Anti-MAPK1/MAPK3 polyclonal antibody

Previously, we detected that 14-3-3 protein epsilon (YWHAE) was involved in the pathogenesis of atopic dermatitis (AD) and tyrosinase-mediated pigmentation. In this study, we aimed to identify critical factors associated with YWHAE in human keratinocytes using high-throughput screening (HTS) approaches to reveal its functions in skin. We overexpressed YWHAE in human HaCaT keratinocytes and then conducted serial HTS studies, including RNA sequencing integrated with antibody arrays and the implementation of bioinformatics algorithms. Cumulatively, these approaches identified several novel genes in keratinocytes associated with the function of YWHAE including KRT9, KRT1, KRT6C, BST2, CIB2, APH1B, ACTC1, IFI27, TUBA1A, CAPN6, UTY, MX2, and MAPK15, based on RNA sequencing data, and MAPK1, MMP2, TYK2, NOS3, and CASP3, based on antibody array data. In particular, CD37 is a unique gene that was detected and validated in all the methods applied in this study. By integrating the datasets obtained from these HTS studies and utilizing the strengths of each method, we obtained new insights into the functional role of YWHAE in skin keratinocytes. The approach used here could contribute to the clinical understanding of YWHAE-associated applications in the treatment of AD disease.

The present study aimed to investigate the existence of immunoregulation-associated long non-coding (lnc)RNAs mediated by T lymphocytes in the wound surfaces of diabetic foot ulcers (DFUs). The wound skin tissues of patients receiving debridement for trauma or DFUs associated with infection were obtained. Dermatological histological changes were observed by pathological staining, and T lymphocyte subsets and inflammation-associated cytokines were identified. Gene chip technology was used to screen for lncRNAs regulated by immune cells. The wound skin structure in the control group was revealed to be complete, and the inflammatory response was not marked. However, the wound skin structure in the ulcer group was disordered and exhibited a notable inflammatory response. Compared with the control group, expression levels of cluster of differentiation (CD)3 and CD8 in the wound surface tissues of the ulcer group were significantly increased, while the expression levels of interleukin (IL)-1, IL-2, IL-10, interferon- and tumor necrosis factor- were significantly upregulated. A target regulatory association was identified between downregulated lncRNA-ENST00000411554 and upregulated mitogen-activated protein kinase (MAPK)1 in DFU tissues, and a negative correlation was detected between this RNA and protein. The present results suggested that an immune functional disorder of T lymphocytes may be closely associated with the development of DFUs. Furthermore, activation of the MAPK signal transduction pathway mediated by the lncRNA-ENST00000411554/MAPK1 axis may affect the DFU immune regulatory imbalance.