Therefore that myosin Va expression is also not required for normal trafficking and packaging of secretory granules into platelets at the level of the megakaryocyte. It is likely that, for this role, myosin II is the predominant motor protein involved. On the other hand, it is also possible that other related myosins are expressed or over-expressed in the Myo5a2/2 platelet, and that redundancy of function with these myosins is such that there is no observable phenotype in the single Myo5a2/2 mouse. Myosin Vb is involved actin-dependent vesicle transport and plasma membrane recycling in various cells, including neurons and oocytes. Myosin Vc localises with membrane compartments involved in transferrin trafficking in epithelial cells and has been shown to function as a molecular motor driving secretory granule transport in lacrimal gland acinar cells and the MCF-7 cell line. To examine the expression of myosin Vb, Vc, and VI, we immunoblotted for these proteins in human, wild-type, and Myo5a2/2 platelets. Myosin Vb and Vc could not be detected in any platelet sample, suggesting that the absence of a platelet defect in myosin Va-deficient mice is not a consequence of normal expression or compensatory upregulation of myosin Vb or Vc. The absence of these proteins is consistent with mRNA analysis of human and mouse platelets. Recently, it has been found that myosin VI regulates fusion pores formed between secretory vesicles and the plasma membrane. In contrast to myosin Vb and Vc, myosin VI was present in human, wild-type and Myo5a2/2 platelets. There was no upregulation of myosin VI detected in myosin Va-deficient platelets, suggesting that its expression does not change in the absence of myosin Va. However, the presence of myosin VI in platelets, and its recently reported role in exocytosis, provides the possibility that this protein is involved in platelet granule secretion, and that there may be redundancy of function between this motor protein and myosin Va in the control of granule secretion. This may be more important in mouse platelets than in human platelets, as mRNA analysis indicates a greater abundance of myo6 mRNA in mouse platelets. The possible role of myosin VI in mouse platelet exocytosis deserves further attention. Epidermis, the outermost part of the skin composed mainly of keratinocytes, is a self-renewing, multilayered, stratified and keratinized squamous epithelium. It provides a physical barrier protecting an organism from dehydration and a variety of environmental insults. To generate the protective barrier continuously, keratinocytes should be well balanced in their proliferation, differentiation and apoptosis programs. The mechanism to control keratinocyte differentiation depend on many factors such as calcium, vitamin D, and reactive oxygen species. Many of intracellular signaling cascades and transcription factors are coordinately regulated by these factors, thereby ensuring the proper expression of differentiation-related genes in a spatiotemporal fashion. For example, p63 is expressed in the basal layer of epidermis and supports the proliferation of keratinocytes. In contrast, Notch signaling is activated in spinous layer and induces keratinocyte differentiation. Also, PKC associated AP1 and C/EBP transcription factors are involved in the induction of keratinocyte differentiation. Although a number of genes required for keratinocyte proliferation and differentiation have been investigated.

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