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DISEASE
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Dermatitis, Atopic
Abnormal expression of the novel epidermal enzyme, glucosylceramide deacylase, and the accumulation of its enzymatic reaction product, glucosylsphingosine, in the skin of patients with atopic dermatitis.
The skin of atopic dermatitis patients contains a novel enzyme, glucosylceramide sphingomyelin deacylase, which cleaves the N-acyl linkage of sphingomyelin and glucosylceramide.
in extracts of whole epidermis biopsies from patients with atopic dermatitis, sphingomyelin deacylase activities are significantly (3-fold) increased over healthy controls in the particulate fraction, whereas there is no significant difference in the activity of sphingomyelinase between atopic dermatitis and healthy control
activity is enhanced more than 5fold in involved stratum corneum, more than 3fold in uninvolved stratum corneum, and approximately 3fold in the involved epidermis from patients with atopic dermatitis compared with healthy controls
from lesional forearm skin (volar side) of patients with atopic dermatitis, sphingomyelin deacylase activity is at least 5times higher than in the stratum corneum of healthy controls. In stratum corneum from nonlesional skin of patients with atopic dermatitis, SM deacylase activity is at least three times higher than in healthy controls. Stratum corneum from contact dermatitis patients shows levels of sphingomyelin deacylase similar to healthy controls
glucosylceramide sphingomyelin deacylase, is expressed in the skin of patients with atopic dermatitis, which plays an important role in ceramide deficiency (including acylceramides) in the stratum corneum
high-expression of sphingomyelin deacylase is an important determinant of ceramide deficiency leading to barrier disruption in atopic dermatitis. The enzyme is highly expressed in the epidermis of patients with atopic dermatitis, and competes with sphingomyelinase or beta-glucocerebrosidase for the common substrate sphingomyelin or glucosylceramide, which leads to the ceramide deficiency of the stratum corneum in atopic dermatitis
the abnormal expression of sphingomyelin deacylase, which acts as a by-pass enzyme and competes with EC 3.1.4.12 (sphingomyelin phosphodiesterase) as well as EC 3.2.1.45 (glucosylceramidase) for N-acyl-sphingosylphosphorylcholine and D-glucosyl-N-acylsphingosine, respectively, is mainly responsible for the ceramide deficiency in patients with atopic dermatitis. The biogenesis of EC 3.1.4.12 (sphingomyelin phosphodiesterase) as well as EC 3.2.1.45 (glucosylceramidase) may be critical to the pathogenesis of atopic dermatitis
glucosylceramide sphingomyelin deacylase, is expressed in the skin of patients with atopic dermatitis, which plays an important role in ceramide deficiency (including acylceramides) in the stratum corneum
Higuchi, K.; Hara, J.; Okamoto, R.; Kawashima, M.; Imokawa, G.
The skin of atopic dermatitis patients contains a novel enzyme, glucosylceramide sphingomyelin deacylase, which cleaves the N-acyl linkage of sphingomyelin and glucosylceramide
A possible mechanism underlying the ceramide deficiency in atopic dermatitis: expression of a deacylase enzyme that cleaves the N-acyl linkage of sphingomyelin and glucosylceramide
Ishibashi, M.; Arikawa, J.; Okamoto, R.; Kawashima, M.; Takagi, Y.; Ohguchi, K.; Imokawa, G.
Abnormal expression of the novel epidermal enzyme, glucosylceramide deacylase, and the accumulation of its enzymatic reaction product, glucosylsphingosine, in the skin of patients with atopic dermatitis