myxoma/tyrosine

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Myxoma virus and Shope fibroma virus encode dual-specificity tyrosine/serine phosphatases which are essential for virus viability.

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Sequence analysis of the genomes of the Leporipoxviruses myxoma virus and Shope fibroma virus (SFV) led to the discovery of open reading frames homologous to the vaccinia H1L gene encoding a soluble protein phosphatase with dual tyrosine/serine specificity. These viral phosphatase genes were

Myxoma and vaccinia viruses exploit different mechanisms to enter and infect human cancer cells.

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Myxoma (MYXV) and vaccinia (VACV) viruses have recently emerged as potential oncolytic agents that can infect and kill different human cancer cells. Although both are structurally similar, it is unknown whether the pathway(s) used by these poxviruses to enter and cause oncolysis in cancer cells are

Myxoma virus induces extensive CD4 downregulation and dissociation of p56lck in infected rabbit CD4+ T lymphocytes.

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Myxoma virus is a pathogenic poxvirus that induces extensive dysregulation of cellular immunity in infected European rabbits. Infection of a rabbit CD4+ T-cell line (RL-5) with myxoma virus results in dramatic reductions of cell surface levels of CD4 as monitored by flow cytometry. The virus-induced

Myxoma virus selectively disrupts type I interferon signaling in primary human fibroblasts by blocking the activation of the Janus kinase Tyk2.

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Poxviruses currently are known to disrupt Jak-STAT signal transduction induced by interferon (IFN) through two distinct mechanisms: (1) secreted poxviral IFN decoy receptors that prevent the initiation of IFN signaling from type I or II receptors at the cell surface; and (2) poxviral phosphatase

Poxvirus infection rapidly activates tyrosine kinase signal transduction.

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Viruses have evolved a number of strategies to gain entry and replicate in host target cells that, for human immunodeficiency virus (HIV) and the poxvirus, myxoma virus, involve appropriating chemokine receptors. In this report we demonstrate that activation of multiple intracellular tyrosine

The role of tumor vascularisation in benign and malignant cardiovascular neoplasms: a comparison of cardiac myxoma and sarcomas of the pulmonary artery.

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Neoangiogenesis is involved in the development and progression of malignant tumors. Vascular endothelial growth factor (VEGF) and its receptors have been designated a central part in this process. Since the significance of the assessment of angiogenesis in soft tissue tumors is still a matter of

Prichard's structures of the fossa ovalis are not histogenetically related to cardiac myxoma.

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OBJECTIVE Cardiac myxomas are neoplasms of unknown histogenesis. They are thought to arise from hypothetical subendothelial vasoformative reserve cells or from primitive cells which reside in the fossa ovalis and surrounding endocardium. In 1951 Prichard described a kind of microscopic endocardial

Oncolytic Virus-Mediated RAS Targeting in Rhabdomyosarcoma.

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Aberrant activation of the receptor tyrosine kinase-mediated RAS signaling cascade is the primary driver of embryonal rhabdomyosarcoma (ERMS), a pediatric cancer characterized by a block in myogenic differentiation. To investigate the cellular function of activated RAS signaling in regulating the

Pathogenic poxviruses reveal viral strategies to exploit the ErbB signaling network.

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Virulence of poxviruses, the causative agents of smallpox, depends on virus-encoded growth factors related to the mammalian epidermal growth factor (EGF). Here we report that the growth factors of Shope fibroma virus, Myxoma virus and vaccinia virus (SFGF, MGF and VGF) display unique patterns of

Nck- and N-WASP-dependent actin-based motility is conserved in divergent vertebrate poxviruses.

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Vaccinia virus enhances its cell-to-cell spread by stimulating actin polymerization via Src- and Abl-mediated phosphorylation of the highly conserved orthopoxvirus protein A36. The Yatapoxvirus, Yaba-like disease virus (YLDV), also induces actin polymerization, although it lacks an obvious A36

Synaptophysin immunoreactivity in primary pigmented nodular adrenocortical disease: neuroendocrine properties of tumors associated with Carney complex.

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Carney complex (CNC) is characterized by lentiginosis and myxomatosis together with a variety of endocrine, neural crest-derived, and other tumors, including primary pigmented nodular adrenocortical disease (PPNAD). PPNAD is characterized by lipofuscin-containing, autonomously functioning,

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