Ecsit-ement on the crossroads of Toll and BMP signal transduction: Figure 1.

Moustakas, Aristidis; Heldin, Carl‐Henrik

doi:10.1101/gad.1161403

Cited by 38 publications

(36 citation statements)

References 38 publications

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“…In fact, subsequent analysis showed that ECSIT can function as a coactivator for effectors of Bmp/ TGF␤ signaling, namely, the Smad transcription factors (Xiao et al 2003). This surprising finding raises the possibility that ECSIT may regulate both TLR and TGF/ Bmp pathways, and hence may help provide an explanation for why these pathways cross-repress one another (Moustakas and Heldin 2003). It is also important to point out that the TAK/TAB proteins were also initially identified and characterized as intermediates in TGF␤ signaling, and hence it is possible that this link between adapters in TLR and TGF signaling pathways may be more extensive than currently imagined.…”

Section: Toll/il-1 Receptor Signaling To Nf-bmentioning

confidence: 99%

Signaling to NF-κB

Hayden¹,

Ghosh²

2004

Genes Dev.

3,618

3,417

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The transcription factor NF-B has been the focus of intense investigation for nearly two decades. Over this period, considerable progress has been made in determining the function and regulation of NF-B, although there are nuances in this important signaling pathway that still remain to be understood. The challenge now is to reconcile the regulatory complexity in this pathway with the complexity of responses in which NF-B family members play important roles. In this review, we provide an overview of established NF-B signaling pathways with focus on the current state of research into the mechanisms that regulate IKK activation and NF-B transcriptional activity.

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Section: Toll/il-1 Receptor Signaling To Nf-bmentioning

confidence: 99%

Signaling to NF-κB

Hayden¹,

Ghosh²

2004

Genes Dev.

3,618

3,417

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“…Intriguingly, hippocampal AD cells show increased expression of BMP4 levels, which signals through BMPr1a receptors and ECSIT, resulting in negative modulation of the proliferation and further inhibition of neurogenesis [79]. The ubiquitination of ECSIT could provide a mechanistic explanation of this process, since it would inactivate the differentiation pathways by precluding its binding to SMAD complexes and impairing their translocation to the nucleus [47,52,80]. Additionally, ECSIT could switch on the MAPK pathway, unleashing a phosphorylation cascade that would result in hyperphosphorylation of tau [81].…”

Section: Neuro-reparative Role Of Ecsit For Cell Damagementioning

confidence: 99%

Towards Alzheimer's root cause: ECSIT as an integrating hub between oxidative stress, inflammation and mitochondrial dysfunction

et al. 2012

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Here we postulate that the adapter protein evolutionarily conserved signalling intermediate in Toll pathway (ECSIT) might act as a molecular sensor in the pathogenesis of Alzheimer's disease (AD). Based on the analysis of our AD‐associated protein interaction network, ECSIT emerges as an integrating signalling hub that ascertains cell homeostasis by the specific activation of protective molecular mechanisms in response to signals of amyloid‐beta or oxidative damage. This converges into a complex cascade of patho‐physiological processes. A failure to repair would generate severe mitochondrial damage and ultimately activate pro‐apoptotic mechanisms, promoting synaptic dysfunction and neuronal death. Further support for our hypothesis is provided by increasing evidence of mitochondrial dysfunction in the disease etiology. Our model integrates seemingly controversial hypotheses for familial and sporadic forms of AD and envisions ECSIT as a biomarker to guide future therapies to halt or prevent AD.Editor's suggested further reading in BioEssays Binding of amyloid peptides to domain‐swapped dimers of other amyloid‐forming protein may prevent their neurotoxicity AbstractPlease, also watch the Video Abstract

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“…TAK1, despite its original name, has also been firmly placed as a crucial signalling intermediate in many pro-inflammatory cytokine and Toll-like receptor signalling pathways (reviewed by Moustakas and Heldin, 2003). In these pathways, TAK1 cooperates with TRAF-mediated signalling to regulate inhibitor of nuclear factor κB (IκB) function.…”

mentioning

confidence: 99%

Non-Smad TGF-β signals

Moustakas

Heldin

2005

Journal of Cell Science

Self Cite

1,016

812

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During the past 10 years, it has been firmly established that Smad pathways are central mediators of signals from the receptors for transforming growth factor β (TGF-β) superfamily members to the nucleus. However, growing biochemical and developmental evidence supports the notion that alternative, non-Smad pathways also participate in TGF-β signalling. Non-Smad signalling proteins have three general mechanisms by which they contribute to physiological responses to TGF-β: (1) non-Smad signalling pathways directly modify (e.g. phosphorylate) the Smads and thus modulate the activity of the central effectors; (2) Smads directly interact and modulate the activity of other signalling proteins (e.g. kinases), thus transmitting signals to other pathways; and (3) the TGF-β receptors directly interact with or phosphorylate non-Smad proteins, thus initiating parallel signalling that cooperates with the Smad pathway in eliciting physiological responses. Thus, non-Smad signal transducers under the control of TGF-β provide quantitative regulation of the signalling pathway, and serve as nodes for crosstalk with other major signalling pathways, such as tyrosine kinase, G-protein-coupled or cytokine receptors.

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Ecsit-ement on the crossroads of Toll and BMP signal transduction: Figure 1.

Cited by 38 publications

References 38 publications

Signaling to NF-κB

Signaling to NF-κB

Towards Alzheimer's root cause: ECSIT as an integrating hub between oxidative stress, inflammation and mitochondrial dysfunction

Non-Smad TGF-β signals

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