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C57BL/6JCya-Atl1em1/Cya
Common Name:
Atl1-KO
Product ID:
S-KO-19022
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Atl1-KO
Strain ID
KOCMP-73991-Atl1-B6J-VB
Gene Name
Atl1
Product ID
S-KO-19022
Gene Alias
4930435M24Rik; Adfsp; Fsp1; Spg3; Spg3a
Background
C57BL/6JCya
NCBI ID
73991
Modification
Conventional knockout
Chromosome
12
Phenotype
MGI:1921241
Document
Click here to download >>
Application
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Rare Disease Data Center >>
Note
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Atl1em1/Cya mice (Catalog S-KO-19022) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000021466
NCBI RefSeq
NM_178628
Target Region
Exon 3
Size of Effective Region
~1.4 kb
Detailed Document
Click here to download >>
Overview of Gene Research
Atlastin-1 (ATL1), a regulator of endoplasmic reticulum (ER) morphology, is crucial for tubular ER formation and protein synthesis [3]. It is involved in the mTOR signaling pathway, which is important in regulating cell growth, proliferation, and survival [1].

ATL1 has been studied in relation to several diseases. In pre-eclampsia (PE), ATL1 is upregulated in patients and placental tissues. Upregulation of ATL1 in HTR-8/SVneo cells inhibits the proliferation and invasion of trophoblast cells via the inhibition of the mTOR signaling pathway [1]. In intracranial aneurysms, the circular RNA circ-ATL1 is increased. Silencing circ-ATL1 suppresses vascular smooth muscle cell (VSMC) migration, proliferation, and phenotypic modulation, suggesting its role in aneurysm development [2]. Additionally, ATL1 is one of the causative genes of hereditary spastic paraplegia (HSP). Mutations in ATL1 can lead to a range of symptoms, and genotype-phenotype correlations have been explored, with de novo variants causing complex and severe symptoms in HSP-ATL1 patients [3,4].

In conclusion, ATL1 is essential for ER formation and protein synthesis. Studies on ATL1 in disease models such as pre-eclampsia, intracranial aneurysms, and HSP have provided insights into its role in these conditions. Understanding ATL1 may offer potential targets for treating related diseases.

References:
1. Zhang, Guanli, Feng, Yan, Wang, Min, Liu, Xin. 2022. ATL1 inhibits the proliferation and invasion of trophoblast cells via inhibition of the mTOR signaling pathway. In Journal of biochemical and molecular toxicology, 37, e23237. doi:10.1002/jbt.23237. https://pubmed.ncbi.nlm.nih.gov/36193555/
2. Xu, Jichong, Fang, Chun. 2023. Circ-ATL1 silencing reverses the activation effects of SIRT5 on smooth muscle cellular proliferation, migration and contractility in intracranial aneurysm by adsorbing miR-455. In BMC molecular and cell biology, 24, 3. doi:10.1186/s12860-022-00461-2. https://pubmed.ncbi.nlm.nih.gov/36717793/
3. Shih, Yu-Tzu, Hsueh, Yi-Ping. 2018. The involvement of endoplasmic reticulum formation and protein synthesis efficiency in VCP- and ATL1-related neurological disorders. In Journal of biomedical science, 25, 2. doi:10.1186/s12929-017-0403-3. https://pubmed.ncbi.nlm.nih.gov/29310658/
4. Alecu, Julian E, Saffari, Afshin, Jordan, Catherine, Blackstone, Craig, Ebrahimi-Fakhari, Darius. . De novo variants cause complex symptoms in HSP-ATL1 (SPG3A) and uncover genotype-phenotype correlations. In Human molecular genetics, 32, 93-103. doi:10.1093/hmg/ddac182. https://pubmed.ncbi.nlm.nih.gov/35925862/
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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