NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis. - Wikidata - awgldk - TriplyDB

NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis.

NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis.

http://www.wikidata.org/entity/Q36011663

about

A multi-scale approach to designing therapeutics for tuberculosis Macrophage polarization drives granuloma outcome during Mycobacterium tuberculosis infection Multiscale computational models of complex biological systems.Multi-scale modeling predicts a balance of tumor necrosis factor-α and interleukin-10 controls the granuloma environment during Mycobacterium tuberculosis infection.Investigating the Role of Gene-Gene Interactions in TB Susceptibility.The COX- inhibitor indomethacin reduces Th1 effector and T regulatory cells in vitro in Mycobacterium tuberculosis infection.The pregnane X receptor in tuberculosis therapeutics.The Role of Prostate Apoptosis Response-4 (Par-4) in Mycobacterium tuberculosis Infected Macrophages.Harnessing the heterogeneity of T cell differentiation fate to fine-tune generation of effector and memory T cells.Systems biology approaches to understanding the cause and treatment of heart, lung, blood, and sleep disorders.Topology, dynamics, and heterogeneity in immune signaling.In silico models of M. tuberculosis infection provide a route to new therapies Strategies for efficient numerical implementation of hybrid multi-scale agent-based models to describe biological systems.Identifying mechanisms driving formation of granuloma-associated fibrosis during Mycobacterium tuberculosis infection.Facing the challenges of multiscale modelling of bacterial and fungal pathogen-host interactions.Signaling via the NFκB system.Mathematical Models for Immunology: Current State of the Art and Future Research Directions.Computational identification and analysis of signaling subnetworks with distinct functional roles in the regulation of TNF production.Mycobacterium tuberculosis PE13 (Rv1195) manipulates the host cell fate via p38-ERK-NF-κB axis and apoptosis.A population model capturing dynamics of tuberculosis granulomas predicts host infection outcomes.Polymorphism in cathelicidin gene (CAMP) that alters Hypoxia-inducible factor (HIF-1α::ARNT) binding is not associated with tuberculosis.Deletion of TGF-β1 Increases Bacterial Clearance by Cytotoxic T Cells in a Tuberculosis Granuloma Model.A Multi-Compartment Hybrid Computational Model Predicts Key Roles for Dendritic Cells in Tuberculosis Infection.System-wide coordinates of higher order functions in host-pathogen environment upon Mycobacterium tuberculosis infection.Isoliquiritigenin attenuates spinal tuberculosis through inhibiting immune response in a New Zealand white rabbit model.Low Levels of T Cell Exhaustion in Tuberculous Lung Granulomas Rv2346c enhances mycobacterial survival within macrophages by inhibiting TNF-α and IL-6 production via the p38/miRNA/NF-κB pathway

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P2860

NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis.

http://www.wikidata.org/entity/Q36011663

description

2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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2012年论文

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2012年论文

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NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis.

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NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis.

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NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis.

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NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis.

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FPHYS.2012.00170

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Frontiers in Physiology

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NF-κB Signaling Dynamics Play a Key Role in Infection Control in Tuberculosis.

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Denise E Kirschner

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Jennifer J Linderman

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Mohammad Fallahi-Sichani

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P2860

De-ubiquitination and ubiquitin ligase domains of A20 downregulate NF-kappaB signalling

Exploring the full spectrum of macrophage activation

Tuberculosis associated with infliximab, a tumor necrosis factor alpha-neutralizing agent

Oscillations in NF-kappaB signaling control the dynamics of gene expression

Differences in reactivation of tuberculosis induced from anti-TNF treatments are based on bioavailability in granulomatous tissue

Identification of key processes that control tumor necrosis factor availability in a tuberculosis granuloma

Modeling a snap-action, variable-delay switch controlling extrinsic cell death

Shared principles in NF-kappaB signaling

Activators and target genes of Rel/NF-kappaB transcription factors

An essential role for NF-kappaB in preventing TNF-alpha-induced cell death

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170

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10.3389/FPHYS.2012.00170

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