坏死性下垂
信号转导
炎症
细胞生物学
生物
蛋白激酶A
ASK1
激酶
癌症研究
免疫学
细胞凋亡
程序性细胞死亡
丝裂原活化蛋白激酶激酶
生物化学
作者
Salin Kiratikanon,Nipon Chattipakorn,Nipon Chattipakorn,Sirinart Kumfu
标识
DOI:10.1016/j.abb.2022.109189
摘要
Protein tyrosine phosphatase non-receptor type 6 (PTPN6) is a key regulatory protein in cellular signal transduction in the control of inflammation and cell death. Impairment of PTPN6 is known to be associated with human inflammatory diseases including neutrophilic dermatosis; however, comprehensive studies of PTPN6-associated neutrophilic dermatosis have not clearly identified the relationships involved. Reports from in vitro and in vivo studies revealed that inflammatory cytokines have increased in the white blood cells from PTPN6-knocked out mice, and systemic inflammation was also increased in these mice, resulting in skin inflammation in this model. Reports of PTPN6 regulatory functions through five pathophysiological mechanisms are summarized and discussed here including inhibition of myeloid differentiation primary response 88, enhancement of the regulatory function of receptor-interacting protein kinase, inhibition of receptor-interacting serine/threonine-protein kinase 3/mixed lineage kinase domain-like protein-dependent necroptosis, inhibition of caspase-8-dependent apoptosis, and inhibition of p38/mitogen-activated protein kinase. Treatments by blocking the pathways involved in signal transduction and inflammatory cytokine release are also summarized. Understanding this underlying mechanism could improve therapeutic strategies for neutrophilic dermatosis.
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