cowpox/hypoxia

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Vaccinia-related kinase 2 modulates the stress response to hypoxia mediated by TAK1.

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Hypoxia represents a major stress that requires an immediate cellular response in which different signaling pathways participate. Hypoxia induces an increase in the activity of TAK1, an atypical mitogen-activated protein kinase kinase kinase (MAPKKK), which responds to oxidative stress by triggering

The extract of inflamed rabbit skin induced by inoculation of vaccinia virus possesses antioxidant and neuroprotective effects in acute ischemic stroke.

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Acute cerebral ischemia remains a major cause for death and disability but current therapeutic options are limited. A mixture of biological agents extracted from the inflamed rabbit skin induced by inoculation of vaccinia virus has been shown to reduce ischemia-induced cerebral edema in vivo. In the

A role for vaccinia virus protein C16 in reprogramming cellular energy metabolism.

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Vaccinia virus (VACV) is a large DNA virus that replicates in the cytoplasm and encodes about 200 proteins of which approximately 50 % may be non-essential for viral replication. These proteins enable VACV to suppress transcription and translation of cellular genes, to inhibit the innate immune

Lister strain vaccinia virus, a potential therapeutic vector targeting hypoxic tumours.

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Hypoxia contributes to the aggressive and treatment-resistant phenotype of pancreatic ductal adenocarcinoma. Oncolytic vaccinia virus has potential as an anti-tumour agent, but the ability to lyse hypoxic tumour cells is vital for clinical efficacy. We hypothesized that unique aspects of the

Vascular endothelial growth factor A promotes vaccinia virus entry into host cells via activation of the Akt pathway.

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Vaccinia virus (VV) is an enveloped DNA virus from the poxvirus family and has played a crucial role in the eradication of smallpox. It continues to be used in immunotherapy for the prevention of infectious diseases and treatment of cancer. However, the mechanisms of poxvirus entry, the host factors

A mechanism for induction of a hypoxic response by vaccinia virus.

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Viruses have evolved sophisticated strategies to exploit host cell function for their benefit. Here we show that under physiologically normal oxygen levels (normoxia) vaccinia virus (VACV) infection leads to a rapid stabilization of hypoxia-inducible factor (HIF)-1α, its translocation into the

Oncolytic vaccinia virus demonstrates antiangiogenic effects mediated by targeting of VEGF.

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Oncolytic vaccinia virus has been shown to induce a profound, rapid and tumor-specific vascular collapse in both preclinical models and clinical studies; however, a complete examination of the kinetics and levels of collapse and revascularization has not been described previously. Contrast-enhanced

Oncolytic vaccinia virus disrupts tumor-associated vasculature in humans.

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Efforts to selectively target and disrupt established tumor vasculature have largely failed to date. We hypothesized that a vaccinia virus engineered to target cells with activation of the ras/MAPK signaling pathway (JX-594) could specifically infect and express transgenes (hGM-CSF, β-galactosidase)

A central role for CK1 in catalyzing phosphorylation of the p53 transactivation domain at serine 20 after HHV-6B viral infection.

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The tumor suppressor protein p53 is activated by distinct cellular stresses including radiation, hypoxia, type I interferon, and DNA/RNA virus infection. The transactivation domain of p53 contains a phosphorylation site at Ser20 whose modification stabilizes the binding of the transcriptional

Neuroprotective effects of neurotropin in a mouse model of hypoxic-ischemic brain injury.

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Ischemic-hypoxic insult leads to detrimental effects on multiple organs. The brain is especially vulnerable, and it is hard to regenerate once damaged. Currently, therapeutic options are very limited. Previous studies have reported neuroprotective effects of neurotropin, a non-protein

Alveolar macrophages are essential for protection from respiratory failure and associated morbidity following influenza virus infection.

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Alveolar macrophages (AM) are critical for defense against bacterial and fungal infections. However, a definitive role of AM in viral infections remains unclear. We here report that AM play a key role in survival to influenza and vaccinia virus infection by maintaining lung function and thereby

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