Mutations in the ATG site normally used as start of translation and other mutations, as indicated by the red X, result in the production of N-terminally truncated elastase lacking the signal peptide (red bars). These truncated proteins are liberated to the cytosol instead of being routed to the endoplasmic reticulum and granules as is wild-type elastase (black bar). See Figure 6 in the article by Tidwell et al that begins on page 562. ER, endoplasmic.

Mutations in the ATG site normally used as start of translation and other mutations, as indicated by the red X, result in the production of N-terminally truncated elastase lacking the signal peptide (red bars). These truncated proteins are liberated to the cytosol instead of being routed to the endoplasmic reticulum and granules as is wild-type elastase (black bar). See Figure 6 in the article by Tidwell et al that begins on page 562. ER, endoplasmic.

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