Panoply™ Human ABL1 Over-expressing Stable Cell Line

The oncogene ABL1 plays a crucial role in various cancers, but its role in pneumonia remains unclear. Here, researchers investigated the role of ABL1 in pneumonia and its potential mechanisms. They used RNA sequencing to detect the expression levels of various kinases in peripheral blood mononuclear cells (PBMCs). A series of overexpression and gene knockout cell lines were constructed. Furthermore, researchers established a mouse model of pneumonia induced by intranasal infection and pre-treated the mice with asciminib. ELISA and qPCR techniques were used to detect the expression levels of target genes. In addition, STRING interaction network analysis and Western blotting were used to detect the interactions between target proteins. The results showed that ABL1 expression levels were elevated in infants with Escherichia coli pneumonia. ABL1 expression levels were positively correlated with inflammatory cytokine levels and NF-κB pathway activation. In vivo experiments showed that inhibiting ABL1 suppressed the production of inflammatory cytokines, reduced bacterial load in the lungs, and improved lung injury scores. ABL1 inhibited the phosphorylation of IκBα and p38 and regulated the ubiquitination of TRAF6. ABL1 partially regulates the inflammatory response in pneumonia by regulating the MAPK and NF-κB pathways and TRAF6 ubiquitination.

By measuring luciferase activity in IL-1β-induced HEK293T cell lines transfected with an NF-κB luciferase reporter gene and various kinase genes, researchers observed that overexpression of ABL1 significantly enhanced luciferase activity (Figure 1A). Interestingly, they found that luciferase activity was positively correlated with ABL1 expression levels (Figure 1B), supporting the regulatory role of ABL1 in the NF-κB pathway. Furthermore, researchers stimulated ABL1-overexpressing RAW264.7 cells with LPS. The results showed that Il6 and Tnf levels were significantly increased in ABL1-overexpressing cells under LPS induction (Figure 1C). To confirm the role of ABL1 in regulating the NF-κB pathway, researchers constructed ABL1 knockout cells (Figure 1D). Interestingly, the levels of pro-inflammatory cytokines were positively correlated with ABL1 expression levels. Pro-inflammatory cytokine levels were decreased in ABL1 knockout cells, while they were increased in ABL1-overexpressing cells (Figure 1E). These results indicate that ABL1 is crucial for inducing pro-inflammatory cytokines and activating the NF-κB pathway.

Figure 1. ABL1 is essential for the induction of inflammatory cytokines and the activation of the NF-kB pathway. (Xu F, et al., 2022)