C57BL/6JCya-Ano10em1flox/Cya
Common Name:
Ano10-flox
Product ID:
S-CKO-00273
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
Quantity
Price:
Contact for Pricing
Basic Information
Strain Name
Ano10-flox
Strain ID
CKOCMP-102566-Ano10-B6J-VA
Gene Name
Product ID
S-CKO-00273
Gene Alias
Tmem16k
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
9
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Ano10em1flox/Cya mice (Catalog S-CKO-00273) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000042546
NCBI RefSeq
NM_133979
Target Region
Exon 7~8
Size of Effective Region
~2.4 kb
Detailed Document
Overview of Gene Research
Ano10, also known as TMEM16K, is a transmembrane protein and member of the anoctamin family. It exhibits functional duality with ion channel and phospholipid scrambling activities. Ano10 is involved in processes like endosomal sorting, spindle assembly, and calcium signalling [2]. Calcium is necessary for its protein activation in either activity. Dysregulation of calcium signalling in Purkinje cells due to Ano10 defects is proposed as the main mechanism leading to spinocerebellar ataxia autosomal recessive type 10 (SCAR10) [2].
Ano10 knockout in epithelial cells leads to defective ion transport, attenuated volume regulation and deranged Ca2+ signalling. Intestinal epithelial cells from Ano10 null mice are reduced in size and show almost abolished spontaneous and TNFα -induced apoptosis. Similar defects are found in mouse peritoneal Ano10 null macrophages and in human THP1 macrophages with reduced Ano10 expression [3]. Biallelic pathogenic variants in the Ano10 gene cause autosomal recessive progressive ataxia (ATX-Ano10), with most patients having loss-of-function variants [1].
In conclusion, Ano10 plays essential roles in ion transport, calcium signalling, and cell-related processes like apoptosis. Ano10 knockout models have been crucial in revealing its role in causing autosomal recessive progressive ataxia and associated cellular defects, thus deepening our understanding of related disease mechanisms [1,3].
References:
1. Milovanović, Andona, Westenberger, Ana, Stanković, Iva, Kostić, Vladimir S, Dragašević-Mišković, Natasa. 2024. ANO10-Related Spinocerebellar Ataxia: MDSGene Systematic Literature Review and a Romani Case Series. In Movement disorders : official journal of the Movement Disorder Society, 39, 887-892. doi:10.1002/mds.29729. https://pubmed.ncbi.nlm.nih.gov/38469933/
2. Chrysanthou, Androniki, Ververis, Antonis, Christodoulou, Kyproula. 2022. ANO10 Function in Health and Disease. In Cerebellum (London, England), 22, 447-467. doi:10.1007/s12311-022-01395-3. https://pubmed.ncbi.nlm.nih.gov/35648332/
3. Wanitchakool, Podchanart, Ousingsawat, Jiraporn, Sirianant, Lalida, Schreiber, Rainer, Kunzelmann, Karl. 2016. Cellular defects by deletion of ANO10 are due to deregulated local calcium signaling. In Cellular signalling, 30, 41-49. doi:10.1016/j.cellsig.2016.11.006. https://pubmed.ncbi.nlm.nih.gov/27838374/
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