Mutation of NEMO Associated with Neutrophil Chemotaxis Abnormality

Alle, D.; Venglarcik, John; Williams, D.; Casanova, Jean‐Laurent; Hostoffer, Robert

doi:10.1016/j.jaci.2005.12.1096

Cited by 1 publication

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“…IRES B of VEGF has also been shown to be selectively repressed by miR-16 targeting, whereas IRES-A remained active, lending to the notion that VEGF isoforms can be selectively expressed from the same mRNA by miR specific targeting (Karaa et al, 2009). VEGF expression is upregulated in HIV-1 or HRV infection, both of which utilize IRES translation (Psarras et al, 2006; Korgaonkar et al, 2008) suggesting the possibility of related translational mechanisms of their respective IRESs.…”

Section: Cellular Ires-containing Genes and Their Roles In Er Stress mentioning

confidence: 99%

IRES-Dependent Translational Control during Virus-Induced Endoplasmic Reticulum Stress and Apoptosis

et al. 2012

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Many virus infections and stresses can induce endoplasmic reticulum (ER) stress response, a host self-defense mechanism against viral invasion and stress. During this event, viral and cellular gene expression is actively regulated and often encounters a switching of the translation initiation from cap-dependent to internal ribosome-entry sites (IRES)-dependent. This switching is largely dependent on the mRNA structure of the 5′ untranslated region (5′ UTR) and on the particular stress stimuli. Picornaviruses and some other viruses contain IRESs within their 5′ UTR of viral genome and employ an IRES-driven mechanism for translation initiation. Recently, a growing number of cellular genes involved in growth control, cell cycle progression and apoptosis were also found to contain one or more IRES within their long highly structured 5′ UTRs. These genes initiate translation usually by a cap-dependent mechanism under normal physiological conditions; however, in certain environments, such as infection, starvation, and heat shock they shift translation initiation to an IRES-dependent modality. Although the molecular mechanism is not entirely understood, a number of studies have revealed that several cellular biochemical processes are responsible for the switching of translation initiation to IRES-dependent. These include the cleavage of translation initiation factors by viral and/or host proteases, phosphorylation (inactivation) of host factors for translation initiation, overproduction of homologous proteins of cap-binding protein eukaryotic initiation factors (eIF)4E, suppression of cap-binding protein eIF4E expression by specific microRNA, activation of enzymes for mRNA decapping, as well as others. Here, we summarize the recent advances in our understanding of the molecular mechanisms for the switching of translation initiation, particularly for the proteins involved in cell survival and apoptosis in the ER stress pathways during viral infections.

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Section: Cellular Ires-containing Genes and Their Roles In Er Stress mentioning

confidence: 99%