Analysis of protein–protein interaction between late cornified envelope proteins and corneodesmosin |
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| Authors: | Ivonne M. J. J. van Vlijmen‐Willems Nathalie Jonca Erwin van Wijk Wiljan J. A. J. Hendriks Patrick L. J. M. Zeeuwen Joost Schalkwijk |
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| Affiliation: | 1. Department of Dermatology, Radboud University Medical Center, , Nijmegen, The Netherlands;2. Unité Différenciation Epidermique et Autoimmunité Rhumato?de, CNRS UMR5165, INSERM U1056, Université Toulouse III, H?pital PURPAN, , Toulouse, France;3. Department of Human Genetics and Department of Otorhinolaryngology, Radboud University Nijmegen Medical Centre, , Nijmegen, The Netherlands;4. Department of Cell Biology, Radboud University Medical Center, , Nijmegen, The Netherlands |
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| Abstract: | Deletion of two members of the late cornified envelope (LCE) family, LCE3B and LCE3C (LCE3C_LCE3B‐del), has been identified as risk factor for psoriasis with a possible role in skin barrier function. Moreover, genetic interaction between LCE3C_LCE3B‐del and HLA‐C*06, located in the psoriasis susceptibility regions 4 and 1 (PSORS4 and 1), has been reported in several populations. Because of high linkage disequilibrium between the PSORS1 genes HLA‐C*06 and corneodesmosin (CDSN), both genes are potentially involved in psoriasis. As corneodesmosin and LCE proteins are both constituents of the stratum corneum, we investigated potential direct protein–protein interactions between six LCE proteins and two corneodesmosin sequence variants. Partial colocalization of LCE2 and CDSN was observed in normal and psoriasis skin using immunofluorescence microscopy. Co‐expression of eCFP‐LCE and mRFP‐CDSN proteins in COS‐1 cells and human adult keratinocytes, and GST pull‐down results did not provide evidence for direct interactions between LCE proteins and CDSN variants. |
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| Keywords: | corneodesmosin HLA‐C keratinocytes late cornified envelope psoriasis |
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