sclerosis pathogenesis. In Frontiers in cellular neuroscience, 9, 336. doi:10.3389/fncel.2015.00336. https://pubmed.ncbi.nlm.nih.gov/26379505/
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
Contact Us
Connect with our experts for your custom animal model needs. Please fill out the form below to start a conversation or request a quote.
Cyagen values your privacy. We’d like to keep you informed about our latest offerings and insights. Your preferences:
You may unsubscribe from these communications at any time. See our Privacy Policy for details on opting out and data protection.
By clicking the button below, you consent to allow Cyagen to store and process the personal information submitted in this form to provide you the content requested.