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Complete sequencing and characterization of 21,243 full-length human cDNAs
There seems to be a slight bias against GC-rich transcripts in current gene prediction procedures in the “full-length long Japan” collection of sequenced human cDNAs.
Synergy between Interferon-γ and Tumor Necrosis Factor-α in Transcriptional Activation Is Mediated by Cooperation between Signal Transducer and Activator of Transcription 1 and Nuclear Factor κB*
The frequently observed synergy between IFNγ and TNFα in promoting inflammatory response depends in part upon cooperation between STAT1α and NF-κB, which is most likely mediated by their independent interaction with one or more components of the basal transcription complex.
Requirement for STAT1 in LPS‐induced gene expression in macrophages
Results indicate that indirect activation of STAT1 by L PS‐induced type I IFN participates in promoting optimal expression of LPS‐inducible genes, and they suggest that STAT1 may play a critical role in innate immunity against gram‐negative bacterial infection.
The interferon-stimulated response element and a kappa B site mediate synergistic induction of murine IP-10 gene transcription by IFN-gamma and TNF-alpha.
Results indicate that the highly synergistic transcriptional activation of the IP-10 gene by IFN-gamma and TNF-alpha involves the cooperation between factors that are independently activated by the two stimuli and that bind to independent sites.
Cooperative interaction between interferon (IFN) stimulus response element and kappa B sequence motifs controls IFN gamma- and lipopolysaccharide-stimulated transcription from the murine IP-10…
Tumor necrosis factor-alpha induces cell type and tissue-specific expression of chemoattractant cytokines in vivo.
- Y. Ohmori, L. Wyner, S. Narumi, D. Armstrong, M. Stoler, T. Hamilton
- Biology, MedicineThe American journal of pathology
- 1 March 1993
The results indicate that TNF-alpha may be an important stimulus for chemoattractant cytokine gene expression in vivo, and the primary cell types responsible may be either stromal fibroblasts, microvascular endothelium, and/or a subset of anchored mononuclear phagocytes.
IL-4-induced STAT6 suppresses IFN-gamma-stimulated STAT1-dependent transcription in mouse macrophages.
It is suggested that IL-4 may suppress IFN-gamma-stimulated transcription of the IRF-1 gene by activation of STAT6, which can compete with STAT1 for occupancy of theIRF- 1 SBE when STAT1 levels are low.
A macrophage LPS-inducible early gene encodes the murine homologue of IP-10.
Interleukin-4/STAT6 Represses STAT1 and NF-κB-dependent Transcription through Distinct Mechanisms*
Results demonstrate that STAT6 mediates suppression of STAT1 and NF-κB-dependent transcription by distinct mechanisms that are dependent upon the STAT6 transactivation domain and may involve sequestration of necessary but different transcriptional coactivator proteins.
Influenza A virus abrogates IFN‐γ response in respiratory epithelial cells by disruption of the Jak/Stat pathway
It is hypothesized that IFN‐γ is not critical in host survival because influenza A virus has mechanisms to evade the antiviral activity of IFN •γ through effects on the intracellular signaling pathways.