Pathological mechanisms of keratinization abnormalities

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We have studied mechanisms of normal keratinization and abnormal keratinization. We have found evidences to suggest that tight junctions are involved in spatially distinct degradation of corneodesmosomes and in lamellar granule transportation and secretion. We have revealed that abnormal transportation and/or secretion of lamellar granules could result in ichthyosis in two genetic diseases, CEDNIK syndrome and ARC syndrome. We found that corneodesmosin in crucial for corneocyte adhesion. We have found evidences to suggest that Rab11 may be involved in lamellar granule transportation.