Relation Results

Identifier	Residue	Organism
SIGNOR-260259		Homo sapiens
pmid	sentence
18231581	Induction and over-production of proinflammatory cytokines and chemokines, such as IL-6, IL-8, TNF-a and INF-c, were considered to be main mediators in the pathogenesis of SARS

Publications:

1

Organism:

Homo Sapiens

Pathways:

Multiple sclerosis, SARS-CoV CYTOKINE STORM

Identifier	Residue	Organism
SIGNOR-260256		Homo sapiens
pmid	sentence
18231581	Induction and over-production of proinflammatory cytokines and chemokines, such as IL-6, IL-8, TNF-a and INF-c, were considered to be main mediators in the pathogenesis of SARS

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, Multiple sclerosis, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM

Identifier	Residue	Organism
SIGNOR-257599		Homo sapiens
pmid	sentence
25910399	Glucocorticoids (GCs) are the most commonly used anti-inflammatory agents to treat inflammatory and immune diseases [.. }The dogma that transrepression of genes, by tethering of the glucocorticoid receptor (GR) to DNA-bound pro-inflammatory transcription factors, is the main anti-inflammatory mechanism, is now challenged.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Glucocorticoid receptor Signaling

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-263462
pmid	sentence
1847994	The C5a receptor mediates the pro-inflammatory and chemotactic actions of the complement anaphylatoxin C5a. In addition to stimulating chemotaxis, granule enzyme release and superoxide anion production, this receptor stimulates upregulation of expression and activity of the adhesion molecule MAC-1, and of CR1, and a decrease in cell-surface glycoprotein 100MEL-14 on neutrophils.

Publications:

1

Pathways:

Complement Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-259288		Mus musculus	Macrophage
pmid	sentence
12150927	IRAK-M(-/-) cells exhibited increased cytokine production upon TLR/IL-1 stimulation and bacterial challenge, and IRAK-M(-/-) mice showed increased inflammatory responses to bacterial infection.

Publications:

1

Organism:

Mus Musculus

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-263461
pmid	sentence
1847994	The C5a receptor mediates the pro-inflammatory and chemotactic actions of the complement anaphylatoxin C5a. In addition to stimulating chemotaxis, granule enzyme release and superoxide anion production, this receptor stimulates upregulation of expression and activity of the adhesion molecule MAC-1, and of CR1, and a decrease in cell-surface glycoprotein 100MEL-14 on neutrophils.

Publications:

1

Identifier	Residue	Organism	Cell Line
SIGNOR-262310		Mus musculus	Macrophage
pmid	sentence
30918468	Our data suggested that both Ang-(1-7) and alamandine, through their respective receptors Mas and MrgD, promote an anti-inflammatory reprogramming of M(LPS+IFN-γ)/M1 macrophages under inflammatory circumstances and potentiate the reprogramming induced by IL-4.

Publications:

1

Organism:

Mus Musculus

Pathways:

SARS-CoV FIBROSIS

Identifier	Residue	Organism	Cell Line
SIGNOR-255494		Homo sapiens	Eosinophil
pmid	sentence
11290754	Our findings indicate that chemokines acting via CCR3-initiated signaling pathways can very rapidly mobilize preformed stores of IL-4 from within human eosinophils. The means of extracellular release was by noncytotoxic, vesicular transport

Publications:

1

Organism:

Homo Sapiens

Pathways:

Multiple sclerosis

Identifier	Residue	Organism
SIGNOR-260346		Homo sapiens
pmid	sentence
32133002	Both the NLRP3 inflammasome activation and the subsequent inflammation play significant roles in defending against viral infections. However, aberrant NLRP3 inflammasome activation or chronic inflammation can also lead to severe pathological injury. Accordingly, activation of the NLRP3 inflammasome and its associated inflammation is a double-edged sword for host to defense viral infection. Modulating the NLRP3 inflammasome activity can prove to be a promising strategy for the intervention of viral diseases.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, EBV infection, Inflammosome Activation, SARS-CoV INFLAMMATORY RESPONSE

Identifier	Residue	Organism
SIGNOR-266901		Homo sapiens
pmid	sentence
25910399	Glucocorticoids (GCs) are the most commonly used anti-inflammatory agents to treat inflammatory and immune diseases [.. }The dogma that transrepression of genes, by tethering of the glucocorticoid receptor (GR) to DNA-bound pro-inflammatory transcription factors, is the main anti-inflammatory mechanism, is now challenged.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Glucocorticoid receptor Signaling

Identifier	Residue	Organism	Cell Line
SIGNOR-262509		Homo sapiens	HEK-293 Cell
pmid	sentence
32995789	Given our finding that COX-2 signaling does not regulate viral entry or replication, the role of COX-2 induction upon SARS-CoV-2 infection remains an area for future investigation. Rather than directly affecting viral entry or replication, COX-2 induction may regulate the severe lung inflammation and injury seen in COVID-19 patients (35, 36), though it is unclear whether COX-2 would be beneficial, neutral, or detrimental to disease. COX-2 could enhance lung injury in COVID-19, as PGE2 has been reported to induce IL-1β and exacerbate lung injury in bone marrow transplant mice

Publications:

1

Organism:

Homo Sapiens

Pathways:

SARS-CoV INFLAMMATORY RESPONSE

Identifier	Residue	Organism
SIGNOR-260258		Homo sapiens
pmid	sentence
18231581	Induction and over-production of proinflammatory cytokines and chemokines, such as IL-6, IL-8, TNF-a and INF-c, were considered to be main mediators in the pathogenesis of SARS

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, EBV infection, Inflammosome Activation, Multiple sclerosis, NF-KB Canonical, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE, TNF-alpha Signaling

Identifier	Residue	Organism
SIGNOR-260228		Homo sapiens
pmid	sentence
23488800	The discovery that Ang-(1-7) offsets the major biological effects of Ang II has contributed to the realization that the RAS is composed of two opposing axes. The first axis is constituted by the enzyme ACE, with Ang II as the end product, and the AT1 receptor as the main effector mediating the biological actions of Ang II. The second axis results from ACE2-mediated hydrolysis of Ang II, leading to production of Ang-(1-7), with Mas receptor as the main effector conveying the vasodilator, antiproliferative, anti-inflammatory and anti-fibrotic effects of Ang-(1-7). Activation of the ACE2/Ang-(1-7)/Mas axis decreases inflammatory cell function and fibrogenesis in diverse models of human diseases.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, Fibrosis, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV FIBROSIS

Identifier	Residue	Organism
SIGNOR-260257		Homo sapiens
pmid	sentence
18231581	Induction and over-production of proinflammatory cytokines and chemokines, such as IL-6, IL-8, TNF-a and INF-c, were considered to be main mediators in the pathogenesis of SARS

Publications:

1

Organism:

Homo Sapiens

Pathways:

SARS-CoV CYTOKINE STORM

Identifier	Residue	Organism
SIGNOR-258988		Homo sapiens
pmid	sentence
23685857	Tumor necrosis factor α (TNF-α, also known as cachectin) is a strong pro-inflammatory cytokine which plays an important role in the immune system during inflammation, cell proliferation, differentiation and apoptosis

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, EBV infection, Inflammosome Activation, Multiple sclerosis, NF-KB Canonical, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE, TNF-alpha Signaling

Identifier	Residue	Organism
SIGNOR-261036		Homo sapiens
pmid	sentence
32446778	The presence of SARS-CoV-2 in the lung induces an uncontrolled generalized immune response. Several immune cells (like T-lymphocytes, macrophages and dendritic cells) sustain the impressive secretion of cytokines and chemokines ultimately leading to acute respiratory distress syndrome. These data clearly indicate that, in SARS-CoV in-fection, ARDS is the ultimate result of a cytokine storm.

Publications:

1

Organism:

Homo Sapiens

Pathways:

SARS-CoV CYTOKINE STORM

Identifier	Residue	Organism	Cell Line
SIGNOR-189109		Homo sapiens	T-lymphocyte, B-lymphocyte
pmid	sentence
19904719	Cd40 has been found to be essential in mediating a broad variety of immune and inflammatory responses including t cell-dependent immunoglobulin class switching, memory b cell development

Publications:

1

Organism:

Homo Sapiens

Pathways:

Multiple sclerosis

Identifier	Residue	Sequence	Organism	Cell Line
SIGNOR-255489
pmid	sentence
25309941	Following GSK3β activation, NF-κB is translocated from the cytoplasm to the nucleus and binds transcriptional sites with CBP leading to an increase in the transcription of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6).

Identifier	Residue	Organism
SIGNOR-245039		Homo sapiens
pmid	sentence
20457564	The nuclear factor NF-kappaB pathway has long been considered a prototypical proinflammatory signaling pathway, largely based on the role of NF-kappaB in the expression of proinflammatory genes including cytokines, chemokines, and adhesion molecules.

Identifier	Residue	Organism
SIGNOR-260445		Homo sapiens
pmid	sentence
24168260	NF-κB, which can be activated by mitogen-activated protein kinases (MAPKs) (12), is responsible for the transcription of inflammatory factors and profibrotic cytokines, which promote an inflammatory response and fibrosis

Publications:

3

Organism:

, Homo Sapiens

Pathways:

B-cell activation, COVID-19 Causal Network, EBV infection, Fibrosis, Glucocorticoid receptor Signaling, Innate Immune Response, IL1 Signaling , Inflammosome Activation, Multiple sclerosis, NF-KB Canonical, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV CYTOKINE STORM, SARS-CoV FIBROSIS, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA, TNF-alpha Signaling

Identifier	Residue	Organism
SIGNOR-260233		Homo sapiens
pmid	sentence
32201502	Ang II binding to AT1 receptors has been implicated in inflammatory responses. Activation of this Ang II–AT1 receptor-dependent pathway is widely accepted to lead to organ damage and fibrosis.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, Fibrosis, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV FIBROSIS

Identifier	Residue	Organism
SIGNOR-171873		Homo sapiens
pmid	sentence
21304099	Interleukin-1 in the pathogenesis and treatment of inflammatory diseases

Publications:

1

Organism:

Homo Sapiens

Pathways:

IL1 Signaling

Identifier	Residue	Organism
SIGNOR-171876		Homo sapiens
pmid	sentence
21304099	The Il-1 family of ligands and receptors is primarily associated with acute and chronic inflammation.

Publications:

1

Organism:

Homo Sapiens

Pathways:

IL1 Signaling , SARS-CoV CYTOKINE STORM

Identifier	Residue	Organism	Cell Line
SIGNOR-263472		Homo sapiens	HMC-1 Cell
pmid	sentence
9108406	In summary, these findings indicate that C3a and C5a serve as chemotaxins for human mast cells. Anaphylatoxin-mediated recruitment of mast cells might play an important role in hypersensitivity and inflammatory processes.

Publications:

1

Organism:

Homo Sapiens

Pathways:

Complement Signaling

Identifier	Residue	Organism
SIGNOR-261317		Homo sapiens
pmid	sentence
32446778	In this scenario,the release by immune effector cells of large amounts of pro-in-flammatory cytokines (IFNŒ±, IFNŒ≥, IL-1Œ≤, IL-6, IL-12, IL-18, IL-33,TNFŒ±, TGFŒ≤) and chemokines (CXCL10, CXCL8, CXCL9, CCL2, CCL3,CCL5) precipitates and sustains the aberrant systemic inflammatory response.

Publications:

1

Organism:

Homo Sapiens

Pathways:

COVID-19 Causal Network, Inflammosome Activation, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM, SARS-CoV INFLAMMATORY RESPONSE

Name	Inflammation
Primary ID	SIGNOR-PH12
Type	phenotype
Description	The immediate defensive reaction (by vertebrate tissue) to infection or injury caused by chemical or physical agents
Relations	25
Pathways	B-cell activation, COVID-19 Causal Network, Complement Signaling, EBV infection, Eosinophil: CCL11, Fibrosis, Glucocorticoid receptor Signaling, iCAF signaling in PDAC, Innate Immune Response, IL1 Signaling , Inflammosome Activation, Multiple sclerosis, NF-KB Canonical, Chemokines PDAC, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV MAPK PERTURBATION, SARS-CoV ATTACHMENT AND ENTRY, SARS-CoV CYTOKINE STORM, SARS-CoV FIBROSIS, SARS-CoV INFLAMMATORY RESPONSE, SARS-CoV INNATE RESPONSE TO dsRNA, TNF-alpha Signaling

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