Cell mutants degradation

The gibberellic acid-induced biosynthesis and release of cell-wall degrading e/jrfo-D-xylanase by isolated aleurone layers of barley have been studied. Studies on the D-xylanase system of Streptomyces species have included a study of the action of the enzyme on various o-xylans and D-xylo-oligosaccharides. The isolation and structural identification of arabino-D-xylo-oligosaccharides arising from action of the enzyme on corn cob arabino-D-xylan were reported. Mutant strains of Trichoderma viride not producing D-xylanase have been induced and isolated with the aid of nystatin selection. ... 

In contrast to c-Jun, phosphorylation of the tumor suppressor p53 by CSN-associated kinases targets the protein for degradation by the Ub system [35]. For p53 stability, modification on Thrl55 is most important as shown by mutational analysis [35] and by using different p53 peptides [31]. Mutation of Thrl55 to Val led to stabilization of the transiently expressed p53 mutant in HeLa as well as in HL60 cells [35]. Inhibitors of CSN-associated kinases such as curcumin [18] caused stabilization of cellular p53 followed by massive cell death [35]. 

Cell cycle is one of the physiological processes in which the role of uhiquitin—proteasome-mediated proteolysis is well established. With the advent of yeast mutants that interfered with various phases of the cell cycle, cyclin-dependent kinases (Cdks) were found to have a critical role in regulating the cell cycle. Typically, Cdks activated hy regulatory proteins are known as cyclins. Different Cdk—cyclin complexes are formed at specific stages of the cell cycle such as the S-phase (in which DNA synthesis occurs) and the metaphase. The transition from metaphase to anaphase depends on degradation of cyclins. " " Systematic biochemical studies showed that cyclins were substrates for the uhiquitin—proteasome pathway (Table 5). 

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