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keratosis/protease

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The serine protease inhibitor of Kazal-type 9 (SPINK9) is expressed in lichen simplex chronicus, actinic keratosis and squamous cell carcinoma.

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The serine protease inhibitor of Kazal-type (SPINK) 9 was reported to be exclusively expressed in palmoplantar skin. SPINK9 is a specific inhibitor of the serine protease kallikrein-related peptidase 5 (KLK5), which contributes to the desquamation process of the stratum corneum. Herein, we

Nagashima-type palmoplantar keratosis: a common Asian type caused by SERPINB7 protease inhibitor deficiency.

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Nagashima-type palmoplantar keratosis (NPPK) is an autosomal recessive diffuse non-epidermolytic palmoplantar keratosis caused by mutations in SERPINB7, a member of the serine protease inhibitor superfamily. Genetic studies suggest that NPPK is the most common palmoplantar keratosis in Japan, and

Mutations in SERPINB7, encoding a member of the serine protease inhibitor superfamily, cause Nagashima-type palmoplantar keratosis.

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"Nagashima-type" palmoplantar keratosis (NPPK) is an autosomal recessive nonsyndromic diffuse palmoplantar keratosis characterized by well-demarcated diffuse hyperkeratosis with redness, expanding on to the dorsal surfaces of the palms and feet and the Achilles tendon area. Hyperkeratosis in NPPK is

Epidermal expression of serine protease, neuropsin (KLK8) in normal and pathological skin samples.

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OBJECTIVE The expression of human neuropsin (KLK8) mRNA in normal and pathological skin samples was analysed and the results compared with those for tissue plasminogen activator (tPA) mRNA. METHODS Northern blot and in situ hybridisation analyses of KLK8 mRNA in normal and lesional skin of patients

[Clinical experience with enzymes (collagenase, protease) in the treatment of skin lesions caused by CO2-laser surgery].

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The authors applied collagenase and protease in lipofil solution for the treatment of skin lesions caused by CO2 laser interventions. 354 surgical interventions were performed on 91 patients (43 verruca vulgaris, 32 naevus intradermalis, 16 keratosis). The laser methods were excision or/and

Highly prevalent SERPINB7 founder mutation causes pseudodominant inheritance pattern in Nagashima-type palmoplantar keratosis.

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BACKGROUND Nagashima-type palmoplantar keratosis (NPPK) is a distinct autosomal recessive genodermatosis characterized by diffuse transgressive palmoplantar keratoderma (PPK). Very recently, putative loss-of-function mutations in SERPINB7, which encodes a member of the serine protease inhibitor

Topical protease therapy as a novel method of epidermal ablation: preliminary report.

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BACKGROUND For more than 50 years, proteolytic enzymes have been extensively used in laboratory settings for the purposes of in vitro epidermal separation and keratinocyte isolation. However, the topical, in vivo pharmacologic properties of these enzymes are virtually unknown. Previous therapeutic

Loss-of-function mutations in the cathepsin C gene result in periodontal disease and palmoplantar keratosis.

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Papillon-Lefèvre syndrome, or keratosis palmoplantaris with periodontopathia (PLS, MIM 245000), is an autosomal recessive disorder that is mainly ascertained by dentists because of the severe periodontitis that afflicts patients. Both the deciduous and permanent dentitions are affected, resulting in

Melanosome degradation in epidermal keratinocytes related to lysosomal protease cathepsin V.

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The cause of hyperpigmentation, such as solar lentigo and seborrheic keratosis, is the excessive accumulation of melanin pigments in the epidermal basal layer. Melanin pigments are synthesized in the melanosomes, which are specific organelles produced by melanocytes in the basal layer. Melanosomes

Loss-of-function mutations in CAST cause peeling skin, leukonychia, acral punctate keratoses, cheilitis, and knuckle pads.

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Calpastatin is an endogenous specific inhibitor of calpain, a calcium-dependent cysteine protease. Here we show that loss-of-function mutations in calpastatin (CAST) are the genetic causes of an autosomal-recessive condition characterized by generalized peeling skin, leukonychia, acral punctate

Down-regulated PAR-2 is associated in part with interrupted melanosome transfer in pigmented basal cell epithelioma.

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In pigmented basal cell epithelioma (BCE), there seems to be an abnormal transfer of melanized melanosomes from proliferating melanocytes to basaloid tumor cells. In this study, the interruption of that melanosome transfer was studied with special respect to the altered function of a phagocytic
Latent transforming growth factor-beta 1 (TGF-beta 1) and its binding protein-1 (LTBP-1) are components of the extracellular matrix microfibrils of cultured human fibroblasts. Using immunohistochemistry we have studied the localization of TGF-beta 1 and LTBP-1 and compared their distribution with

Aminopeptidase M and dipeptidyl peptidase IV activity in epithelial skin tumors: a histochemical study.

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The activities of microsomal alanylaminopeptidase (APM EC 3.4.11.2) and of dipeptidyl dipeptidase IV (DPP IV EC 3.4.14.5) were histochemically studied in frozen sections of normal skin, seborrheic keratosis, basal cell carcinoma, solar keratosis, Bowen's disease and squamous cell carcinoma using

A genome scan for epidermal skin pattern in adolescent twins reveals suggestive linkage on 12p13.31.

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Deterioration in stratum corneum reticular patterning (skin pattern or skin wrinkling) has been associated with increased rates of solar keratoses and skin cancer. A previous analysis of data from the twin sample used in this investigation has shown that 86% of the variation in skin pattern is

Expression of stratum corneum chymotryptic enzyme in ichthyoses and squamoproliferative processes.

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OBJECTIVE Stratum corneum chymotryptic enzyme (SCCE) is a serine protease, which is thought to play a role in the desquamation of skin via the proteolysis of desmosomes in the stratum corneum. The objective of this study was to investigate the expression of SCCE in ichthyoses and squamoproliferative
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