Anti-KSR1 (aa 301-400) polyclonal antibody

BRAF is an oncogenic protein kinase that drives cell growth and proliferation through the MEK-ERK signaling pathway. BRAF inhibitors have demonstrated antitumor efficacy in melanoma therapy but have also been found to be associated with the development of cutaneous squamous cell carcinomas (cSCCs) in certain patients. Here, we report that BRAF is phosphorylated at Ser729 by AMP-activated protein kinase (AMPK), a critical energy sensor. This phosphorylation promotes the association of BRAF with 14-3-3 proteins and disrupts its interaction with the KSR1 scaffolding protein, leading to attenuation of the MEK-ERK signaling. We also show that phosphorylation of BRAF by AMPK impairs keratinocyte cell proliferation and cell-cycle progression. Furthermore, AMPK activation attenuates BRAF inhibitor-induced ERK hyperactivation in keratinocytes and epidermal hyperplasia in mouse skin. Our findings reveal a mechanism for regulating BRAF signaling in response to energy stress and suggest a strategy for preventing the development of cSCCs associated with BRAF-targeted therapy.

This paper investigates the influence of various sintering temperatures on the microstructure and photoluminescence properties of KSr0.99PO4:Eu-0.01(3+) phosphors prepared by microwave-assisted sintering. The package properties of KSr0.99PO4:Eu-0.01(3+) phosphors combined with a n-UV InGaN chip are also investigated. To achieve maximum luminescence, the optimum sintering temperature for KSr0.99PO4:Eu-0.01(3+) phosphors prepared by microwave assisted-sintering is 1200 degrees C due to the pure phase and uniform and large particles (as identified by XRD and SEM). The results of the package properties showed that KSr1-xPO4:xEu(3+) (x = 0.01) phosphor sintered at 1200 degrees C by microwave-assisted sintering could emit orange-red light via the n-UV InGaN chip.