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Lipniacki2004 - Mathematical model of NFKB regulatory module

ABSTRACT: its a mathematical model studying impact of TNF on NFKB nuclear dynamics. This model is derived from Hoffmann2002 (PMID:12424381).

SUBMITTER: Krishna Kumar Tiwari

PROVIDER: BIOMD0000000786 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000786?filename=Lipniacki2004-biopax2.owl	Owl
	BIOMD0000000786?filename=Lipniacki2004-biopax3.owl	Owl
	BIOMD0000000786?filename=Lipniacki2004-matlab.m	Other
	BIOMD0000000786?filename=Lipniacki2004-octave.m	Other
	BIOMD0000000786?filename=Lipniacki2004.cps	Other

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Publications

Mathematical model of NF-kappaB regulatory module.

Lipniacki Tomasz T Paszek Pawel P Brasier A R Allan R AR Luxon Bruce B Kimmel Marek M

Journal of theoretical biology 20040501 2

The two-feedback-loop regulatory module of nuclear factor kappaB (NF-kappaB) signaling pathway is modeled by means of ordinary differential equations. The constructed model involves two-compartment kinetics of the activators IkappaB (IKK) and NF-kappaB, the inhibitors A20 and IkappaBalpha, and their complexes. In resting cells, the unphosphorylated IkappaBalpha binds to NF-kappaB and sequesters it in an inactive form in the cytoplasm. In response to extracellular signals such as tumor necrosis f ...[more]

PMID: 15094015

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Project description:its a mathematical model studying impact of b_TrCP on NFKB nuclear dynamics. This model is derived from Lipniacki2004 (PMID:15094015).

2024-09-02 | BIOMD0000000794 | BioModels

Tiwari2019 - Mathematical model of NFKB regulatory module with TNF and ROS

Project description:It is a dynamic model containing elements of two different model as one. It contains the impact of TNF on SOD and impact of ROS on A20 behavior.

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TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron

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A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma (part 2)

Project description:SUMMARY Despite numerous genome-wide association studies involving glioblastoma (GBM), few therapeutic targets have been identified for this disease. Using patient derived glioma sphere cultures (GSCs), we have found that a subset of the proneural (PN) GSCs undergo transition to a mesenchymal (MES) state in a TNFa/NFkB dependent manner with an associated enrichment of CD44 sub-populations and radio-resistant phenotypes. To the contrary, MES GSCs exhibit constitutive NFkB activation, CD44 enrichment and radio-resistance. Patients whose tumors exhibit a higher MES metagene, increased expression of CD44, or activated NFkB were associated with poor radiation response and shorter survival. Our results indicate that NFkB activation mediated MES differentiation and radiation resistance presents an attractive therapeutic target for GBM. SIGNIFICANCE In this study, we show plasticity between the proneural (PN) and mesenchymal (MES) transcriptome signatures observed in glioblastoma (GBM). Specifically, we show that PN glioma sphere cultures (GSCs) can be induced to a MES state with an associated enrichment of CD44 expressing cells and a gain of radio-resistance, which we implicate as NFkB- dependent. Newly diagnosed GBM samples show a direct correlation between radiation response, higher MES metagene, CD44 expression, and NFkB activation. This correlation is also observed in the subset of GBM samples that do not exhibit IDH1 mutation, a favorable prognostic marker. Our results uncover a previously unknown link between subtype plasticity that is regulated by NFkB. Inhibition of NFkB activation can directly impact radio-resistance and presents an attractive therapeutic target for GBM. 4 treatments

2013-08-15 | E-GEOD-49162 | biostudies-arrayexpress

A Proneural to Mesenchymal Transition Mediated by NFkB Promotes Radiation Resistance in Glioblastoma (part 1)

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TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (scRNA-Seq)

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TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (RNA-Seq)

Project description:TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (RNA-Seq)

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TNF-NFkB-p53 axis restricts in vivo survival of hPSC-derived dopamine neuron (CRISPR screen)

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Acute TNF-induced repression of cell identity genes is mediated by NFkB-directed redistribution of cofactors from super-enhancers

Project description:The proinflammatory cytokine tumor necrosis factor (TNF) plays a central role in low-grade adipose tissue inflammation and development of insulin resistance during obesity. In this context, nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB), is directly involved and required for the acute activation of the inflammatory gene program. Here we show that the major transactivating subunit of NF?B, v-rel avian reticuloendotheliosis viral oncogene homolog A (RELA), is also required for acute TNF-induced suppression of adipocyte genes. Notably, this repression does not involve RELA binding to the associated enhancers but rather loss of cofactors and enhancer RNA (eRNA) selectively from high occupancy sites within super-enhancers. Based on these data we have developed models that with high accuracy predict which enhancers and genes are repressed by TNF in adipocytes. We show that these models are applicable to other cell types where TNF represses genes associated with super-enhancers in a highly cell type-specific manner. Our results propose a novel paradigm for NF?B-mediated repression, whereby NF?B selectively redistributes cofactors from high occupancy enhancers, thereby specifically repressing super-enhancer-associated cell identity genes. Genome-wide assesment of the acute transcriptional response to TNF in human SGBS adipocytes using RNA- ChIP- and DHS-seq. Total RNA-seq and RNAPII-ChIP seq for vehicle and TNF treated adipocytes are available under GSE60462

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NFkB perturbation followed by genome-wide allelic-expression data assessment

Project description:We developed a method that perturbs transcription factor followed by monitoring genome-wide allelic expression measurements in living cells. As a model for this novel approach, we chose the factor NFÎºB. We performed TNF-Î± induction coupled to inhibition of NFÎºB in LCLs followed by Allelic Expression (AE) analysis on Illumina HumanOmni5-Quad BeadChips. Samples used included two HapMap trios: one from the CEU (GM12891, GM12892, and GM12878) and one from the YRI (GM19239, GM19238, and GM19240) population. NF-ÎºB knockdown was validated using RT-PCR of known gene targets for NFkB. Differential AE was assessed on Illumina HumanOmni5-Quad BeadChips for each experimental condition: (1) inhibition with Helenanin followed 1 hour later by activation by TNF-Î± (TN); (2) activation by TNF-Î± (tnfalpha); (3) DMSO; (4) no treatment (notmt).

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