Autophagosomal IκBα Degradation Plays a Role in the Long Term Control of Tumor Necrosis Factor-α-induced Nuclear Factor-κB (NF-κB) Activity

Colleran, Amy; Ryan, Aideen E.; O'Gorman, Angela; Mureau, Coralie; Liptrot, Catherine H.; Dockery, Peter; Fearnhead, Howard O.; Egan, Laurence J.

doi:10.1074/jbc.m110.199950

Cited by 57 publications

(51 citation statements)

References 44 publications

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“…Support of this hypothesis is provided by a recent systems biology publication by Garmaroudi et al where they showed that IB-␣ is a hub signaling molecule activated throughout the life-cycle of CVB3 in cardiomyocytes. 156 Consistent with the intimate connection of TNF-␣ 157 and IL-1␤ 158 signaling with NF-B and IB-␣ activation, the authors showed that replication of CVB3 could be abrogated by antagonizing IL-1␤ and TNF-␣ signaling in infected cells. These results suggest that proinflammatory signals provided by TNF-␣ and IL-1␤ will boost proviral signaling in infected tissue.…”

Section: Virus Replication and Inflammation Are Caught In A Synergistmentioning

confidence: 48%

Inflammation in Myocardial Diseases

Marchant

Boyd

Lin

et al. 2012

Circulation Research

252

165

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Inflammatory processes underlie a broad spectrum of conditions that injure the heart muscle and cause both structural and functional deficits. In this article, we address current knowledge regarding 4 common forms of myocardial inflammation: myocardial ischemia and reperfusion, sepsis, viral myocarditis, and immune rejection. Each of these pathological states has its own unique features in pathogenesis and disease evolution, but all reflect inflammatory mechanisms that are partially shared. From the point of injury to the mobilization of innate and adaptive immune responses and inflammatory amplification, the cellular and soluble mediators and mechanisms examined in this review will be discussed with a view that both beneficial and adverse consequences arise in these human conditions. (Circ Res. 2012;110:126-144.)

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Section: Virus Replication and Inflammation Are Caught In A Synergistmentioning

confidence: 48%

Inflammation in Myocardial Diseases

Marchant

Boyd

Lin

et al. 2012

Circulation Research

252

165

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“…These proteins have been described to take part in a broad range of processes related to autophagy, such as immunity (NFKBIA/IκBα, 51 IRF1 [interferon regulatory factor 1], 52,53 PPP1R13L/iASPP, 54 EIF2AK2/PKR, 55 RELA/NF-κB-p65 56,57 ) or oncogenesis (BRCA1, 58,59 MYC, 60,61 RB1 [retinoblastoma 1], 62,63 TSC2/Tuberin, 64 FOXO1, 65 XIAP 66,67 ). A few posttranslational modification enzymes have also been identified, such as 2 ubiquitin ligases (HERC1 68,69 and XIAP 66,67 ), 4 kinases (PKD2/polycystin 2, 70,71 MARK4, 72 SIK2, 73 CAMKK2/CaMKKβ 74 ), one deacetylase (HDAC4 75 ), one methyltransferase (EHMT2/G9a 76,77 ) and one phosphatase (PTPN13/PTPL1 78 ) (Table S3).…”

Section: Resultsmentioning

confidence: 99%

iLIR database: A web resource for LIR motif-containing proteins in eukaryotes

et al. 2016

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Atg8-family proteins are the best-studied proteins of the core autophagic machinery. They are essential for the elongation and closure of the phagophore into a proper autophagosome. Moreover, Atg8-family proteins are associated with the phagophore from the initiation of the autophagic process to, or just prior to, the fusion between autophagosomes with lysosomes. In addition to their implication in autophagosome biogenesis, they are crucial for selective autophagy through their ability to interact with selective autophagy receptor proteins necessary for the specific targeting of substrates for autophagic degradation. In the past few years it has been revealed that Atg8-interacting proteins include not only receptors but also components of the core autophagic machinery, proteins associated with vesicles and their transport, and specific proteins that are selectively degraded by autophagy. Atg8-interacting proteins contain a short linear LC3-interacting region/LC3 recognition sequence/Atg8-interacting motif (LIR/LRS/AIM) motif which is responsible for their interaction with Atg8-family proteins. These proteins are referred to as LIR-containing proteins (LIRCPs). So far, many experimental efforts have been carried out to identify new LIRCPs, leading to the characterization of some of them in the past 10 years. Given the need for the identification of LIRCPs in various organisms, we developed the iLIR database (https://ilir.warwick.ac.uk) as a freely available web resource, listing all the putative canonical LIRCPs identified in silico in the proteomes of 8 model organisms using the iLIR server, combined with a Gene Ontology (GO) term analysis. Additionally, a curated text-mining analysis of the literature permitted us to identify novel putative LICRPs in mammals that have not previously been associated with autophagy.

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“…Similarly, TNF␣-induced NF-B activation represses autophagy in different cancer cell lines that originate from breast cancer, acute promyelocytic leukemia, and Ewing sarcoma [58]. Moreover, sustained TNF-induced activation of NF-B in intestinal epithelial cells was associated with the promotion of autophagosomal-controlled IkB␣ degradation [59]. Autophagy inhibition leads to IKK/NF-B recovery from geldanamycin (GA) in malignant cells and significantly dampen the cytotoxicity of GA.…”

Section: Nf-äb Pathwaymentioning

confidence: 98%