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Vaccinia growth factor stimulates cellular proliferation (hyperplasia) around infected cells.
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NF-kappaB was activated in 293T cells transfected with a plasmid encoding the C11R gene. Silencing by small interfering RNA or deletion of the C11R gene reduced both MVA-induced ERK2 and NF-kappaB activation in 293T cells or the keratinocyte line Hacat.
Vaccinia growth factor stimulates an epidermal growth factor receptor-MEK-dependent pro-survival pathway that synergizes with F1L to counteract an infection-induced apoptotic pathway that predominantly involves the BH3-only protein Bad.
Vaccinia growth factor stimulates cellular proliferation (hyperplasia) around infected cells. This effect is beneficial for virus replication in vivo, because poxviruses replicate possibly better in proliferating cells than in quiescent cells. Acts by binding host EGFR, inducing its dimerization, autophosphorylation and leading to activation of several cellular pathways regulating cell proliferation or cell survival. The activation by host EFGR of mitogen activated protein kinases (MAPK) and extracellular- signal regulated kinases (ERK) are essential for the positive effect of vaccinia growth factor on poxvirus virulence in vivo.
epidermal growth factor-like protein (EGF-like protein)