Caspase 2 (Phospho-Ser157) ELISA Kit

Autophagy is an essential component of host immunity and used by viruses for survival. However, the autophagy signaling pathways involved in virus replication are poorly documented. Here, we observed that rabies virus (RABV) infection triggered intracellular autophagosome accumulation and results in incomplete autophagy by inhibiting autophagy flux. Subsequently, we found that RABV infection induced the reduction of CASP2/caspase 2 and the activation of AMP-activated protein kinase (AMPK)-AKT-MTOR (mechanistic target of rapamycin) and AMPK-MAPK (mitogen-activated protein kinase) pathways. Further investigation revealed that BECN1/Beclin 1 binding to viral phosphoprotein (P) induced an incomplete autophagy via activating the pathways CASP2-AMPK-AKT-MTOR and CASP2-AMPK-MAPK by decreasing CASP2. Taken together, our data first reveals a crosstalk of BECN1 and CASP2-dependent autophagy pathways by RABV infection.

Performance in the three Critical Assessment of protein Structure Prediction (CASP) experiments has been compared in the areas of alignment accuracy for models based on homology and three-dimensional accuracy for models produced by using ab initio prediction methods. The homologous models span the comparative modeling and fold-recognition regimes. Each CASP target is assigned a relative difficulty based on the extent of sequence identity and the degree of structural overlap with the best available template. There is a clear improvement in alignment accuracy between CASP1 and CASPs 2 and 3 over much of the difficulty scale but no apparent improvement between CASP2 and CASP3. Encouragingly, the best ab initio models of small targets are clearly more accurate in CASP3 than in CASPs 1 and 2. Published 1999 Wiley-Liss, Inc.dagger.