mProX™ Human CXCR3 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- GPCR Cell Lines
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Published Data
Fig.1 Silencing CXCR3 thwarts mitochondrial DNA harm within an in vitro model of steatohepatitis.
An assay for oxidative mitochondrial DNA damage quantified 8-OHdG, an oxidative DNA damage marker, in AML-12 cells cultured in MCD medium and HepG2 hepatocytes treated with palmitic acid. These cells were transfected with either si-CXCR3 or si-control. The data presented here represent results from three distinct experiments, with MCD referring to methionine-and-choline-deficient and PA denoting palmitic acid.
Ref: Du, Jinghua, et al. "Pro-inflammatory CXCR3 impairs mitochondrial function in experimental non-alcoholic steatohepatitis." Theranostics 7.17 (2017): 4192.
Pubmed: 29158819
DOI: 10.7150/thno.21400
Research Highlights
Zacharias ZR, Houtman JCD. "OMIP-099: 31-color spectral flow cytometry panel to investigate the steady-state ." Cytometry. Part A : the journal of the International Society for Analytical , 2023.
The authors have developed a 31-color panel in order to identify and characterize the steady-state phenotype of T cells in human peripheral blood (Table 1). The panel was optimized using cryopreserved peripheral blood mononuclear cells (PBMC) and includes markers such as CD45RA, CD45RO, CCR7, and CD95 to differentiate different subpopulations of T cells (e.g., naive, T(EM), T(CM), T(EMRA), T(SCM), etc.) of CD4, CD8, and gammadelta T cells. Additionally, the panel includes markers for differentiation status (CD27, CD28), activation/antigen experience (CD11a, CD49d, CD38, HLA-DR, CD56, and CD39), co-inhibitory markers (PD-1, TIM-3), and CD4 T helper subsets (CXCR3, CXCR5, CCR4, CCR6, Foxp3, CD25, and CD127). This optimized panel offers a comprehensive evaluation of human T cell phenotype under steady-state conditions.
Pubmed:
37814476
DOI:
10.1002/cyto.a.24799
Singh A, et al. "CXCR3 antagonist rescues ER stress and reduces inflammation and JEV infection in ." Cytokine, 2023.
The effect of eIF2alpha:CHOP on mitochondrial ROS generation, inflammation, and apoptotic cell death has been studied. Treatment with AMG487 was found to alleviate these effects and increase interferon (IFN)-alpha/beta production in the brains of JEV-infected mice. These findings suggest a potential therapeutic benefit of using a CXCR3 antagonist against JEV infection.
Pubmed:
37812996
DOI:
10.1016/j.cyto.2023.156380
