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Induction of IFIT1 in response to H9N2 virus infection or viral particle inoculation was more sensitive in HUVECs than in BEAS-2Bs. Data offers new insight into the innate immune response of endothelial cells to H9N2 virus infection.
Human IFIT1 and mouse IFIT1B have divergent antiviral specificities: only IFIT1 proteins inhibit a virus encoding a cap 2'O-methyltransferase.
Taken together, this study revealed that IFIT1 played an important antiviral role in human cytomegalovirus infected fetal astrocytes.
Glioblastoma patients with high IFIT1 and low MGMT expression have an improved prognosis.
IFIT1 significantly inhibited human parainfluenza virus type 3, whereas IFIT2, IFIT3, and IFIT5 were less effective or not at all.
All the rubulaviruses tested were sensitive to the antiviral action of ISG56/IFIT1.
IFIT1 is involved in the regulation of IFNalpha treatment for chronic hepatitis B and its polymorphism rs303218 can predict the end point virological response.
there is a positive feedback loop between phosphorylated STAT1 and ISG56, ISG54 or ISG60.
Data show that interferon-induced proteins with tetratricopeptide repeats 1 and 2 (IFIT1 and IFIT2) contribute to the regulation of hepatitis B virus (HBV) replication, likely at both transcriptional and posttranscriptional steps.
IFIT1 is not a dominant restriction factor against three different families of negative-sense RNA viruses.
Reovirus T3D infection induced STAT-1, ISG-15, IFIT-1, Mx1, and IFIT-3 expression.
protein expression is inhibited by hepatitis C virus
The specificity of IFIT1 for 2'O-unmethylated RNA serves as potent antiviral mechanism against viruses lacking 2'O-methyltransferase activity and at the same time allows unperturbed progression of the antiviral program in infected cells.
TLR4 signaling, induced by LPS, increases the expression of melanoma differentiation-associated gene 5 (MDA5) and interferon
ISG56 may play a role in immune and inflammatory reactions induced by toll-like receptor 3 signaling in human mesangial cells.
Results indicate that miR-203 is an interferon-inducible miRNA that can negatively regulate a number of cellular mRNAs, including an interferon-stimulated gene target, IFIT1/ISG56, by destabilizing its mRNA transcript.
Data suggested that PIV5 mRNAs are methylated at the 2'-hydroxyl group and that ISG56/IFIT1 inhibits the translation of PIV5 mRNA by some unrecognized mechanism. Also ISG56/IFIT1 is primarily responsible for the IFN-induced inhibition of PIV5.
crystal structures of human IFIT5, its complex with PPP-RNAs, and an amino-terminal fragment of IFIT1
Hepatitis C virus infection suppresses the upregulation of a subset of effector molecules, including ISG56 and IFITM1.
ISG56 interacts with ribosomal protein L15 in gastric cancer cells.
ISG20 acts as an indirect regulator of RNA virus replication in the cytoplasm through the upregulation of many other ISGs.
IFIT1 expression is associated with podocytes damage, and capable of suppressing some proteins essential to glomerular filtration.
Human IFIT1 and mouse IFIT1 have divergent antiviral specificities: only IFIT1 proteins inhibit a virus encoding a cap 2'O-methyltransferase.
the mechanism for the observed differential induction of the mouse Ifit1, Ifit2, and Ifit3 genes in B cells and demonstrated that the repressive effect of the transcription factor interferon regulatory factor 8 (IRF8), which is highly expressed in B cells, played an essential role in this regulation.
Data suggest that, with up-regulation of IFIT1, alphaviruses (Venezuelan equine encephalitis virus; Chikungunya virus) with wild-type 5' untranslated regions are inducers of type I IFN (interferon), suggesting a new mechanism of type I IFN induction.
Targeted expression of Ifit1 in hepatocytes protects mice from lipopolysaccharide and D-galactosamine induced lethal hepatitis.
Thus, Ifit1 inhibits replication of MTase-defective Japanese encephalitis virus by inhibiting mRNA translation through direct binding to mRNA 5' structures.
Study identified Ifit1 as an important innate immune bottleneck.
results suggest that virulent strains of West Nile virus have largely evaded the antiviral effects of Ifit1, and viral mutants lacking 2'-O methylation are controlled in vivo by Ifit1-dependent and -independent mechanisms in different cell types
IFIT1 bound PPP-RNA antagonizes viruses by sequestering specific viral nucleic acids.
results demonstrate that the 2'-O methylation of the 5' cap of viral RNA functions to subvert innate host antiviral responses through escape of IFIT-mediated suppression
Under some stressful stimulations IFIT1 may participate in cell death pathways by interaction with eEF1A.
block different functions of eIF3 by binding to its different subunits.
Expression increased significantly during LCMV and WNV infection, being widespread and localized predominantly to common as well as distinct neuronal populations in the brain.
Our findings provide the first evidence of a differential pattern of expression of ISG54 and ISG56 genes by IFN-alpha and IFN-beta.
This gene encodes a protein containing tetratricopeptide repeats that was originally identified as induced upon treatment with interferon. The encoded protein may inhibit viral replication and translational initiation. This gene is located in a cluster on chromosome 10 with five other closely related genes. There is a pseudogene for this gene on chromosome 13. Alternatively spliced transcript variants encoding multiple isoforms have been observed.
interferon, alpha-inducible protein (MW 56kD)
, interferon-induced 56 kDa protein
, interferon-inducible mRNA 561
, glucocorticoid-attenuated response gene 16 protein
, glucocorticoid-attenuated response gene 16 product
, interferon-induced protein with tetratricopeptide repeats 1-like protein
, interferon-induced protein with tetratricopeptide repeats 1
, interferon-induced protein with tetratricopeptide repeats 5-like
, interferon-induced protein with tetratricopeptide repeats 1-like
, interferon-stimulated protein 56