mProX™ Human TREM2 Stable Cell Line
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- Membrane Protein Stable Cell Lines
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Published Data
Fig.1 The efficiencies of knockdown and overexpression of TREM2 were confirmed by Western blot.
Scramble siRNA or TREM2 siRNA was transiently transfected into BV2 microglial cells for a duration of 48 hours. Detection of the knockdown efficiency of TREM2 siRNA was performed using western blot analysis. Confirmation of TREM2 overexpression in BV2 cells was achieved through the assessment of Flag expression, which was tagged in the C-terminal of Adv-TREM2, via western blot analysis.
Ref: Guo, Ying, et al. "TREM2 deficiency aggravates α-synuclein-induced neurodegeneration and neuroinflammation in Parkinson's disease models." The FASEB Journal 33.11 (2019): 12164.
Pubmed: 31370707
DOI: 10.1096/fj.201900992R
Research Highlights
Zhang, Xingyu. et al. "Soluble TREM2 ameliorates tau phosphorylation and cognitive deficits through activating transgelin-2 in Alzheimer's disease." Nature communications, 2023.
The transmembrane protein, Triggering receptor expressed on myeloid cells 2 (TREM2), is predominantly expressed by microglia in the brain. When proteolytically shed, TREM2 releases a soluble form known as sTREM2. Studies have shown that levels of sTREM2 are increased in the cerebrospinal fluid of patients with Alzheimer's disease (AD), but it is unclear whether sTREM2 plays a role in the disease's pathogenesis. The authors of this study have identified transgelin-2 (TG2), expressed on neurons, as the receptor for sTREM2. They found that microglia-derived sTREM2 binds to TG2, leading to RhoA phosphorylation and inactivation of the RhoA-ROCK-GSK3β pathway. This process decreases tau protein phosphorylation, which is associated with AD. Their research also identified a specific fragment of sTREM2, sTREM2 (77-89), as the active sequence responsible for activating TG2. This segment mimics the effects of sTREM2 on reducing tau phosphorylation. Additional experiments in mice showed that overexpression of sTREM2 or administration of the active peptide improved tau pathology and behavioral impairment in a mouse model of tau pathology. Collectively, these findings suggest that the interaction between sTREM2 and TG2 serves as a means of communication between microglia and neurons. The researchers propose that targeting sTREM2 or its active peptides may be a potential therapeutic approach for treating tauopathies, including AD.
Zhang, Xingyu. et al. "Soluble TREM2 ameliorates tau phosphorylation and cognitive deficits through activating transgelin-2 in Alzheimer's disease." Nature communications, 2023.
Pubmed:
37865646
DOI:
10.1038/s41467-023-42505-x
Evans, Frances. et al. "CD300f immune receptor contributes to healthy aging by regulating inflammaging, metabolism, and cognitive decline." Cell reports, 2023.
Recent discoveries have indicated a potential role for immune receptors in various aging-related functions, including energy regulation, inflammation, and cognitive deterioration. One such receptor, CD300f, bears strong resemblance to the TREM2 lipid-sensing receptor and uniquely combines both activating and inhibitory cell signaling mechanisms to influence inflammation, efferocytosis, and microglial metabolic health. The authors propose that CD300f may serve as a regulator of systemic aging processes and contribute to overall longevity. To test this hypothesis, multiple groups of two strains of mice lacking CD300f were closely monitored over an extended period.
Evans, Frances. et al. "CD300f immune receptor contributes to healthy aging by regulating inflammaging, metabolism, and cognitive decline." Cell reports, 2023.
Pubmed:
37864797
DOI:
10.1016/j.celrep.2023.113269