Regular articleInvolvement of protein kinase C in translocation of desmoplakins from cytosol to plasma membrane during desmosome formation in human squamous cell carcinoma cells grown in low to normal calcium concentration☆
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IgG against the Membrane-Proximal Portion of the Desmoglein 3 Ectodomain Induces Loss of Keratinocyte Adhesion, a Hallmark in Pemphigus Vulgaris
2023, Journal of Investigative DermatologyCitation Excerpt :In addition, there are critical heterophilic interactions between DSG3 and desmocollins, which strengthen the cohesion of the desmosomal cell‒cell contacts (Heupel et al., 2008; Mavropoulos et al., 2013; Nose et al., 1990; Spindler et al., 2009; Syed et al., 2002). In vitro, Ca2+ concentrations over 0.1 mM rapidly induce cell adhesion of HaCaT KCs and formation of functional desmosomes within 5 hours, whereas Ca2+ concentrations below 0.1 mM prevent desmosome formation (Kitajima et al., 1999; Sheu et al., 1989). The extracellular domain of DSG3, similar to those of other cadherins, consists of five subdomains (EC1‒5), which share high structural homology, except for the COOH-terminal EC5 domain (Koch et al., 1990).
The desmosome as a model for lipid raft driven membrane domain organization
2020, Biochimica et Biophysica Acta - BiomembranesNew insights into desmosome regulation and pemphigus blistering as a desmosome-remodeling disease
2013, Kaohsiung Journal of Medical SciencesCitation Excerpt :Based on results presented to date, it appears plausible that Dsgs and Dscs might interact with each other by homophilic and/or heterophilic binding mechanisms. Keratinocytes that are cultured in media containing low Ca2+ concentrations (below 0.1 mM) proliferate without differentiation and do not form desmosomes [16–18]. Increasing the Ca2+ concentration in the culture medium to greater than 0.1 mM induces cell–cell contacts (mainly adherens junctions) within 5 minutes, and desmosome formation within 2 hours [18,19] (Fig. 3).
PKC-δ and-η, MEKK-1, MEK-6, MEK-3, and p38-δ Are essential mediators of the response of normal human epidermal keratinocytes to differentiating agents
2010, Journal of Investigative DermatologyDesmosomes: New perspectives on a classic
2007, Journal of Investigative DermatologyCitation Excerpt :Interestingly, knockdown of the α-isoform of PKC impairs calcium-dependent desmosome formation (Hobbs RP, Hsieh SN, et al., personal communication) and results in retention of DP along IF in a manner similar to that observed for the S2849G DP mutant. Activation of PKC had previously been reported to trigger desmosome formation in low-calcium conditions, or in cells lacking desmosomes owing to mutation of adherens junction proteins (Sheu et al., 1989; Hengel et al., 1997). Thus, PKC may act as a rheostat to control both the availability of DP for junction assembly and the rate at which DP reinforcements are assembled into particles and traffic to join their counterparts already building up the desmosomal plaque.
Structure and Function of Desmosomes
2007, International Review of CytologyCitation Excerpt :On the other hand, H‐7 interfered with calcium‐dependent disassembly and internalization after desmosomal splitting (Denisenko et al., 1994; Pasdar et al., 1995a). It was therefore suggested that the different sensitivities are mediated by calcium‐dependent intracellular signal transduction pathways (Pasdar et al., 1995a), most likely by PKC (Citi, 1992; Sheu et al., 1989). Probably one of the most compelling examples of regulation of desmosomal properties and dynamics has been provided by Wallis et al. (2000).
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This work was supported by a grant (B, 01480267) from the Scientific Research Fund of the Ministry of Education Science and Culture, Japan.
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Present address: Department of Dermatology, Kaohsiung Medical College No. 100, Shih-Chuan 1st Road, Kaohsiung, Taiwan, Republic of China.