C57BL/6JCya-Slc9a1em1flox/Cya
Common Name
Slc9a1-flox
Product ID
S-CKO-18194
Backgroud
C57BL/6JCya
Strain ID
CKOCMP-20544-Slc9a1-B6J-VB
Status
When using this mouse strain in a publication, please cite “Slc9a1-flox Mouse (Catalog S-CKO-18194) 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
Slc9a1-flox
Strain ID
CKOCMP-20544-Slc9a1-B6J-VB
Gene Name
Product ID
S-CKO-18194
Gene Alias
swe, Apnh, Nhe1, Mir5122, mir-5122
Background
C57BL/6JCya
Gene Full Name
solute carrier family 9 (sodium/hydrogen exchanger), member 1
Modification
Conditional knockout
NCBI ID
Phenotype
Chromosome
Chr 4 (Mouse)
Application
--
Datasheet
Strain Description
Ensembl Transcript ID
ENSMUST00000030669
NCBI Transcript ID
NM_016981
Target Region
Exon 5
Size of Effective Region
~1.0 kb
Overview of Gene Research
Slc9a1, encoding the sodium/hydrogen exchanger isoform one (NHE1), is crucial for maintaining intracellular pH homeostasis by exchanging one intracellular proton for one extracellular sodium ion [3,4]. This process is involved in multiple biological pathways and is of great biological importance. Genetic models, such as knockout mouse models, have been valuable in studying its functions.
In conditional Slc9a1 knockout (cKO) mouse models, deletion of Slc9a1 in Cx3cr1+ cells led to expansion of a microglial subgroup with elevated transcription of white matter myelination genes. This subgroup also showed more acidic pHi and upregulated CREB signaling. Moreover, there was an enrichment of a corresponding oligodendrocyte subgroup in the white matter tissues, indicating stimulation of microglia-oligodendrocyte crosstalk for remyelination [1].
In mice, the Slc9a1 inhibitor decreased the transport efficiency of chitosan oligosaccharide (COS) both in vitro and in vivo, and overexpression of Slc9a1 in MODE-K cells increased COS transport, suggesting its role in COS transport across the intestinal mucosa [2].
Mice with a homozygous null mutation in Slc9a1 exhibited ataxia, recurrent seizures, and selective neuronal cell death, and in humans, mutations in SLC9A1 are associated with cerebellar ataxia, sensorineural hearing loss, and neuromuscular disorders [3,4].
In gliomas, higher SLC9A1 mRNA levels in higher-grade gliomas were correlated with worsened survival probabilities, and inhibition of NHE1 protein reduced glioma volume and invasion in mouse models [5]. Adipose mesenchymal stem cell-derived exosomal microRNA-1236 reduced breast cancer cells' resistance to cisplatin by suppressing SLC9A1 [6].
In conclusion, Slc9a1 plays essential roles in maintaining intracellular pH, microglia-oligodendrocyte crosstalk, intestinal transport, and is associated with various diseases including neurological disorders and cancers. The Slc9a1 KO/CKO mouse models have significantly contributed to understanding its functions in these disease-related biological processes.
References：
1. Song, Shanshan, Oft, Helena, Metwally, Shamseldin, Kohanbash, Gary, Sun, Dandan. 2024. Deletion of Slc9a1 in Cx3cr1+ cells stimulated microglial subcluster CREB1 signaling and microglia-oligodendrocyte crosstalk. In Journal of neuroinflammation, 21, 69. doi:10.1186/s12974-024-03065-z. https://pubmed.ncbi.nlm.nih.gov/38509618/
2. Wen, Jiaying, Chen, Shengwei, Bao, Minglong, Abd El-Aty, A M, Ju, Xianghong. 2022. Slc9a1 plays a vital role in chitosan oligosaccharide transport across the intestinal mucosa of mice. In Carbohydrate polymers, 299, 120179. doi:10.1016/j.carbpol.2022.120179. https://pubmed.ncbi.nlm.nih.gov/36876794/
3. Iwama, Kazuhiro, Osaka, Hitoshi, Ikeda, Takahiro, Mizuguchi, Takeshi, Matsumoto, Naomichi. 2018. A novel SLC9A1 mutation causes cerebellar ataxia. In Journal of human genetics, 63, 1049-1054. doi:10.1038/s10038-018-0488-x. https://pubmed.ncbi.nlm.nih.gov/30018422/
4. Guissart, Claire, Li, Xiuju, Leheup, Bruno, Fliegel, Larry, Koenig, Michel. 2014. Mutation of SLC9A1, encoding the major Na⁺/H⁺ exchanger, causes ataxia-deafness Lichtenstein-Knorr syndrome. In Human molecular genetics, 24, 463-70. doi:10.1093/hmg/ddu461. https://pubmed.ncbi.nlm.nih.gov/25205112/
5. Guan, Xiudong, Luo, Lanxin, Begum, Gulnaz, Sun, Dandan, Jia, Wang. 2018. Elevated Na/H exchanger 1 (SLC9A1) emerges as a marker for tumorigenesis and prognosis in gliomas. In Journal of experimental & clinical cancer research : CR, 37, 255. doi:10.1186/s13046-018-0923-z. https://pubmed.ncbi.nlm.nih.gov/30333031/
6. Jia, Zhongming, Zhu, Huamin, Sun, Hongguang, Jiang, Jingru, Wang, Xiaohong. 2020. Adipose Mesenchymal Stem Cell-Derived Exosomal microRNA-1236 Reduces Resistance of Breast Cancer Cells to Cisplatin by Suppressing SLC9A1 and the Wnt/β-Catenin Signaling. In Cancer management and research, 12, 8733-8744. doi:10.2147/CMAR.S270200. https://pubmed.ncbi.nlm.nih.gov/33061571/
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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