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1 ing for the accelerated recovery kinetics in epidermolytic hyperkeratosis.
2 nical disorder with histological findings of epidermolytic hyperkeratosis.
3 ve been identified as the molecular basis of epidermolytic hyperkeratosis.
4 including epidermolysis bullosa simplex and epidermolytic hyperkeratosis.
5 d barrier recovery kinetics in patients with epidermolytic hyperkeratosis.
6 kin blistering phenotype mimicking a form of epidermolytic hyperkeratosis, a keratin gene disorder.
7 calcium in outer stratum granulosum cells in epidermolytic hyperkeratosis after barrier disruption.
8 the keratin 10 deficient mouse, a model for epidermolytic hyperkeratosis, and a mouse model for Bloo
9 erythrodermic psoriasis, atopic dermatitis, epidermolytic hyperkeratosis, and Netherton's syndrome.
11 baseline permeability barrier abnormality in epidermolytic hyperkeratosis can be attributed to abnorm
12 t causes the autosomal dominant skin disease epidermolytic hyperkeratosis (EHK) is an arginine to his
15 or the major inherited blistering disorders, epidermolytic hyperkeratosis, epidermolysis bullosa simp
19 autosomal-dominant skin blistering disorder, epidermolytic hyperkeratosis (MIM 113800), which is caus
20 mal dominant genodermatosis characterized by epidermolytic hyperkeratosis restricted to the palm and
21 mately 3-fold, recovery rates were faster in epidermolytic hyperkeratosis than in age-matched control
22 o ((157)NQSLLQPL --> (157)NQSPLQPL) leads to epidermolytic hyperkeratosis, we tested and showed that
23 x, neurofibromatosis type 1, Bloom syndrome, epidermolytic hyperkeratosis, X-linked ichthyosis, Nethe
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