BCR signaling can in principle bind and phosphorylate calponin-3. Thus, it may very well be that phosphorylation under physiological conditions takes place and is 12 / 16 Calponin-3 in B Lymphocyte Development functionally relevant, but is below the detection limit. Indeed, although the role of phosphorylation 
for the regulation of calponins has been established in numerous in vitro experiments, the detection of phospho-calponins under physiological in vivo conditions has been difficult. In contrast to the conditional deletion of calponin-3 in B cells, the whole body knockout animals showed a strong neuronal phenotype, which is in correspondence with the high expression of calponin-3 in neuronal tissue. Such a phenotype has already been PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19710468 proposed based on the high expression of calponin-3 in the early stages of hippocampal development compared to its low expression in adult hippocampi, suggesting a role in neural cell proliferation and migration. Whether loss of calponin-3 also affects neural plasticity, as has been postulated based on in vitro data, needs to be investigated in the future. Besides the neuronal phenotype, embryos appeared to be morphologically normal, which is surprising given the broad expression pattern of calponin-3-GFP observed in the knock-in animals, e.g. in the skin. However, we cannot rule out that other calponin family members may be able to compensate the loss of calponin-3 in these tissues. Whether deletion of calponin-3 affects trophoblast fusion, myoblast fusion or wound healing in vivo, as has PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19710561 been suggested, remains to be determined. In summary, here we have identified calponin-3 as a putative element downstream of preBCR signaling. Deletion of calponin-3 in B cells, however, did not lead to a profound phenotype, arguing against an important role in B cell development. Nevertheless, the mouse model we generated in the course of this project will be of benefit for assessing the role of calponin-3 under physiological conditions. It not only simplifies the identification and tracking of calponin-3-expressing cells in vivo, but also allows its analysis in a loss-of-function approach. Crossing our mice with a Cre-transgenic strain of choice will reveal the tissue-specific function of calponin-3, and thus will help to shed light on the role of calponin-3 in muscle and nonmuscle cells. ~~ Melanogenesis is the physiological process by which melanin is synthesized in melanocytes located in the basal layer of the epidermis to purchase MRT-67307 protect the skin from UV irradiation. UVB-exposed keratinocytes secrete cytokines and growth factors, including endothelin 1, that stimulate cellular functions, especially proliferation and melanization, of adjacent melanocytes in the epidermis. The corresponding specific receptors are constitutively expressed by human melanocytes and the binding of cytokines and growth factors to their receptors transduces intracellular signals to initiate melanogenesis through specific signaling cascades. On the other hand, UVB radiation directly induces the generation of reactive oxygen species in epidermal keratinocytes and melanocytes and stimulates stress activated protein kinases, such as p38, c-jun N-terminal kinase or extracellular regulated protein kinase . In UVB-exposed human melanocytes, the p38 pathway predominantly contributes to the increased expression of microphthalmia-associated transcription factor , a master regulator of melanocyte functions, including differentiation, proliferation, surviva
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