ArticleProceedings of the National Academy of Sciences of the United States of America2006
LPS-induced TNF-alpha factor (LITAF)-deficient mice express reduced LPS-induced cytokine: Evidence for LITAF-dependent LPS signaling pathways.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed.
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- Cannabis Oil and Exploratory Gut-Immune Signatures During Breast Cancer Chemotherapy: A Randomized Pilot Trial.Biomedicines · 2026Article
- Senescent hepatic stellate cells drive inflammation and disease progression in MASH (Review).Experimental and therapeutic medicine · 2026Review
- MiR-497-5p Ameliorates Deep Venous Thrombosis by Facilitating Endothelial Progenitor Cell Migration and Angiogenesis by Regulating LITAF.Biochemical genetics · 2025Article
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- A dynamic peripheral immune landscape during human pregnancy.Fundamental research · 2025Article
- SPP1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- LINC00173 silence and estrone supply suppress ERCancer science · 2024Article
- Multiomic analyses uncover immunological signatures in acute and chronic coronary syndromes.Nature medicine · 2024Article
- Peimine ameliorates LPS-induced acute lung injury by regulating Nrf2 and NF-κB pathways.American journal of translational research · 2024Article
- Effects of sustained hyperprolactinemia in late gestation on the mammary parenchymal tissue transcriptome of gilts.BMC genomics · 2023Article
- Diclofenac Disrupts the Circadian Clock and through Complex Cross-Talks Aggravates Immune-Mediated Liver Injury-A Repeated Dose Study in Minipigs for 28 Days.International journal of molecular sciences · 2023Article
- Diversity and heterogeneity in human breast cancer adipose tissue revealed at single-nucleus resolution.Frontiers in immunology · 2023Article
- Effects of Copper Exposure on Oxidative Stress, Apoptosis, Endoplasmic Reticulum Stress, Autophagy and Immune Response in Different Tissues of Chinese Mitten Crab (Antioxidants (Basel, Switzerland) · 2022Article
- TPL-2 Inhibits IFN-β Expression via an ERK1/2-TCF-FOS Axis in TLR4-Stimulated Macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- Variation of TNF modulates cellular immunity of gregarious and solitary locusts against fungal pathogenProceedings of the National Academy of Sciences of the United States of America · 2022Article
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- Gene signatures associated with barrier dysfunction and infection in oral lichen planus identified by analysis of transcriptomic data.PloS one · 2021Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
4 authors.
Funding
Abstract
Previously we identified a transcription factor, LPS-Induced TNF-alpha Factor (LITAF), mediating inflammatory cytokine expression in LPS-induced processes. To characterize the role of LITAF in vivo, we generated a macrophage-specific LITAF-deficient mouse (macLITAF(-/-)). Our data demonstrate that in macrophages (i) several cytokines (such as TNF-alpha, IL-6, sTNF-RII, and CXCL16) are induced at lower levels in macLITAF(-/-) compared with LITAF(+/+) control macrophages; (ii) macLITAF(-/-) mice are more resistant to LPS-induced lethality. To further identify LITAF signaling pathways, we tested mouse TLR-2(-/-), -4(-/-), and -9(-/-) and WT peritoneal macrophages exposed to LPS. Using these cells, we now show that LITAF expression can be induced after challenge either with LPS from Porphyromonas gingivalis via agonism at TLR-2, or with LPS from Escherichia coli via agonism at TLR-4, both requiring functional MyD88. We also show that, in response to LPS, the MyD88-dependent LITAF pathway differs from the NF-kappaB pathway. Furthermore, using a kinase array, p38alpha was found to mediate LITAF phosphorylation and the inhibition of p38alpha with a p38-specific inhibitor (SB203580) blocked LITAF nuclear translocation and reduced LPS-induced TNF-alpha protein levels. Finally, macLITAF(-/-) macrophages rescued by LITAF cDNA transfection restored levels of TNF-alpha similar to those observed in WT cells. We conclude that LITAF is an important mediator of the LPS-induced inflammatory response that can be distinguished from NF-kappaB pathway and that p38alpha is the specific kinase involved in the pathway linking LPS/MyD88/LITAF to TNF.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.