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Fig. 9. Adhesion defects in laminin 5 or integrin ß4 chronically elevate ATF3. (A) Cryostat sections of skin from wild type neonatal mouse (a,d) and laminin 5 null neonatal mouse (b,c,e,f,) were stained with an anti-ATF3 (a,b,c) or anti-integrin ß4 antibody (d,e,f). ATF3 protein is not detectable in wild type mouse epidermis (arrows identify epidermal basal cells). ß4 was continuous and polarized to the basement membrane (d, arrow identifies ß4 staining in the basement membrane zone). In contrast, laminin 5 null mouse skin (
3-/-) exhibited increased levels of nuclear ATF3 protein expression (b, c, arrow identifies ATF3 staining). Integrin ß4 was polarized to the basement membrane zone in laminin 5 null keratinocytes but was discontinuous (e,f) (arrows identify discontinuities in ß4 integrin). (B) Cryostat sections of skin from a normal control individual (a) and from an individual with null defects in the INTB4 gene encoding the integrin ß4 subunit (b) were stained with anti-ATF3 antibodies. ATF3 was elevated in most cell layers in the ß4 null epidermis. Bar, 20 µm (A); 20 µm (B).
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