Publications by authors named "JiangFeng Fei"
Our recent study demonstrated eIF3a loss contributes to vemurafenib resistance in melanoma by activating ERK. However, overexpression of eIF3a in the clinic is not feasible to produce vemurafenib re-sensitization, and ERK inhibitors combined with vemurafenib still exhibit limited effectiveness in the treatment of melanoma. Here, using the human receptor tyrosine kinase phosphorylation antibody array, we observed that silencing eIF3a could activate BMX, a tyrosine kinase.
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- Vemurafenib is effective in treating melanoma but often faces issues with drug resistance, highlighting the need for strategies to overcome this challenge.
- A protein called eIF3a plays a key role in mediating resistance to vemurafenib, with lower levels found in resistant melanoma cells compared to sensitive ones.
- Overexpressing eIF3a can enhance sensitivity to BRAF inhibitors by lowering ERK activity, suggesting that targeting eIF3a could be a new approach to improve patient responses to treatment.
[structure: see text] A versatile strategy for the synthesis of polymerizable derivatives of the redox-active indicator dye 2,2'-azino-bis(3-ethylbenzthiazoline-6-sulfonic acid) (ABTS) is reported. Two products are shown to illustrate how the final step in the synthetic strategy can be used to alter the physical properties of the product. Both products were characterized spectroscopically and electrochemically.
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