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Mutations in keratins, the epithelial-specific intermediate filament proteins, result in aberrant cytoskeletal networks which present clinically as a variety of epithelial fragility phenotypes.

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In this chapter, I review what is known about the cytoskeletons of intermediate filaments and their associated proteins.

Given that identical inherited mutations in this gene can cause either pachyonychia congenita or steatocystoma multiplex, the features of this mouse model suggest that this clinical heterogeneity arises from a cell type-specific, genetically determined compensation by related keratins.

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The type II hair keratin clone (hHaKB2-1, 829 bp) also encoded 2B helix and C-terminal regions and was 95% homologous to mouse.

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In diabetes mellitus, hyperglycemia has been found to result in increased levels of dialglycerol, which in turn activates the protein kinase C (PKC) pathway.

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In this review a brief synopsis is done about the pathophysiology and etiology of CME, the different diagnostic methods for evaluating the CME are described and finally the therapeutic approaches of the disease are evaluated.

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Pachyonychia congenita (PC) is a skin disorder resulting from mutations in keratin (K) proteins including K6a, K6b, K16, and K17.

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Investigators in one study theorized that some persons have an inherited tendency for weak melanocytes that respond to inflammation by decreasing melanin production, or for strong melanocytes that respond by increasing melanin production.

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Moreover, the processing of intermediates was also affected by transcription, suggesting that ODN-directed gene repair may be linked to transcription-coupled repair.

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Since 1991, mutations in several keratin genes have been found to cause a variety of human diseases affecting the epidermis and other epithelial structures.

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The invention further relates to the use of a combination of pharmaceutical agents which comprise: (a) a compound of formula (I); and (b) one or more pharmaceutically active agents for the manufacture of a medicament for the treatment of a disease or disorder which responds to a c-Met tyrosine kinase, especially a proliferative disorder or disease, in particular a cancer.

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Abstract: Twelve cases of pachyonychia congenita were reviewed.

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Mitochondrial dehydrogenase (WST-1) assay for rat embryonal neurosensory precursor retinal cells after 24-hour exposure to dexamethasone solution (Dex-S), dexamethasone powder solubilized in DMSO (Dex-P), DMSO at an equivalent dose used to solubilize the powder, and untreated controls.

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In retinal vein occlusion, both ranibizumab and Ozurdex have been shown to be effective, although their relative efficacy has not been determined in head-to-head clinical trials.

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Analysis of both phenotype and genotype data led to the following conclusions: (i) K6a or K16 mutations produce the pachyonychia congenita type 1 phenotype, whereas K17 (or K6b) mutations cause pachyonychia congenita type 2; (ii) the presence of pilosebaceous cysts following puberty is the best indicator of pachyonychia congenita type 2; (iii) prepubescent patients are more difficult to classify due to the lack of cysts; and (iv) natal teeth are indicative of pachyonychia congenita type 2, although their absence does not preclude the pachyonychia congenita type 2 phenotype.

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At the molecular level it has been shown that mutations in keratin K6a or K16 cause PC-1 whereas those in K6b or K17 lead to PC-2.

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