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1  cell superantigenic activity retained their epidermolytic activity (although some of these mutants r
2 utants that lost esterase activity also lost epidermolytic activity.
3 inally, we correlated esterase activity with epidermolytic activity.
4 tivities such as lymphocyte mitogenicity and epidermolytic activity.
5 t causes the autosomal dominant skin disease epidermolytic hyperkeratosis (EHK) is an arginine to his
6 n disorder with clinical features similar to epidermolytic hyperkeratosis (EHK).
7 tant, Dsk12, which models the human disease, epidermolytic hyperkeratosis (EHK).
8 autosomal-dominant skin blistering disorder, epidermolytic hyperkeratosis (MIM 113800), which is caus
9 calcium in outer stratum granulosum cells in epidermolytic hyperkeratosis after barrier disruption.
10 d pathogenesis of the barrier abnormality in epidermolytic hyperkeratosis are unknown, however.
11 baseline permeability barrier abnormality in epidermolytic hyperkeratosis can be attributed to abnorm
12                                              Epidermolytic hyperkeratosis is a dominantly inherited i
13                                              Epidermolytic hyperkeratosis is a hallmark feature of li
14                                              Epidermolytic hyperkeratosis is characterized by tonofil
15 mal dominant genodermatosis characterized by epidermolytic hyperkeratosis restricted to the palm and
16 mately 3-fold, recovery rates were faster in epidermolytic hyperkeratosis than in age-matched control
17 kin blistering phenotype mimicking a form of epidermolytic hyperkeratosis, a keratin gene disorder.
18  the keratin 10 deficient mouse, a model for epidermolytic hyperkeratosis, and a mouse model for Bloo
19  erythrodermic psoriasis, atopic dermatitis, epidermolytic hyperkeratosis, and Netherton's syndrome.
20 or the major inherited blistering disorders, epidermolytic hyperkeratosis, epidermolysis bullosa simp
21 o ((157)NQSLLQPL --> (157)NQSPLQPL) leads to epidermolytic hyperkeratosis, we tested and showed that
22 x, neurofibromatosis type 1, Bloom syndrome, epidermolytic hyperkeratosis, X-linked ichthyosis, Nethe
23 d barrier recovery kinetics in patients with epidermolytic hyperkeratosis.
24 ing for the accelerated recovery kinetics in epidermolytic hyperkeratosis.
25 nical disorder with histological findings of epidermolytic hyperkeratosis.
26 ve been identified as the molecular basis of epidermolytic hyperkeratosis.
27  including epidermolysis bullosa simplex and epidermolytic hyperkeratosis.
28                                              Epidermolytic ichthyosis (EI) due to KRT10 mutations is
29                                      Annular epidermolytic ichthyosis is a distinct phenotypic varian
30 hroderma, n = 6; lamellar ichthyosis, n = 7; epidermolytic ichthyosis, n = 5; and Netherton syndrome,
31 We now describe a third kindred with annular epidermolytic ichthyosis.
32                                              Epidermolytic palmoplantar keratoderma (EPPK) is an auto
33                                              Epidermolytic palmoplantar keratoderma (EPPK) is one of
34                                              Epidermolytic palmoplantar keratoderma (EPPK, MIM #14420
35 of pachyonychia congenita (PC) and focal non-epidermolytic palmoplantar keratoderma (FNEPPK).
36                                    Focal non-epidermolytic palmoplantar keratoderma (PPK or palmoplan
37                           Tylosis (focal non-epidermolytic palmoplantar keratoderma) is an autosomal
38  mutations in the K9 gene are known to cause epidermolytic palmoplantar keratoderma, a rare dominant-
39 perkeratosis, epidermolysis bullosa simplex, epidermolytic palmoplantar keratoderma, junctional epide
40 tient with extensive mucocutaneous blisters, epidermolytic palmoplantar keratoderma, nail dystrophy,

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