Disease relevance of Smtn

• A smoothelin-deficient mouse model may help to establish the role of smoothelin-A in intestinal contraction and provide a model for myogenic chronic intestinal pseudo-obstruction [1].

High impact information on Smtn

• By deletion of exons 18, 19, and 20 from the smoothelin gene, the expression of both smoothelin isoforms was disrupted [1].
• The latter consisted of staining UA cross sections for the differentiation markers smooth muscle alpha-actin and smoothelin, and for the proliferation marker MKI67 [2].
• Our findings indicate that CHASM is a novel member of the smoothelin protein family that elicits Ca2+ desensitization in smooth muscle [3].
• Among those phosphoproteins identified was calponin homology-associated smooth muscle (CHASM), a novel protein that contains a calponin homology domain and shares sequence similarity with the smoothelin family of smooth muscle specific proteins [3].
• Structure and chromosome location of Smtn, the mouse smoothelin gene [4].

Biological context of Smtn

• Smooth muscle cell proliferation increased in midpregnancy and was paralleled by a transient decrease in smoothelin and smooth muscle alpha-actin expression [5].

Anatomical context of Smtn

• The epithelioid cells examined showed only a weak expression of the protein smoothelin, which occurs exclusively in contractile smooth muscle cells [6].

Analytical, diagnostic and therapeutic context of Smtn

• Western blot analysis showed expression of smoothelin in the cells from passages 3, 7, and 11 in A(1)WT and A(1)KO mice [7].

References