Evidence map›Paper›PMID 33893499›Full record

ArticleIntegrative biology : quantitative biosciences from nano to macro2021

Mechanistic dissection of spatial organization in NF-κB signaling pathways by hybrid simulations.

Yinghao Wu, Kalyani Dhusia, Zhaoqian Su

Open access · greenAbstract read
In one paragraph

Article in Integrative biology : quantitative biosciences from nano to macro, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 64% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Yinghao WuDepartment of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY, USA.ORCID 0000-0003-1181-5670
Kalyani DhusiaDepartment of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY, USA.
Zhaoqian SuDepartment of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, NY, USA.
Albert Einstein College of Medicine · US

Funding

A multiscale model for binding kinetics of membrane receptors on cell surfacesR01GM120238 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WU, YINGHAO · 2016 to 2020
$1.6M
Computational models for the signaling of tumor necrosis factor receptor on cell surfacesR01GM122804 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI WU, YINGHAO · 2017 to 2020
$1.3M
NIGMS NIH HHS R01 GM120238NIGMS NIH HHS R01 GM122804
6 · The paper itself

Abstract

The nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) is one of the most important transcription factors involved in the regulation of inflammatory signaling pathways. Inappropriate activation of these pathways has been linked to autoimmunity and cancers. Emerging experimental evidences have been showing the existence of elaborate spatial organizations for various molecular components in the pathways. One example is the scaffold protein tumor necrosis factor receptor associated factor (TRAF). While most TRAF proteins form trimeric quaternary structure through their coiled-coil regions, the N-terminal region of some members in the family can further be dimerized. This dimerization of TRAF trimers can drive them into higher-order clusters as a response to receptor stimulation, which functions as a spatial platform to mediate the downstream poly-ubiquitination. However, the molecular mechanism underlying the TRAF protein clustering and its functional impacts are not well-understood. In this article, we developed a hybrid simulation method to tackle this problem. The assembly of TRAF-based signaling platform at the membrane-proximal region is modeled with spatial resolution, while the dynamics of downstream signaling network, including the negative feedbacks through various signaling inhibitors, is simulated as stochastic chemical reactions. These two algorithms are further synchronized under a multiscale simulation framework. Using this computational model, we illustrated that the formation of TRAF signaling platform can trigger an oscillatory NF-κB response. We further demonstrated that the temporal patterns of downstream signal oscillations are closely regulated by the spatial factors of TRAF clustering, such as the geometry and energy of dimerization between TRAF trimers. In general, our study sheds light on the basic mechanism of NF-κB signaling pathway and highlights the functional importance of spatial regulation within the pathway. The simulation framework also showcases its potential of application to other signaling pathways in cells.

Indexed as

NF-kappa BSignal TransductionNF-kappa Bhybrid simulationsligand–receptor oligomerizationNF-κB signaling pathways

Identifiers

PMID33893499
PMCPMC8129552
OpenAlexW3154472100

What OpenQuestion holds

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Registered trials

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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.