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C57BL/6JCya-Slc30a10em1/Cya
Common Name:
Slc30a10-KO
Product ID:
S-KO-06017
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
Price:
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Basic Information
Strain Name
Slc30a10-KO
Strain ID
KOCMP-226781-Slc30a10-B6J-VA
Gene Name
Slc30a10
Product ID
S-KO-06017
Gene Alias
E130106K10Rik; Gm212
Background
C57BL/6JCya
NCBI ID
226781
Modification
Conventional knockout
Chromosome
1
Phenotype
MGI:2685058
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/6JCya-Slc30a10em1/Cya mice (Catalog S-KO-06017) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000061093
NCBI RefSeq
NM_001033286
Target Region
Exon 3~4
Size of Effective Region
~2.2 kb
Detailed Document
Click here to download >>
Overview of Gene Research
Slc30a10, a manganese (Mn) efflux transporter, is crucial for maintaining Mn homeostasis. It is involved in excreting Mn from hepatocytes into bile and from enterocytes into the gastrointestinal tract lumen, thus preventing Mn toxicity [3,5,7]. Mutations in this gene can lead to familial parkinsonism associated with Mn retention and other severe symptoms, highlighting its significance in preventing Mn-induced neurotoxicity and related disorders [3,4,6]. Genetic models, such as knockout (KO) mice, have been instrumental in studying its function [1,2,5].

In pan-neuronal/glial Slc30a10 knockout mice, Mn levels were elevated in specific brain regions during early postnatal development, and adolescent or adult knockouts exhibited neuromotor deficits and reduced striatal dopamine release without neurodegeneration or changes in striatal dopamine levels. This indicates that brain Slc30a10 regulates Mn levels in early postnatal life, protecting against deficits in neuromotor function and dopaminergic neurotransmission [1]. Whole-body Slc30a10-deficient mice developed severe Mn excess and impaired systemic and biliary Mn excretion, while liver-or small intestine-specific knockouts had less severe Mn excess, suggesting that Slc30a10 in these tissues is essential for Mn excretion [5].

In conclusion, Slc30a10 is essential for Mn excretion and maintaining Mn homeostasis, protecting against Mn-induced toxicity. Studies using KO mouse models have revealed its role in preventing deficits in neuromotor function, dopaminergic neurotransmission, and in physiological Mn excretion. Understanding Slc30a10 function is crucial for treating Mn-related diseases, such as familial parkinsonism and Mn-induced neurotoxicity.

References:

1. Taylor, Cherish A, Grant, Stephanie M, Jursa, Thomas, Gonzales, Rueben A, Mukhopadhyay, Somshuvra. . SLC30A10 manganese transporter in the brain protects against deficits in motor function and dopaminergic neurotransmission under physiological conditions. In Metallomics : integrated biometal science, 15, . doi:10.1093/mtomcs/mfad021. https://pubmed.ncbi.nlm.nih.gov/36990693/

2. Prajapati, Milankumar, Pettiglio, Michael A, Conboy, Heather L, Fukada, Toshiyuki, Bartnikas, Thomas B. 2021. Characterization of in vitro models of SLC30A10 deficiency. In Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine, 34, 573-588. doi:10.1007/s10534-021-00296-y. https://pubmed.ncbi.nlm.nih.gov/33713241/

3. Mukhopadhyay, Somshuvra. 2017. Familial manganese-induced neurotoxicity due to mutations in SLC30A10 or SLC39A14. In Neurotoxicology, 64, 278-283. doi:10.1016/j.neuro.2017.07.030. https://pubmed.ncbi.nlm.nih.gov/28789954/

4. Chen, Pan, Bowman, Aaron B, Mukhopadhyay, Somshuvra, Aschner, Michael. 2015. SLC30A10: A novel manganese transporter. In Worm, 4, e1042648. doi:10.1080/21624054.2015.1042648. https://pubmed.ncbi.nlm.nih.gov/26430566/

5. Mercadante, Courtney J, Prajapati, Milankumar, Conboy, Heather L, Rao, Deepa B, Bartnikas, Thomas B. . Manganese transporter Slc30a10 controls physiological manganese excretion and toxicity. In The Journal of clinical investigation, 129, 5442-5461. doi:10.1172/JCI129710. https://pubmed.ncbi.nlm.nih.gov/31527311/

6. Carmona, Asuncion, Zogzas, Charles E, Roudeau, Stéphane, Mukhopadhyay, Somshuvra, Ortega, Richard. 2018. SLC30A10 Mutation Involved in Parkinsonism Results in Manganese Accumulation within Nanovesicles of the Golgi Apparatus. In ACS chemical neuroscience, 10, 599-609. doi:10.1021/acschemneuro.8b00451. https://pubmed.ncbi.nlm.nih.gov/30272946/

7. Prajapati, Milankumar, Zhang, Jared Z, Chiu, Lauren, Aghajan, Mariam, Bartnikas, Thomas B. 2024. Hepatic HIF2 is a key determinant of manganese excess and polycythemia in SLC30A10 deficiency. In JCI insight, 9, . doi:10.1172/jci.insight.169738. https://pubmed.ncbi.nlm.nih.gov/38652538/

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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