mProX™ Human CD38 Stable Cell Line
- Product Category:
- Membrane Protein Stable Cell Lines
- Subcategory:
- Immune Checkpoint Cell Lines
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Published Data
Fig.1 Suppression of CD38 expression resulted in a reduction in Angiotensin II-triggered production of reactive oxygen species (ROS).
Assessment of ROS generation involved the examination of both a negative control group and H9c2 cells with a CD38 gene knockdown. These cells were treated with CM-H2DCFDA and subsequently exposed to a 20-minute Ang-II stimulation. The quantification of ROS production was performed using a fluorescence-activated cell sorter.
Ref: Guan, Xiao-Hui, et al. "CD38 promotes angiotensin II-induced cardiac hypertrophy." Journal of cellular and molecular medicine 21.8 (2017): 1492-1502.
Pubmed: 28296029
DOI: 10.1111/jcmm.13076
Research Highlights
Jia, Guiquan. et al. "An interleukin 6 responsive plasma cell signature is associated with disease progression in systemic sclerosis interstitial lung disease." iScience, 2023.
In the study of Systemic sclerosis (SSc) interstitial lung disease (ILD), it has been found to be a leading cause of SSc-related morbidity and mortality. Previous studies have shown that To**mab (T*Z, anti-IL6RA) has led to a reduced rate of pulmonary function decline in SSc-ILD patients. A transcriptome analysis was conducted on skin biopsy samples from the faSScinate and focuSSced trials to determine gene networks associated with T*Z treatment. One module, linked to disease progression, showed changes with T*Z treatment and consisted of plasma cell (PC) genes. These genes were also found to be increased in fibrotic SSc and IPF lungs compared to controls. Further analysis via scRNAseq showed that these genes were expressed in CD38 and CD138 expressing PC subsets in SSc lungs. These findings suggest the potential role of PC in disease progression and the mechanism of action of T*Z in fibrotic interstitial lung diseases.
Jia, Guiquan. et al. "An interleukin 6 responsive plasma cell signature is associated with disease progression in systemic sclerosis interstitial lung disease." iScience, 2023.
Pubmed:
37867940
DOI:
10.1016/j.isci.2023.108133
Gu, Xiao-Jing. et al. "Expanding causal genes for Parkinson's disease via multi-omics analysis." NPJ Parkinson's disease, 2023.
Researchers integrated genetic data from various tissues with Parkinson's disease (PD) studies to identify potential causal genes and drug targets. They employed a comprehensive analytical approach, including Mendelian randomization and protein-protein network analysis. The study highlighted GPNMB's significant role in PD at both protein and transcriptional levels across blood, cerebrospinal fluid, and brain. It also discovered CD38's protective role and DGKQ's inconsistent effects on PD. Additionally, nine other proteins were linked to PD risk. These insights enhance understanding of PD's genetic foundation and aid in developing future therapies.
Gu, Xiao-Jing. et al. "Expanding causal genes for Parkinson's disease via multi-omics analysis." NPJ Parkinson's disease, 2023.
Pubmed:
37865667
DOI:
10.1038/s41531-023-00591-0
