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Inhibition of Integrin αβ-FAK-MAPK signaling constrains the invasion of T-ALL cells.The role of adhesion receptor integrin αvβ3 in T-ALL was unclear. Firstly, we performed quantitative real-time PCR to assess medullary expression of integrin β3(ITGB3) in T-ALL patients and high ITGB3 expression was relevant with the central nervous system leukemia(CNSL) incidence. Decreasing of cell invasion was observed in Jurkat and Molt4 treated with integrin αvβ3 specific antibody and inhibitor as well as cells with ITGB3 interference. Further, phosphorylation of FAK, cRAF, MEK and ERK decreased in cells with integrin αvβ3 inhibition or interference. Invasion decreased in T-ALL cells treated with FAK and ERK inhibitors. In conclusion, inhibition of integrin αvβ3 signals significantly limits the cell invasion of T-ALL cells.
Lan Huang, Yao Zhu, Qinglin Kong, Xianmin Guan, Xiaoying Lei, Luying Zhang, Hui Yang, Xinyuan Yao, Shaoyan Liang, Xizhou An, Jie Yu
2787 related Products with: Inhibition of Integrin αβ-FAK-MAPK signaling constrains the invasion of T-ALL cells.1.5 x 10^6 cells2 Pieces/Box 5 G1.5x10(6) cells1 Set100ug100ug Lyophilized10ml100ug Lyophilized100ug5 mg1.00 flask
#36944397 2023/03/19 To Up
Modulating CD40 and integrin signaling in the proinflammatory nexus using a 15-amino acid peptide, KGYY.CD40-signaling has long been a target in autoimmunity. Attempts to block signaling between CD40 and CD154 during clinical trials using monoclonal antibodies suffered severe adverse events. Previously, we developed a peptide, KGYY, that targets CD40 and, in preclinical trials, prevents Type 1 Diabetes in >90% of cases and reverses new onset hyperglycemia in 56% of cases. It did so by establishing normal effector T cell levels rather than ablating the cells and causing immunosuppression. However, the relationship between KGYY and other elements of the complex signaling network of CD40 is not clear. Studying interactions between proteins from autoimmune and non-autoimmune mice, we demonstrate interactions between CD40 and integrin CD11a/CD18, which complicates the understanding of the inflammatory nexus and how to prevent auto-inflammation. In addition to interacting with CD40, KGYY interacts with the integrins CD11a/CD18 and CD11b/CD18. We argue that modulation of CD40-CD154 signaling may be more advantageous than complete inhibition because it may preserve normal immunity to pathogens.
GiselaM Vaitaitis, DavidH Wagner