Appears in Networks 15

Endothelial Innate Immune Activation-2.0-Hs v2.0

The Endothelial Innate Immune Activation network depicts the causal mechanisms that describe acute response of healthy pulmonary endothelium to pro-inflammatory stimuli. These response mechanisms include production of the inflammatory chemokines, adhesion molecules and other mediators during endothelial cells activation leading to lung microvascular endothelial cells dysfunction. The network also includes causal mechanisms associated with angiogenic regulation by immune cells, including drivers of VEGF secretion and other related signaling pathways that crosstalk between the immune system and angiogenesis.

Wound Healing-2.0-Hs v2.0

The Wound Healing network describes the causal mechanisms involved in the wound healing response in pulmonary tissue following exposure to cigarette smoke. This includes processes related to cell migration as a result of MMP degradation of matrix components and progenitor cell differentiation mediated by NOTCH1, SOX2, KRT14 and CTNNB1.

Apoptosis-2.0-Mm v2.0

The Apoptosis network describes causal mechanisms in several different signaling pathways that are involved in the induction of apoptosis in response to environmental cues. The pathways include ER stress signaling, particularly the PERK-eIF2alpha-ATF4-CHOP pathway, MAPK components that regulate the pro-apoptotic proteins (Bad,Bax, Bim) via PI3K/AKT and JNK pathways, NFkB signaling which induces downstream expressions of anti-apoptotic proteins, PKC-mediated apoptosis, and activation of TNFR1 and Fas receptor leading to downstream signaling of caspase-8. The network also characterizes the transcriptional role of TP53 in apoptosis through the presence of its downstream anti-apoptotic and pro-apoptotic targets. \nReviewed during Jamboree2014

Endothelial Innate Immune Activation-2.0-Mm v2.0

The Endothelial Innate Immune Activation network depicts the causal mechanisms that describe acute response of healthy pulmonary endothelium to pro-inflammatory stimuli. These response mechanisms include production of the inflammatory chemokines, adhesion molecules and other mediators during endothelial cells activation leading to lung microvascular endothelial cells dysfunction. The network also includes causal mechanisms associated with angiogenic regulation by immune cells, including drivers of VEGF secretion and other related signaling pathways that crosstalk between the immune system and angiogenesis.

Fibrosis-2.0-Mm v2.0

The Fibrosis network depicts causal mechanisms that describe fibrosis and epithelial-to-mesenchymal cell transition (EMT) in lung tissue repair, including distinct characteristics of lung fibrosis such as TGFB1, collagen and MMPs. The network also contains signaling components of the Wnt, Hedgehog, and EGFR pathways that promote fibrosis and EMT.

Wound Healing-2.0-Mm v2.0

The Wound Healing network describes the causal mechanisms involved in the wound healing response in pulmonary tissue following exposure to cigarette smoke. This includes processes related to cell migration as a result of MMP degradation of matrix components and progenitor cell differentiation mediated by NOTCH1, SOX2, KRT14 and CTNNB1.

Apoptosis-2.0-Rn v2.0

The Apoptosis network describes causal mechanisms in several different signaling pathways that are involved in the induction of apoptosis in response to environmental cues. The pathways include ER stress signaling, particularly the PERK-eIF2alpha-ATF4-CHOP pathway, MAPK components that regulate the pro-apoptotic proteins (Bad,Bax, Bim) via PI3K/AKT and JNK pathways, NFkB signaling which induces downstream expressions of anti-apoptotic proteins, PKC-mediated apoptosis, and activation of TNFR1 and Fas receptor leading to downstream signaling of caspase-8. The network also characterizes the transcriptional role of TP53 in apoptosis through the presence of its downstream anti-apoptotic and pro-apoptotic targets. \nReviewed during Jamboree2014

Endothelial Innate Immune Activation-2.0-Rn v2.0

The Endothelial Innate Immune Activation network depicts the causal mechanisms that describe acute response of healthy pulmonary endothelium to pro-inflammatory stimuli. These response mechanisms include production of the inflammatory chemokines, adhesion molecules and other mediators during endothelial cells activation leading to lung microvascular endothelial cells dysfunction. The network also includes causal mechanisms associated with angiogenic regulation by immune cells, including drivers of VEGF secretion and other related signaling pathways that crosstalk between the immune system and angiogenesis.

Fibrosis-2.0-Rn v2.0

The Fibrosis network depicts causal mechanisms that describe fibrosis and epithelial-to-mesenchymal cell transition (EMT) in lung tissue repair, including distinct characteristics of lung fibrosis such as TGFB1, collagen and MMPs. The network also contains signaling components of the Wnt, Hedgehog, and EGFR pathways that promote fibrosis and EMT.

Wound Healing-2.0-Rn v2.0

The Wound Healing network describes the causal mechanisms involved in the wound healing response in pulmonary tissue following exposure to cigarette smoke. This includes processes related to cell migration as a result of MMP degradation of matrix components and progenitor cell differentiation mediated by NOTCH1, SOX2, KRT14 and CTNNB1.

Alzheimer's Disease Knowledge Assembly v5.0.4

This knowledge assembly is specific to Alzheimer's Disease for the AETIONOMY project. It encodes the pathological mechanisms in neurons in the human brain as well as additional evidence from mice and rats. This model includes different pathways such as apoptosis signaling, calcium signaling, cholesterol homeostasis, endocytosis, GSK activation, inflammatory responses, oxidative stress of mitochondria and endoplasmic reticulum, etc. In this version, we have added additional mechanisms/pathways to describe the functional consequences of SNPs linked with genes implicated in Alzheimer's Disease through GWAS.

Alzheimer's Disease Knowledge Assembly v5.0.6

This knowledge assembly is specific to Alzheimer's Disease for the AETIONOMY project. It encodes the pathological mechanisms in neurons in the human brain as well as additional evidence from mice and rats. This model includes different pathways such as apoptosis signaling, calcium signaling, cholesterol homeostasis, endocytosis, GSK activation, inflammatory responses, oxidative stress of mitochondria and endoplasmic reticulum, etc. In this version, we have added additional mechanisms/pathways to describe the functional consequences of SNPs linked with genes implicated in Alzheimer's Disease through GWAS.

Alzheimer's Disease Knowledge Assembly v5.0.9

This knowledge assembly is specific to Alzheimer's Disease for the AETIONOMY project. It encodes the pathological mechanisms in neurons in the human brain as well as additional evidence from mice and rats. This model includes different pathways such as apoptosis signaling, calcium signaling, cholesterol homeostasis, endocytosis, GSK activation, inflammatory responses, oxidative stress of mitochondria and endoplasmic reticulum, etc. In this version, we have added additional mechanisms/pathways to describe the functional consequences of SNPs linked with genes implicated in Alzheimer's Disease through GWAS.

colorectal cancer Knowledge Assembly - Drugs v1.0.1

colorectal cancer Knowledge Assembly with drug associations.

colorectal cancer Drugs resistance v1.0.1.0

colorectal cancer Knowledge Assembly with drug associations.

About

BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of the open source project, PyBEL. Please feel free to contact us here to give us feedback or report any issues.