Anti-MAPKAPK2 monoclonal antibody, clone FQS6468 Knockout Validated

We have identified a novel series of substituted N,N'-diarylurea p38 alpha inhibitors. The inhibitory activity of the target compounds against the enzyme p38 alpha, MAPKAPK2 in BHK cells, TNF-alpha release in LPS-stimulated THP-1 cells and p38 alpha binding experiments were tested. Among these compounds, 25a inhibited the p38 alpha enzyme with an IC50 value of 0.47 nM and a KD value of 1.54 x 10(-8) and appears to be the most promising one in the series.

Severe inflammation can lead to multiple organ dysfunction syndrome, which has high mortality. Adipose-derived stem cells have been shown to affect the inflammatory response of macrophages. However, the molecular mechanism of the anti-inflammatory capacity of adipose-derived stem cells (ADSCs) remains to be understood. In the present study, a macrophage inflammation model was established by LPS, and treated with different volumes of ADSC supernatant. Then, we investigated the key genes in the LPS group and treatment group by RT-PCR, RNA sequencing technology, and bioinformatics analysis. A total of 26 miRNAs and 11,882 mRNAs were differentially expressed between them. The expression of 15 of the miRNAs (9 upregulated and 6 downregulated) was confirmed by RT-PCR. GO and KEGG pathway analyses of the targets of the 9 significantly upregulated miRNAs showed that they were related to immune system process, inflammatory response, lipopolysaccharide, and TNF-alpha, NF-kappa B, Toll-like receptor, and MAPK signaling pathways. Moreover, a miRNA-mRNA network also revealed 8 important genes (Mapkapk2, Sepp1, Cers6, Snn, ZfP568, Ccdc93, Pofut1, Pik3cd). We finally confirmed the expression of these 8 targeted genes by performing the RT-PCR analysis. This study may provide a new understanding of the molecular mechanism of ADSCs in the inflammatory response related to multiple miRNAs and mRNAs.