C57BL/6JCya-Trem2em1flox/Cya
Common Name:
Trem2-flox
Product ID:
S-CKO-17045
Background:
C57BL/6JCya
Product Type
Age
Genotype
Sex
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Basic Information
Strain Name
Trem2-flox
Strain ID
CKOCMP-83433-Trem2-B6J-VA
Gene Name
Product ID
S-CKO-17045
Gene Alias
TREM-2; Trem2a; Trem2b; Trem2c
Background
C57BL/6JCya
NCBI ID
Modification
Conditional knockout
Chromosome
17
Phenotype
Document
Application
--
Note: When using this mouse strain in a publication, please cite “C57BL/6JCya-Trem2em1flox/Cya mice (Catalog S-CKO-17045) were purchased from Cyagen.”
Strain Description
Ensembl Number
ENSMUST00000113237
NCBI RefSeq
NM_001272078
Target Region
Exon 2~5
Size of Effective Region
~4.1 kb
Detailed Document
Overview of Gene Research
TREM2, Triggering receptor expressed on myeloid cells 2, is a surface receptor on myeloid cells. It's crucial for microglial responses to neurodegeneration, including processes like proliferation, survival, clustering, and phagocytosis [1]. It has been implicated in multiple pathways related to metabolism, such as the mammalian target of rapamycin (mTOR) signaling pathway, influencing ATP levels and biosynthetic pathways [1]. TREM2 is of great biological importance, especially in neurodegenerative diseases, as well as in tumor microenvironments and liver-related diseases. Genetic models, like gene knockout (KO) mouse models, have been instrumental in studying its functions.
In Alzheimer's disease (AD), TREM2-deficient mice with AD-like pathology show abnormal autophagy due to defective mTOR signaling, resulting in metabolic derailment. Dietary cyclocreatine can offset these effects, restoring microglial clustering around plaques and reducing plaque-adjacent neuronal dystrophy, indicating TREM2's role in maintaining microglial metabolic fitness during AD [1]. In glioblastomas (GBM), genetic or pharmacological TREM2 deficiency promotes GBM progression in vivo, suggesting a distinct immunoprotective role of TREM2 in central nervous system cancers compared to peripheral cancers [2]. In non-alcoholic fatty liver disease (NAFLD) and sepsis, Trem2-deficient macrophages release exosomes that impair hepatocytic mitochondrial structure and energy supply, accelerating NAFLD progression and sepsis susceptibility in a mouse model, while TREM2 overexpression in liver macrophages improves the outcome [3].
In conclusion, TREM2 is essential for maintaining microglial metabolic fitness, especially in AD. It also plays distinct roles in different types of cancers and in the coordination between hepatocyte-macrophage metabolism in NAFLD and sepsis. The use of KO mouse models has significantly advanced our understanding of TREM2's functions in these disease conditions, providing potential targets for therapeutic interventions.
References:
1. Ulland, Tyler K, Song, Wilbur M, Huang, Stanley Ching-Cheng, Holtzman, David M, Colonna, Marco. . TREM2 Maintains Microglial Metabolic Fitness in Alzheimer's Disease. In Cell, 170, 649-663.e13. doi:10.1016/j.cell.2017.07.023. https://pubmed.ncbi.nlm.nih.gov/28802038/
2. Zhong, Jian, Xing, Xudong, Gao, Yixin, Bai, Fan, Zhang, Nu. 2024. Distinct roles of TREM2 in central nervous system cancers and peripheral cancers. In Cancer cell, 42, 968-984.e9. doi:10.1016/j.ccell.2024.05.001. https://pubmed.ncbi.nlm.nih.gov/38788719/
3. Hou, Jinchao, Zhang, Jue, Cui, Ping, Colonna, Marco, Fang, Xiangming. . TREM2 sustains macrophage-hepatocyte metabolic coordination in nonalcoholic fatty liver disease and sepsis. In The Journal of clinical investigation, 131, . doi:10.1172/JCI135197. https://pubmed.ncbi.nlm.nih.gov/33586673/
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