Dataset Information

Padala2017- ERK, PI3K/Akt and Wnt signalling network (PTEN mutation)

ABSTRACT: Padala2017- ERK, PI3K/Akt and Wnt signalling network (PTEN mutation) Crosstalk model of the ERK, Wnt and Akt Signalling pathways with PTEN mutation. This model is described in the article: Cancerous perturbations within the ERK, PI3K/Akt, and Wnt/?-catenin signaling network constitutively activate inter-pathway positive feedback loops. Padala RR, Karnawat R, Viswanathan SB, Thakkar AV, Das AB. Mol Biosyst 2017 May; 13(5): 830-840 Abstract: Perturbations in molecular signaling pathways are a result of genetic or epigenetic alterations, which may lead to malignant transformation of cells. Despite cellular robustness, specific genetic or epigenetic changes of any gene can trigger a cascade of failures, which result in the malfunctioning of cell signaling pathways and lead to cancer phenotypes. The extent of cellular robustness has a link with the architecture of the network such as feedback and feedforward loops. Perturbation in components within feedback loops causes a transition from a regulated to a persistently activated state and results in uncontrolled cell growth. This work represents the mathematical and quantitative modeling of ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk to show the dynamics of signaling responses during genetic and epigenetic changes in cancer. ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk networks include both intra and inter-pathway feedback loops which function in a controlled fashion in a healthy cell. Our results show that cancerous perturbations of components such as EGFR, Ras, B-Raf, PTEN, and components of the destruction complex cause extreme fragility in the network and constitutively activate inter-pathway positive feedback loops. We observed that the aberrant signaling response due to the failure of specific network components is transmitted throughout the network via crosstalk, generating an additive effect on cancer growth and proliferation. This model is hosted on BioModels Database and identified by: BIOMD0000000655. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

SUBMITTER: Emma Fairbanks

PROVIDER: BIOMD0000000655 | BioModels | 2024-09-02

REPOSITORIES: BioModels

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			Action	DRS
	BIOMD0000000655?filename=BIOMD0000000655-biopax2.owl	Owl
	BIOMD0000000655?filename=BIOMD0000000655-biopax3.owl	Owl
	BIOMD0000000655?filename=BIOMD0000000655.m	Other
	BIOMD0000000655?filename=BIOMD0000000655.png	Other
	BIOMD0000000655?filename=BIOMD0000000655.sci	Other

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Publications

Cancerous perturbations within the ERK, PI3K/Akt, and Wnt/β-catenin signaling network constitutively activate inter-pathway positive feedback loops.

Padala Rahul Rao RR Karnawat Rishabh R Viswanathan Satish Bharathwaj SB Thakkar Abhishek Vijay AV Das Asim Bikas AB

Molecular bioSystems 20170501 5

Perturbations in molecular signaling pathways are a result of genetic or epigenetic alterations, which may lead to malignant transformation of cells. Despite cellular robustness, specific genetic or epigenetic changes of any gene can trigger a cascade of failures, which result in the malfunctioning of cell signaling pathways and lead to cancer phenotypes. The extent of cellular robustness has a link with the architecture of the network such as feedback and feedforward loops. Perturbation in comp ...[more]

PMID: 28367561

Publication: 1/2

Similar Datasets

Project description:Padala2017- ERK, PI3K/Akt and Wnt signalling network (PI3K mutated) Crosstalk model of the ERK, Wnt and Akt signalling pathways with mutated PI3K. This model is described in the article: Cancerous perturbations within the ERK, PI3K/Akt, and Wnt/?-catenin signaling network constitutively activate inter-pathway positive feedback loops. Padala RR, Karnawat R, Viswanathan SB, Thakkar AV, Das AB. Mol Biosyst 2017 May; 13(5): 830-840 Abstract: Perturbations in molecular signaling pathways are a result of genetic or epigenetic alterations, which may lead to malignant transformation of cells. Despite cellular robustness, specific genetic or epigenetic changes of any gene can trigger a cascade of failures, which result in the malfunctioning of cell signaling pathways and lead to cancer phenotypes. The extent of cellular robustness has a link with the architecture of the network such as feedback and feedforward loops. Perturbation in components within feedback loops causes a transition from a regulated to a persistently activated state and results in uncontrolled cell growth. This work represents the mathematical and quantitative modeling of ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk to show the dynamics of signaling responses during genetic and epigenetic changes in cancer. ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk networks include both intra and inter-pathway feedback loops which function in a controlled fashion in a healthy cell. Our results show that cancerous perturbations of components such as EGFR, Ras, B-Raf, PTEN, and components of the destruction complex cause extreme fragility in the network and constitutively activate inter-pathway positive feedback loops. We observed that the aberrant signaling response due to the failure of specific network components is transmitted throughout the network via crosstalk, generating an additive effect on cancer growth and proliferation. This model is hosted on BioModels Database and identified by: BIOMD0000000652. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

Project description:Padala2017- ERK, PI3K/Akt and Wnt signalling network (EGFR overexpression) Crosstalk model of the ERK, Wnt and Akt signalling pathways with EGFR overexpression. This model is described in the article: Cancerous perturbations within the ERK, PI3K/Akt, and Wnt/?-catenin signaling network constitutively activate inter-pathway positive feedback loops. Padala RR, Karnawat R, Viswanathan SB, Thakkar AV, Das AB. Mol Biosyst 2017 May; 13(5): 830-840 Abstract: Perturbations in molecular signaling pathways are a result of genetic or epigenetic alterations, which may lead to malignant transformation of cells. Despite cellular robustness, specific genetic or epigenetic changes of any gene can trigger a cascade of failures, which result in the malfunctioning of cell signaling pathways and lead to cancer phenotypes. The extent of cellular robustness has a link with the architecture of the network such as feedback and feedforward loops. Perturbation in components within feedback loops causes a transition from a regulated to a persistently activated state and results in uncontrolled cell growth. This work represents the mathematical and quantitative modeling of ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk to show the dynamics of signaling responses during genetic and epigenetic changes in cancer. ERK, PI3K/Akt, and Wnt/?-catenin signaling crosstalk networks include both intra and inter-pathway feedback loops which function in a controlled fashion in a healthy cell. Our results show that cancerous perturbations of components such as EGFR, Ras, B-Raf, PTEN, and components of the destruction complex cause extreme fragility in the network and constitutively activate inter-pathway positive feedback loops. We observed that the aberrant signaling response due to the failure of specific network components is transmitted throughout the network via crosstalk, generating an additive effect on cancer growth and proliferation. This model is hosted on BioModels Database and identified by: BIOMD0000000656. To cite BioModels Database, please use: Chelliah V et al. BioModels: ten-year anniversary. Nucl. Acids Res. 2015, 43(Database issue):D542-8. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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