PERM is the most efficient approach for solv- ing protein folding problem based on simple lattice model. In this article a personification explanation of PERM is pro- posed. A new version of PERM, population control a...PERM is the most efficient approach for solv- ing protein folding problem based on simple lattice model. In this article a personification explanation of PERM is pro- posed. A new version of PERM, population control algorithm with two main improvements is presented: one is that it is able to redefine the weight and its predicted value in PERM, and the other is that it is able to unify the calculation of weight when choosing possible branches. The improved PERM is more efficient than the previous version; specifi- cally it can find the known lowest energy states for the four well-known difficult instances and is generally several to hundreds times faster than PERM. It is noteworthy that with the improved PERM we found new lowest energy configura- tions of three of the four difficult problems missed in previ- ous papers.展开更多
This article is to summarize the molecular and functional analysis of the gene “suppression of tumorigenicity 13” (ST13). ST13 is in fact the gene encoding Hsp70 interacting protein (Hip), a co-factor (co-chaperone)...This article is to summarize the molecular and functional analysis of the gene “suppression of tumorigenicity 13” (ST13). ST13 is in fact the gene encoding Hsp70 interacting protein (Hip), a co-factor (co-chaperone) of the 70-kDa heat shock proteins (Hsc/Hsp70). By collaborating with other positive co-factors such as Hsp40 and the Hsp70-Hsp90 organizing protein (Hop), or competing with negative co-factors such as Bcl2-associated athanogen 1 (Bag1), Hip facilitates may facilitate the chaperone function of Hsc/Hsp70 in protein folding and repair, and in controlling the activity of regulatory proteins such as steroid receptors and regulators of proliferation or apoptosis. Although the nomenclature of ST13 implies a role in the suppression of tumorigenicity (ST), to date available experimental data are not sufficient to support its role in cancer development, except for the possible down-regulation of ST13 in gastric and colorectal cancers. Further investigation of this gene at the physiological level would benefit our understanding of diseases such as endocrinological disorders, cancer, and neurodegeneration commonly associated with protein misfolding.展开更多
文摘PERM is the most efficient approach for solv- ing protein folding problem based on simple lattice model. In this article a personification explanation of PERM is pro- posed. A new version of PERM, population control algorithm with two main improvements is presented: one is that it is able to redefine the weight and its predicted value in PERM, and the other is that it is able to unify the calculation of weight when choosing possible branches. The improved PERM is more efficient than the previous version; specifi- cally it can find the known lowest energy states for the four well-known difficult instances and is generally several to hundreds times faster than PERM. It is noteworthy that with the improved PERM we found new lowest energy configura- tions of three of the four difficult problems missed in previ- ous papers.
基金Project supported by the National Basic Research Program (973) of China (No. 2004CB518707)the National Natureal Science Foundation of China (No. 30400521)
文摘This article is to summarize the molecular and functional analysis of the gene “suppression of tumorigenicity 13” (ST13). ST13 is in fact the gene encoding Hsp70 interacting protein (Hip), a co-factor (co-chaperone) of the 70-kDa heat shock proteins (Hsc/Hsp70). By collaborating with other positive co-factors such as Hsp40 and the Hsp70-Hsp90 organizing protein (Hop), or competing with negative co-factors such as Bcl2-associated athanogen 1 (Bag1), Hip facilitates may facilitate the chaperone function of Hsc/Hsp70 in protein folding and repair, and in controlling the activity of regulatory proteins such as steroid receptors and regulators of proliferation or apoptosis. Although the nomenclature of ST13 implies a role in the suppression of tumorigenicity (ST), to date available experimental data are not sufficient to support its role in cancer development, except for the possible down-regulation of ST13 in gastric and colorectal cancers. Further investigation of this gene at the physiological level would benefit our understanding of diseases such as endocrinological disorders, cancer, and neurodegeneration commonly associated with protein misfolding.
