Stress transcriptional, processes

Glucocorticoids alter the DNA transcription process in their target tissues. They adapt the body to stress. Glucocorticoids also promote the rapid provision of glucose and fatty acids for energy and permit the responses of the circulation required in reaction to stressful events. When glucocorticoid secretion is chronically increased, there is suppression of the immune system patients experience poor wound healing and increased susceptibility to infection. 

Moreover, overexpression of the same mutants inhibit DNA replication and block the cells at the Gl/S-phase transition (Kim et al, 2005), emphasizing the potential role of nucleolin mobilization. It is therefore highly probable that two different processes help the formation of RPA-nucleolin complexes after a genotoxic stress a post-transcriptional modification of nucleolin that renders the GAR domain of nucleolin accessible to RPA, and its p53-dependent relocalization to the nucleoplasm where a higher amount of RPA is available. Of importance, nucleolin relocalization is transient and lasts far less than replication inhibition (Daniely and Borowiec, 2000). This means that nucleolin-RPA interaction is only an initial event and that other mechanisms account for prolonged replication inhibition. 

HO-1 is controlled at the level of transcription by oxidative stress and several inducers such as porphyrins, metals, and progesterone (8). The absence of HO-1 is associated with severe growth retardation, anemia, and enhanced endothelial cell injury 156, 157). In addition, HO-1 has been implicated in protection against transplant rejection 158, 159). HO-2 is constitutively expressed, and its presence in brain and the noted similar effects of CO and NO has led to the proposal that CO-generated by HO-2 is involved in signaling processes 8, 160-162). 

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