C57BL/6NCya-Asgr1em1flox/Cya
Common Name:
Asgr1-flox
Product ID:
S-CKO-01318
Background:
C57BL/6NCya
Product Type
Age
Genotype
Sex
Quantity
Price:
Contact for Pricing
Basic Information
Strain Name
Asgr1-flox
Strain ID
CKOCMP-11889-Asgr1-B6N-VA
Gene Name
Product ID
S-CKO-01318
Gene Alias
ASGPR1; Asgr; Asgr-1; HL-1
Background
C57BL/6NCya
NCBI ID
Modification
Conditional knockout
Chromosome
11
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6NCya-Asgr1em1flox/Cya mice (Catalog S-CKO-01318) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000146411
NCBI RefSeq
NM_001291131
Target Region
Exon 3~9
Size of Effective Region
~2.1 kb
Detailed Document
Overview of Gene Research
Asgr1, also known as asialoglycoprotein receptor 1, is a C-type lectin receptor [4]. It is primarily expressed in the liver and mediates the internalization and lysosomal degradation of blood asialoglycoproteins. Asgr1 is involved in cholesterol metabolism and also plays a role in the body's response to liver injury and sepsis-induced liver injury [1,2,3]. Genetic models, such as gene knockout mouse models, have been crucial for studying its functions.
In gene knockout mouse models, Asgr1 deficiency has been shown to have multiple effects. It decreases lipid levels in serum and liver by stabilizing LXRα, which upregulates ABCA1 and ABCG5/G8, promoting cholesterol transport to high-density lipoprotein and excretion to bile and faeces, respectively [1]. Additionally, Asgr1 deficiency exacerbates liver injury in male mice, as it increases circulating levels of GP73, a mediator of endoplasmic reticulum stress, leading to liver injury [2]. In sepsis-induced liver injury, ASGR1-knockdown mice show suppressed monocyte-to-macrophage differentiation, alleviated liver injury, and improved survival [3]. In ApoE-/-mice, Asgr1 deficiency improves atherosclerosis but also causes broader alterations in liver metabolism and a deterioration of liver injury [5].
In conclusion, Asgr1 plays essential roles in cholesterol metabolism, liver injury, and sepsis-induced liver injury as revealed through gene knockout mouse models. These studies contribute to understanding the biological functions of Asgr1 in related disease areas, such as hypercholesterolemia, liver diseases, and sepsis-related liver injuries, providing potential directions for therapeutic interventions [1,2,3,5].
References:
1. Wang, Ju-Qiong, Li, Liang-Liang, Hu, Ao, Luo, Jie, Song, Bao-Liang. 2022. Inhibition of ASGR1 decreases lipid levels by promoting cholesterol excretion. In Nature, 608, 413-420. doi:10.1038/s41586-022-05006-3. https://pubmed.ncbi.nlm.nih.gov/35922515/
2. Zhang, Zhe, Leng, Xiang Kai, Zhai, Yuan Yuan, Tao, Kai Shan, Wu, Jiang Wei. 2024. Deficiency of ASGR1 promotes liver injury by increasing GP73-mediated hepatic endoplasmic reticulum stress. In Nature communications, 15, 1908. doi:10.1038/s41467-024-46135-9. https://pubmed.ncbi.nlm.nih.gov/38459023/
3. Shi, Rui, Wang, Jiangang, Zhang, Zhen, Leng, Yiping, Chen, Alex F. 2023. ASGR1 promotes liver injury in sepsis by modulating monocyte-to-macrophage differentiation via NF-κB/ATF5 pathway. In Life sciences, 315, 121339. doi:10.1016/j.lfs.2022.121339. https://pubmed.ncbi.nlm.nih.gov/36621538/
4. Hoober, J Kenneth. 2020. ASGR1 and Its Enigmatic Relative, CLEC10A. In International journal of molecular sciences, 21, . doi:10.3390/ijms21144818. https://pubmed.ncbi.nlm.nih.gov/32650396/
5. Svecla, Monika, Moregola, Annalisa, Dalt, Lorenzo Da, Bonacina, Fabrizia, Norata, Giuseppe Danilo. 2024. ASGR1 deficiency improves atherosclerosis but alters liver metabolism in ApoE-/- mice. In Cardiovascular diabetology, 23, 428. doi:10.1186/s12933-024-02507-5. https://pubmed.ncbi.nlm.nih.gov/39616371/
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