Accordingly, six sites were identified within the catalytic segment of PC2.

No significant effect of line was found for PC2 scores, associated with risk assessment behavior.

This study provides novel evidence regarding the role of PC2 in skeletal muscle cell atrophy.

The role of PC2 in the control of atrophy and autophagy in skeletal muscle remains unknown.

In oat, victorin sensitivity is conferred by the Vb gene, which is genetically inseparable from the Pc2 resistance gene.

In vivo treatment with SQ22,536 significantly reduced liver cystic area and cell proliferation in PC2-defective mice.

PC2 was associated with older age, less education, never having smoked, a lower BMI and waist:hip ratio and lower levels of physical activity.

PC2 consisted of measures of good metabolic and cardiovascular function with an estimated heritability of 27%.

In these cells, expression of native PC2 does not result in the secretion of measurable in vitro activity against a pentapeptide fluorogenic substrate.

In addition, we show that inhibition of mTORC1, by starvation or rapamycin is inhibited in cells when PC2 is silenced.

Here, we show that PC2 is required for the induction of atrophy in C2C12 myotubes caused by nutrient deprivation or rapamycin exposure.

PC2 was found in A and in some D cells more than in B cells and PC1 was evident only in B cells.

Deletion of PC2 increases cAMP levels, which can be corrected by reexpression of wild-type PC2 but not by a mutant lacking calcium channel activity.