C57BL/6NCya-Coro1aem1/Cya
Common Name:
Coro1a-KO
Product ID:
S-KO-16243
Background:
C57BL/6NCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Coro1a-KO
Strain ID
KOCMP-12721-Coro1a-B6N-VB
Gene Name
Product ID
S-KO-16243
Gene Alias
Clabp; Lmb3; TACO; p57
Background
C57BL/6NCya
NCBI ID
Modification
Conventional knockout
Chromosome
7
Phenotype
Document
Application
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Note: When using this mouse strain in a publication, please cite “C57BL/6NCya-Coro1aem1/Cya mice (Catalog S-KO-16243) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000106364
NCBI RefSeq
NM_001301374
Target Region
Exon 3~11
Size of Effective Region
~2.5 kb
Detailed Document
Overview of Gene Research
Coro1a, short for Coronin 1A, is an actin-binding protein that plays crucial roles in multiple biological processes. It is involved in cytoskeleton remodeling, which is essential for processes like receptor-mediated endocytosis, neuronal morphogenesis, and the regulation of autophagy [1,2,4]. It participates in pathways related to steroidogenesis, neuronal development, and autophagic flux, highlighting its overall biological importance. Genetic models, such as gene knockout (KO) or conditional knockout (CKO) mouse models, are valuable for studying its functions.
In Cd-exposed Leydig cells, up-regulation of Coro1a leads to F-actin disassembly, reducing LDL uptake, total cholesterol, and progesterone production. Silencing Coro1a in Cd-treated R2C cells rescues these phenotypes, indicating its role in Cd-induced steroid hormone deficiency [1]. In neuronal morphogenesis, loss of Coro1a leads to similar phenotypes as loss of TRIM67, and a Coro1a mutant unable to bind TRIM67 cannot rescue the loss-of-function phenotypes, suggesting their collaborative role in netrin-dependent neuronal morphogenesis [2]. In triple-negative breast cancer (TNBC), promoting the neddylation-mediated degradation of Coro1a via TRIM4 using a molecular glue (Aurovertin B) inhibits various cellular processes and exerts antitumor effects [3]. In hepatocytes, CREBH inhibits Coro1a expression, and overexpression of Coro1a in LO2 liver cells inhibits autophagic flux and elevates inflammatory cytokine levels [4].
In summary, Coro1a is essential for cytoskeleton-related functions in processes like steroidogenesis, neuronal development, and autophagy. Studies using KO/CKO mouse models (or equivalent loss-of-function experiments) have revealed its significant contributions to diseases such as Cd-induced steroid hormone deficiency, TNBC, and non-alcoholic steatohepatitis (NASH), providing insights into potential therapeutic targets.
References:
1. Wang, Youjin, Li, Teng, Li, Haoji, Huang, Yadong, Zhang, Qihao. 2022. CORO1A regulates lipoprotein uptake in Leydig cells exposed to cadmium. In Ecotoxicology and environmental safety, 232, 113255. doi:10.1016/j.ecoenv.2022.113255. https://pubmed.ncbi.nlm.nih.gov/35121256/
2. Ho, Chris T, Evans, Elliot B, Lukasik, Kimberly, Bear, James E, Gupton, Stephanie L. 2025. Coro1A and TRIM67 collaborate in netrin-dependent neuronal morphogenesis. In bioRxiv : the preprint server for biology, , . doi:10.1101/2025.03.20.644333. https://pubmed.ncbi.nlm.nih.gov/40166342/
3. Gu, Wen-Jie, Liu, Xiao-Xia, Shen, Yi-Wen, Jin, Jin-Mei, Luan, Xin. 2024. TRIM4 enhances small-molecule-induced neddylated-degradation of CORO1A for triple negative breast cancer therapy. In Theranostics, 14, 7023-7041. doi:10.7150/thno.97662. https://pubmed.ncbi.nlm.nih.gov/39629122/
4. Deng, Xiaoling, Liu, Beibei, Jiang, Qianqian, Li, Jiahuan, Xu, Keshu. 2023. CREBH promotes autophagy to ameliorate NASH by regulating Coro1a. In Biochimica et biophysica acta. Molecular basis of disease, 1870, 166914. doi:10.1016/j.bbadis.2023.166914. https://pubmed.ncbi.nlm.nih.gov/37837948/
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