CSA-dependent degradation of CSB by the ubiquitin-proteasome pathway establishes a link between complementation factors of the Cockayne syndrome

Article Abstract:

Mutations in the CSA or CSB complementation genes cause the Cockayne syndrome, a severe genetic disorder that results in patients' death in early adulthood. Following UV irradiation, CSB is degraded at a late stage of the repair process in a proteasome- and CSA-dependent manner. The importance of CSB degradation for post-transcription-coupled repair (TCR) recovery of transcription and for the Cockayne syndrome is demonstrated, which unravel for the first time the functional relationship between CSA and CSB.

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A subcomplex of the proteasome regulatory particle required for ubiquitin-conjugate degradation and related to the COP9-signalosome and elF3

Article Abstract:

A study was conducted on two subcomplexes, the lid and the base, of the proteasome regulatory particle. Results showed that the base suffices the activation of the core particle for degradation of peptides or a nonubiquitinated protein, while the lid is needed for ubiquitin-dependent degradation. Moreover, the lid subunits have similar sequence motifs with components of the COP9/signalosome and elF3.

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The ubiquitin ligase activity in the DDB2 and CSA complexes is differentially regulated by COP9 signalosome in response to DNA damage

Article Abstract:

Research has been conducted on nucleoside excision repair. The authors demonstrate that UV response of the DDB2 and CSA complexes affect nucleoside excision repair mechanism.

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