mProX™ Human TREM1 Stable Cell Line
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- Membrane Protein Stable Cell Lines
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Published Data
Fig.1 The suppression of LPS-induced GFAP and Iba-1 expressions was observed in response to TREM1-KD.
A 24-hour TREM1 knockdown (KD) treatment was administered to AST and BV2 cells, which were subsequently exposed to LPS stimulation for another 24 hours, as part of the ensuing investigations. Western blot analysis of GFAP and Iba-1 was performed in AST and BV2 cells, respectively.
Ref: Li, Zhenhuan, et al. "Inhibition of TREM1 reduces inflammation and oxidative stress after spinal cord injury (SCI) associated with HO-1 expressions." Biomedicine & Pharmacotherapy 109 (2019): 2014-2021.
Pubmed: 30551457
DOI: 10.1016/j.biopha.2018.08.159
Research Highlights
Yao, Yao. et al. "Identification of Targets for Subsequent Treatment of Crohn's Disease Patients After Failure of Anti-TNF Therapy." Journal of inflammation research, 2023.
In current medical practice, Anti-TNF medications are widely recognized as the primary treatment for Crohn's Disease (CD), yet a considerable number of patients remain unresponsive to this therapy. To address this issue, the present study employs bioinformatics technology to identify potential intervention targets for non-responders to anti-TNF treatment. Through this research, it is hoped that a more effective and individualized approach to managing CD can be developed for those who do not benefit from traditional treatment methods.
Yao, Yao. et al. "Identification of Targets for Subsequent Treatment of Crohn's Disease Patients After Failure of Anti-TNF Therapy." Journal of inflammation research, 2023.
Pubmed:
37868830
DOI:
10.2147/JIR.S422881
R Rashed, Hebatallah. et al. "Nerve transcriptomes in autoimmune and genetic demyelinating neuropathies: Pathogenic pathway assessment of nerve demyelination." Journal of neuroimmunology, 2023.
The pathogenesis of autoimmune demyelinating neuropathies remains unclear in comparison to inherited forms. Through a whole transcriptome approach using RNA-Seq on nerve biopsy tissues, the differences in gene expression were investigated in patients with various autoimmune and inherited demyelinating neuropathies (CIDP n = 10, POEMS n = 18, DADS n = 3, CMT1 n = 3) and healthy controls (n = 6). A limited number of differentially expressed genes were identified when compared to the healthy controls (POEMS = 125, DADS = 15, CMT = 14, CIDP = 5). Divergent pathogenic pathways, including those involved in inflammation, demyelination, and neurite regeneration, such as the triggering receptor expressed on myeloid cells (TREM1) from the immunoglobulin superfamily and RhoGD1, were found. This study also revealed both shared and distinct pathogenic mechanisms between autoimmune and inherited forms of demyelinating neuropathies.
R Rashed, Hebatallah. et al. "Nerve transcriptomes in autoimmune and genetic demyelinating neuropathies: Pathogenic pathway assessment of nerve demyelination." Journal of neuroimmunology, 2023.
Pubmed:
37857228
DOI:
10.1016/j.jneuroim.2023.578220
