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C57BL/6NCya-Atg13em1/Cya
Common Name:
Atg13-KO
Product ID:
S-KO-10280
Background:
C57BL/6NCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Atg13-KO
Strain ID
KOCMP-51897-Atg13-B6N-VA
Gene Name
Atg13
Product ID
S-KO-10280
Gene Alias
1110053A20Rik; D2Ertd391e; Harbi1
Background
C57BL/6NCya
NCBI ID
51897
Modification
Conventional knockout
Chromosome
2
Phenotype
MGI:1196429
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/6NCya-Atg13em1/Cya mice (Catalog S-KO-10280) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000076803
NCBI RefSeq
NM_145528
Target Region
Exon 3~9
Size of Effective Region
~8.9 kb
Detailed Document
Click here to download >>
Overview of Gene Research
Atg13, a key component in the autophagy process, is part of the Atg1 kinase complex in yeast and the orthologous ULK1 kinase complex in vertebrates. It functions in initiating autophagy, sensing nutritional status signals, recruiting downstream ATG proteins to the autophagosome formation site, and governing autophagosome formation. Autophagy is an intracellular degradation process involved in recycling cytoplasmic components and removing various cellular elements [2,3].

In PM2.5-induced pulmonary fibrosis, PM2.5-downregulated ALKBH5 promotes m6A modification of Atg13 mRNA at site 767 in lung epithelial cells. Atg13-mediated ULK complex positively regulates autophagy and inflammation in these cells. Knockout of ALKBH5 in mice further accelerates ULK complex-regulated autophagy, inflammation, and pulmonary fibrosis, highlighting the role of site-specific m6A methylation on Atg13 mRNA in autophagy-dependent pulmonary fibrosis [1]. Atg13-deficient mice die in utero, showing growth retardation and myocardial growth defects. In cultured fibroblasts, Atg13 deficiency blocks autophagosome formation at an upstream step, and deletion of Atg13 enhances sensitivity to TNF-α-induced apoptosis [4].

In conclusion, Atg13 is essential for autophagy, with its deficiency having significant impacts on cardiac development and apoptosis sensitivity. In the context of PM2.5-induced pulmonary fibrosis, its mRNA methylation is crucial in autophagy-related disease progression. Studies using Atg13-deficient mouse models have provided valuable insights into its role in these biological processes and disease conditions.

References:

1. Ning, Jie, Pei, Zijie, Wang, Mengruo, Leng, Shuguang, Zhang, Rong. 2023. Site-specific Atg13 methylation-mediated autophagy regulates epithelial inflammation in PM2.5-induced pulmonary fibrosis. In Journal of hazardous materials, 457, 131791. doi:10.1016/j.jhazmat.2023.131791. https://pubmed.ncbi.nlm.nih.gov/37295326/

2. Alers, Sebastian, Wesselborg, Sebastian, Stork, Björn. . ATG13: just a companion, or an executor of the autophagic program? In Autophagy, 10, 944-56. doi:10.4161/auto.28987. https://pubmed.ncbi.nlm.nih.gov/24879146/

3. Wang, Qiuling, Hou, Suiwen. 2022. The emerging roles of ATG1/ATG13 kinase complex in plants. In Journal of plant physiology, 271, 153653. doi:10.1016/j.jplph.2022.153653. https://pubmed.ncbi.nlm.nih.gov/35255243/

4. Kaizuka, Takeshi, Mizushima, Noboru. 2015. Atg13 Is Essential for Autophagy and Cardiac Development in Mice. In Molecular and cellular biology, 36, 585-95. doi:10.1128/MCB.01005-15. https://pubmed.ncbi.nlm.nih.gov/26644405/

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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