Melanin provides protection against excess exposure to solar ultraviolet radiation (UVR) and related adverse health effects. Diffuse reflectance spectroscopy (DRS) can be used to calculate cutaneous melanin and erythema, but this is complex and has been mostly used for light-to-medium pigmented skin. Handheld reflectance spectrophotometers, such as the Mexameter(®) MX18, can also be used.
View Article and Find Full Text PDFCa(2+)mobilization in response to cross-linking of IgE bound to its high affinity receptor, FcεRI, on mast cells is central to immune allergic responses. Stimulated tyrosine phosphorylation caused by this cross-linking activates store-operated Ca(2+)entry that results in sustained Ca(2+)oscillations dependent on Rho family GTPases and phosphoinositide synthesis. Coupling of the endoplasmic reticulum (ER) Ca(2+)sensor, stromal interaction molecule 1 (STIM1), to the Ca(2+)-selective channel, Orai1, is regulated by these elements and depends on membrane organization, both at the plasma membrane and at the ER.
View Article and Find Full Text PDFBackground: Skin colour is an important factor in skin-related diseases. Accurate determination of skin colour is important for disease prevention and supporting healthy sun behaviour, yet such data are lacking for dark skin types.
Methods: Self-perceived, natural skin colour and sun-skin reaction were compared with objectively measured skin colour among an African population with predominantly dark skin.
Antigen stimulation of mast cells via FcεRI, the high-affinity receptor for IgE, triggers a signaling cascade that requires Ca(2+) mobilization for exocytosis of secretory granules during the allergic response. To characterize the role of Rho GTPases in FcεRI signaling, we utilized a mutant RBL cell line, B6A4C1, that is deficient in antigen-stimulated Cdc42 activation important for these processes. Recently the importance of stimulated intracellular oscillations has emerged, and we find that B6A4C1 cells exhibit severely attenuated Ca(2+) oscillations in response to antigen, which are restored to wild-type RBL-2H3 levels by expression of constitutively active Cdc42 G12V or by a GEF for Cdc42, DOCK7, but not when the C-terminal di-arginine motif of active Cdc42 is mutated to di-glutamine.
View Article and Find Full Text PDFThe proto-oncogene proviral integration site for moloney murine leukemia virus (PIM) kinases (PIM-1, PIM-2, and PIM-3) are serine/threonine kinases that are involved in a number of signaling pathways important to cancer cells. PIM kinases act in downstream effector functions as inhibitors of apoptosis and as positive regulators of G1-S phase progression through the cell cycle. PIM kinases are upregulated in multiple cancer indications, including lymphoma, leukemia, multiple myeloma, and prostate, gastric, and head and neck cancers.
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