TNF and MAP kinase signalling pathways

Sabio, Guadalupe; Davis, Roger J.

doi:10.1016/j.smim.2014.02.009

Cited by 567 publications

(460 citation statements)

References 126 publications

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“…The latter results indicate that the relevance of our work may extend beyond the regulation of oncogenic signaling to other diseases in which abnormal ERK activity has been implicated. These include inflammatory disease, cardiac hypertrophy, metabolic disorders and neurodegenerative conditions, such as Alzheimer's disease (50)(51)(52)(53).…”

Section: Discussionmentioning

confidence: 99%

Dual-specificity phosphatase 5 controls the localized inhibition, propagation, and transforming potential of ERK signaling

Kidger

Rushworth

Stellzig

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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The authors wish to note the following: "Since the publication of our paper, we have become aware that the quantitative data presented in Fig. 1B do not represent the full raw data set provided in the supporting information deposited online at https://doi.org/ 10.15125/BATH-00317. We are therefore publishing a corrected version of Fig. 1 in which the graphs in panel B have been replaced by those generated from the complete online dataset. The result and the conclusions drawn are unchanged. A minor correction has also been made to the figure legend to reflect the altered P values that result from use of the complete dataset." The corrected Fig. 1 and its corrected legend appear below.

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Section: Discussionmentioning

confidence: 99%

Dual-specificity phosphatase 5 controls the localized inhibition, propagation, and transforming potential of ERK signaling

Kidger

Rushworth

Stellzig

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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“…The importance of the different kinases appears to be cell typedependent and context-specific (18). The isoforms p38α/β regulate, for example, TNF-α expression (18). In our model, TNF-α or NF-κB (tissue mRNA, proteome profiler/ELISA and WB) were not clearly involved.…”

Section: Factor Analysis Identified Cinc1-3 Mip-1/3` Mig Rantes Anmentioning

confidence: 81%

“…Four members of the p38 MAP kinase family have been identified (p38α, p38β, p38γ, p38δ). The importance of the different kinases appears to be cell typedependent and context-specific (18). The isoforms p38α/β regulate, for example, TNF-α expression (18).…”

Section: Factor Analysis Identified Cinc1-3 Mip-1/3` Mig Rantes Anmentioning

confidence: 99%

GPR84 and TREM-1 Signaling Contribute to the Pathogenesis of Reflux Esophagitis

Abdel-Aziz

Schneider

Neuhuber

et al. 2015

Mol Med

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Gastro-esophageal reflux disease (GERD) is one of the most common disorders in gastroenterology. Patients present with or without increased acid exposure indicating a nonuniform etiology. Thus, the common treatment with proton pump inhibitors (PPIs) fails to control symptoms in up to 40% of patients. To further elucidate the pathophysiology of the condition and explore new treatment targets, transcriptomics, proteomics and histological methods were applied to a surgically induced subchronic reflux esophagitis model in Wistar rats after treatment with either omeprazole (PPI) or STW5, a herbal preparation shown to ameliorate esophagitis without affecting refluxate pH. The normal human esophageal squamous cell line HET-1A and human endoscopic biopsies were used to confirm our findings to the G-protein-coupled receptor (GPR) 84 in human tissue. Both treatments reduced reflux-induced macroscopic and microscopic lesions of the esophagi as well as known proinflammatory cytokines. Proteomic and transcriptomic analyses identified CINC1-3, MIP-1/3α, MIG, RANTES and interleukin (IL)-1β as prominent mediators in GERD. Most regulated cyto-/chemokines are linked to the TREM-1 signaling pathway. The fatty acid receptor GPR84 was upregulated in esophagitis but significantly decreased in treated groups, a finding supported by Western blot and immunohistochemistry in both rat tissue and HET-1A cells. GPR84 was also found to be significantly upregulated in patients with grade B reflux esophagitis. The expression of GPR84 in esophageal tissue and its potential involvement in GERD are reported for the first time. IL-8 (CINC1-3) and the TREM-1 signaling pathway are proposed, besides GPR84, to play an important role in the pathogenesis of GERD.

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“…Signaling via the JNK module results from the sequential activation of a MAP3K, MAP2K, and JNK, complexed via a scaffold protein (7,8). Cytokine binding to cognate TNF and IL-1/TLR receptors triggers activation of the TRAF 2 family of atypical ubiquitin ligases and promotes Lys-63-linked ubiquitination and autophosphorylation of MAP3Ks (9 -11), including MLK3 (12)(13)(14).…”

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confidence: 99%