mumps/tyrosine

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Roles of Sialic Acid, AXL, and MER Receptor Tyrosine Kinases in Mumps Virus Infection of Mouse Sertoli and Leydig Cells

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The mumps virus (MuV) causes epidemic parotitis. MuV also frequently infects the testis and induces orchitis, an important etiological factor contributing to male infertility. However, mechanisms underlying MuV infection of the testis remain unknown. Here, we describe that sialic acid, AXL, and MER

Suppression of thermotolerance in mumps virus-infected cells is caused by lack of HSP27 induction contributed by STAT-1.

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Viral infection modulates the regulation of apoptosis in host cells. Here, we report a novel mechanism by which human cells infected with mumps virus become susceptible to apoptosis caused by extracellular stresses. Mumps virus stimulates proteasome-dependent degradation of STAT-1 by action of viral

Inclusion body myositis: investigation of the mumps virus hypothesis by polymerase chain reaction.

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Inclusion body myositis (IBM) is a distinctive form of chronic inflammatory myopathy characterized pathologically by the finding of rimmed vacuoles and 15-18nm microtubular filamentous inclusions in muscle fiber nuclei and cytoplasm. The observation that these filaments resembled nucleocapsids of

Novel polyvalent live vaccine against varicella-zoster and mumps virus infections.

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The varicella-zoster virus (VZV) Oka vaccine strain (vOka) is a highly immunogenic and safe live vaccine that has long been used worldwide. Because its genome is large, making it suitable for inserting foreign genes, vOka is considered a candidate vector for novel polyvalent vaccines. Previously, a

C-terminal tyrosine residues modulate the fusion activity of the Hendra virus fusion protein.

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The paramyxovirus family includes important human pathogens such as measles, mumps, respiratory syncytial virus, and the recently emerged, highly pathogenic Hendra and Nipah viruses. The viral fusion (F) protein plays critical roles in infection, promoting both the virus-cell membrane fusion events

Mumps virus V protein antagonizes interferon without the complete degradation of STAT1.

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Mumps virus (MuV) has been shown to antagonize the antiviral effects of interferon (IFN) through proteasome-mediated complete degradation of STAT1 by using the viral V protein (T. Kubota et al., Biochem. Biophys. Res. Commun. 283:255-259, 2001). However, we found that MuV could inhibit IFN signaling

STAT3 ubiquitylation and degradation by mumps virus suppress cytokine and oncogene signaling.

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Mumps virus is a common infectious agent of humans, causing parotitis, meningitis, encephalitis, and orchitis. Like other paramyxoviruses in the genus Rubulavirus, mumps virus catalyzes the proteasomal degradation of cellular STAT1 protein, a means for escaping antiviral responses initiated by

Genome-wide SNP associations with rubella-specific cytokine responses in measles-mumps-rubella vaccine recipients.

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Genetic polymorphisms are known to affect responses to both viral infection and vaccination. Our previous work has described genetic polymorphisms significantly associated with variations in immune response to rubella vaccine from multiple gene families with known immune function, including HLA,

Temsirolimus in overtreated metastatic renal cancer with subsequent use of sunitinib: A case report.

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During the last decade, we have been developing new therapeutic strategies for the treatment of renal cancer, based on knowledge derived from molecular biology. We report a case of long-term renal metastatic cancer progression despite therapy with sunitinib and interleukin, which are the most active

Paramyxovirus strategies for evading the interferon response.

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Two genera, the Respirovirus (Sendai virus (SeV) and human parainfluenza virus (hPIV3) and the Rubulavirus (simian virus (SV) 5, SV41, mumps virus and hPIV2), of the three in the subfamily Paramyxovirinae inhibit interferon (IFN) signalling to circumvent the IFN response. The viral protein

The relationship between humoral and cellular immunity to IA-2 in IDDM.

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Autoantibodies to the neuroendocrine protein insulinoma-associated protein 2 (IA-2), a member of the tyrosine phosphatase family, have been observed in individuals with or at increased risk for IDDM. Because this disease is thought to result from a T-cell-mediated autoimmune destruction of the

Herpes simplex encephalitis in a patient with a distinctive form of inherited IFNAR1 deficiency

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Inborn errors of TLR3-dependent IFN-α/β- and -λ-mediated immunity in the central nervous system (CNS) can underlie herpes simplex virus 1 (HSV-1) encephalitis (HSE). The respective contributions of IFN-α/β and -λ are unknown. We report a child homozygous for a genomic deletion of the entire coding

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