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The epidermal integrin α3β1 promotes skin tumorigenesis in experimental models; yet, the underlying molecular mechanisms remain mostly unclear. In their article, Ramovs et al. (2020a) identify two spatially separated α3β1-dependent signaling branches fostering skin tumor outgrowth. In basal keratinocytes, α3β1/laminin (LN)-332 drives FAK/Src activation, whereas in suprabasal layers, junctional α3β1 and the tetraspanin CD151 mediate signal transducer and protein kinase B (Akt)‒dependent survival that is independent of LN-332 binding.Tradit
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