Commit 50b0459a authored by Marek Ostaszewski's avatar Marek Ostaszewski
Browse files

Author information

parent f194f0d8
This diff is collapsed.
<?xml version="1.0" encoding="UTF-8"?>
<sbml xmlns="http://www.sbml.org/sbml/level2/version4" xmlns:celldesigner="http://www.sbml.org/2001/ns/celldesigner" level="2" version="4">
<model metaid="mitochondrium" id="mitochondrium" sboTerm="SBO:0000231">
<notes>
<html xmlns="http://www.w3.org/1999/xhtml">
<head>
<title/>
</head>
<body>
Authors: Julia Scheel, University of Rostock, Germany
Description: The diagram describes the disruption of the Electron Transport Chain by the SARS-CoV-2 proteins
</body>
</html>
</notes>
<annotation>
<celldesigner:extension>
<celldesigner:modelVersion>4.0</celldesigner:modelVersion>
......
......@@ -6,8 +6,11 @@
<head>
<title/>
</head>
<body>Author(s):
<body>
Author:
Julia Sommers, Oregon Health and Science University (OHSU), United States
Description:
The pathway of heme metabolism under COVID-19, involving Orf3a and Orf9c
</body>
</html>
</notes>
......@@ -8160,7 +8163,7 @@ Description:
<head>
<title/>
</head>
<body>Interaction is sparsely described, and does not elaborate on which PKC (PRKCA or PRKCB)
<body>Interaction is sparsely described, and does not elaborate on which PKC (PRKCA or PRKCB)
</body>
</html>
</notes>
......
<?xml version="1.0" encoding="UTF-8"?>
<sbml xmlns="http://www.sbml.org/sbml/level2/version4" xmlns:celldesigner="http://www.sbml.org/2001/ns/celldesigner" level="2" version="4">
<model metaid="pyrimidine_biosyth_1" id="pyrimidine_deprivation">
<notes>
<html xmlns="http://www.w3.org/1999/xhtml">
<head>
<title/>
</head>
<body>
Author:
Zsolt Bocskei, Sanofi R&D
Description:
Pyrimidine deprivation and immune response related to human coronavirus infection
</body>
</html>
</notes>
<annotation>
<celldesigner:extension>
<celldesigner:modelVersion>4.0</celldesigner:modelVersion>
......
......@@ -7,20 +7,11 @@
<title/>
</head>
<body>
[-:-] Given input is not a valid SBGN-ML file.
[macromolecule multimer:glyph28] 1 Set the default value of 2.
[macromolecule multimer:glyph30] 1 Set the default value of 2.
[macromolecule multimer:glyph26] 1 Set the default value of 2.
[macromolecule multimer:glyph22] 1 Set the default value of 2.
[macromolecule multimer:glyph24] 1 Set the default value of 2.
[macromolecule multimer:glyph31] 1 Set the default value of 2.
[macromolecule multimer:glyph29] 1 Set the default value of 2.
[macromolecule multimer:glyph27] 1 Set the default value of 2.
[macromolecule multimer:glyph32] 1 Set the default value of 2.
[macromolecule multimer:glyph21] 1 Set the default value of 2.
[macromolecule multimer:glyph23] 1 Set the default value of 2.
[macromolecule multimer:glyph25] 1 Set the default value of 2.
[SquareCompartment:glyph1] CellDesigner requires thickness to be at least: 2.5
Authors:
Falk Schreiber, Helena Borlinghaus, Universität Konstanz, Germany
Tobias Czauderna, Monash University, Australia
Description:
Assembly of the Replication Transcription Complex and Transcription of SARS-CoV-2
</body>
</html>
</notes>
......
......@@ -6,8 +6,12 @@
<head>
<title/>
</head>
<body>Authors:
<body>
Authors:
Corinna Montrone, Gisela Fobo, Andreas Ruepp, Helmholtz Zentrum München / Institute of Experimental Genetics, Germany
Enrico Glaab, Luxembourg Centre for Systems Biomedicine (LCSB), Luxembourg
Description:
The role of the interaction between the SARS-CoV-2 Spike protein and the renin-angiotensin pathway, in particular human ACE2 in pulmonary blood pressure regulation
</body>
</html>
</notes>
......
......@@ -6,8 +6,12 @@
<head>
<title/>
</head>
<body>Authors:
Description:
<body>
Authors:
Corinna Montrone, Gisela Fobo, Andreas Ruepp, Helmholtz Zentrum München / Institute of Experimental Genetics, Germany
Enrico Glaab, Luxembourg Centre for Systems Biomedicine (LCSB), Luxembourg
Description:
The role of the interaction between the SARS-CoV-2 Spike protein and the renin-angiotensin pathway, in particular human ACE2 in pulmonary blood pressure regulation
</body>
</html>
</notes>
......@@ -2180,7 +2184,7 @@ Description:
<head>
<title/>
</head>
<body>Ang I can be cleaved by NEP to Ang (1–7).
<body>Ang I can be cleaved by NEP to Ang (1–7).
ACE and NEP hydrolysed Ang I efficiently, whereas ACE2 hydrolysed Ang I only very slowly.
PMID:15283675
</body>
......@@ -4791,7 +4795,7 @@ Angiotensin peptides are metabolized by several subsequent enzymatic steps: Firs
<head>
<title/>
</head>
<body>Although treatment with AGTR1 antagonist (losartan) or AGTR2 agonist (CGP42112A) inhibits tumor progression in several cancer cells, their combined treatment has not been reported. PMID:25014541
<body>Although treatment with AGTR1 antagonist (losartan) or AGTR2 agonist (CGP42112A) inhibits tumor progression in several cancer cells, their combined treatment has not been reported. PMID:25014541
</body>
</html>
</notes>
......@@ -5982,7 +5986,7 @@ PMID:26171856
<head>
<title/>
</head>
<body>Angiotensin II (ANGII) signaling, mediated via angiotensin II receptor type 1 (AGTR1) or type 2 (AGTR2), controls tissue remodeling in fibrosis, but the relevance of AGTR2 remains elusive. PMID:17630322
<body>Angiotensin II (ANGII) signaling, mediated via angiotensin II receptor type 1 (AGTR1) or type 2 (AGTR2), controls tissue remodeling in fibrosis, but the relevance of AGTR2 remains elusive. PMID:17630322
Chronic activation of the myocardial renin angiotensin system (RAS) elevates the local level of angiotensin II (Ang II) thereby inducing pathological cardiac hypertrophy, which contributes to heart failure. The authors report a novel paracrine mechanism between cardiac fibroblasts (CF)s and cardiomyocytes whereby Ang II induces pathological cardiac hypertrophy. In cultured CFs, Ang II treatment enhanced exosome release via the activation of Ang II receptor types 1 (AT1R) and 2 (AT2R), whereas lipopolysaccharide, insulin, endothelin (ET)-1, transforming growth factor beta (TGFbeta)1 or hydrogen peroxide did not. PMID:26497614
Both, ANG II and ANG IV act primarily via the angiotensin II receptor type 1 (AGTR1). PMID:32333398
Ang A has the same affinity to the AT1 receptor as Ang II, but a higher affinity to the AT2 receptor. PMID:17138938
......@@ -6123,7 +6127,7 @@ Ang A has the same affinity to the AT1 receptor as Ang II, but a higher affinity
<head>
<title/>
</head>
<body>Because AT1R seems to be essential for Ang-II–mediated ACE2 internalization, we also tested whether ACE2 and AT1R physically interact. Coimmunoprecipitation experiments confirmed this dimerization in control conditions (Figure 5B, second lane). However, Ang-II treatment decreased this interaction in a time-dependent manner [...]. PMID:25225202
<body>Because AT1R seems to be essential for Ang-II–mediated ACE2 internalization, we also tested whether ACE2 and AT1R physically interact. Coimmunoprecipitation experiments confirmed this dimerization in control conditions (Figure 5B, second lane). However, Ang-II treatment decreased this interaction in a time-dependent manner [...]. PMID:25225202
</body>
</html>
</notes>
......@@ -7366,7 +7370,7 @@ Since angiotensin-(1-12) [Ang-(1-12)] is a non-renin dependent alternate precurs
<head>
<title/>
</head>
<body>&quot;In support of this hypothesis we show that the non-peptide MAS agonist AR234960 increases both mRNA and protein levels of CTGF via ERK1/2 signaling in HEK293-MAS cells and adult human cardiac fibroblasts.&quot; PMID:29287092
<body>&quot;In support of this hypothesis we show that the non-peptide MAS agonist AR234960 increases both mRNA and protein levels of CTGF via ERK1/2 signaling in HEK293-MAS cells and adult human cardiac fibroblasts.&quot; PMID:29287092
</body>
</html>
</notes>
......
......@@ -6,8 +6,12 @@
<head>
<title/>
</head>
<body>Authors:
<body>
Authors:
Corinna Montrone, Gisela Fobo, Andreas Ruepp, Helmholtz Zentrum München / Institute of Experimental Genetics, Germany
Enrico Glaab, Luxembourg Centre for Systems Biomedicine (LCSB), Luxembourg
Description:
The role of the interaction between the SARS-CoV-2 Spike protein and the renin-angiotensin pathway, in particular human ACE2 in pulmonary blood pressure regulation
</body>
</html>
</notes>
......@@ -2219,7 +2223,7 @@ Description:
<head>
<title/>
</head>
<body>Ang I can be cleaved by NEP to Ang (1–7).
<body>Ang I can be cleaved by NEP to Ang (1–7).
ACE and NEP hydrolysed Ang I efficiently, whereas ACE2 hydrolysed Ang I only very slowly.
PMID:15283675
</body>
......@@ -3639,7 +3643,7 @@ PMID:15283675
<head>
<title/>
</head>
<body>&quot;We investigated RB150, a dimer of the selective aminopeptidase A inhibitor, EC33, generated by creating a disulfide bond&quot; PMID:18362226
<body>&quot;We investigated RB150, a dimer of the selective aminopeptidase A inhibitor, EC33, generated by creating a disulfide bond&quot; PMID:18362226
&quot;QGC001 (originally named RB150) is a prodrug of the specific and selective APA inhibitor EC33,...&quot; PMID:24337978)
</body>
</html>
......@@ -4875,7 +4879,7 @@ Angiotensin peptides are metabolized by several subsequent enzymatic steps: Firs
<head>
<title/>
</head>
<body>Although treatment with AGTR1 antagonist (losartan) or AGTR2 agonist (CGP42112A) inhibits tumor progression in several cancer cells, their combined treatment has not been reported. PMID:25014541
<body>Although treatment with AGTR1 antagonist (losartan) or AGTR2 agonist (CGP42112A) inhibits tumor progression in several cancer cells, their combined treatment has not been reported. PMID:25014541
</body>
</html>
</notes>
......@@ -6102,7 +6106,7 @@ PMID:26171856
<head>
<title/>
</head>
<body>Angiotensin II (ANGII) signaling, mediated via angiotensin II receptor type 1 (AGTR1) or type 2 (AGTR2), controls tissue remodeling in fibrosis, but the relevance of AGTR2 remains elusive. PMID:17630322
<body>Angiotensin II (ANGII) signaling, mediated via angiotensin II receptor type 1 (AGTR1) or type 2 (AGTR2), controls tissue remodeling in fibrosis, but the relevance of AGTR2 remains elusive. PMID:17630322
Chronic activation of the myocardial renin angiotensin system (RAS) elevates the local level of angiotensin II (Ang II) thereby inducing pathological cardiac hypertrophy, which contributes to heart failure. The authors report a novel paracrine mechanism between cardiac fibroblasts (CF)s and cardiomyocytes whereby Ang II induces pathological cardiac hypertrophy. In cultured CFs, Ang II treatment enhanced exosome release via the activation of Ang II receptor types 1 (AT1R) and 2 (AT2R), whereas lipopolysaccharide, insulin, endothelin (ET)-1, transforming growth factor beta (TGFbeta)1 or hydrogen peroxide did not. PMID:26497614
Both, ANG II and ANG IV act primarily via the angiotensin II receptor type 1 (AGTR1). PMID:32333398
Ang A has the same affinity to the AT1 receptor as Ang II, but a higher affinity to the AT2 receptor. PMID:17138938
......@@ -6245,7 +6249,7 @@ Ang A has the same affinity to the AT1 receptor as Ang II, but a higher affinity
<head>
<title/>
</head>
<body>Because AT1R seems to be essential for Ang-II–mediated ACE2 internalization, we also tested whether ACE2 and AT1R physically interact. Coimmunoprecipitation experiments confirmed this dimerization in control conditions (Figure 5B, second lane). However, Ang-II treatment decreased this interaction in a time-dependent manner [...]. PMID:25225202
<body>Because AT1R seems to be essential for Ang-II–mediated ACE2 internalization, we also tested whether ACE2 and AT1R physically interact. Coimmunoprecipitation experiments confirmed this dimerization in control conditions (Figure 5B, second lane). However, Ang-II treatment decreased this interaction in a time-dependent manner [...]. PMID:25225202
</body>
</html>
</notes>
......@@ -7487,7 +7491,7 @@ Since angiotensin-(1-12) [Ang-(1-12)] is a non-renin dependent alternate precurs
<head>
<title/>
</head>
<body>&quot;In support of this hypothesis we show that the non-peptide MAS agonist AR234960 increases both mRNA and protein levels of CTGF via ERK1/2 signaling in HEK293-MAS cells and adult human cardiac fibroblasts.&quot; PMID:29287092
<body>&quot;In support of this hypothesis we show that the non-peptide MAS agonist AR234960 increases both mRNA and protein levels of CTGF via ERK1/2 signaling in HEK293-MAS cells and adult human cardiac fibroblasts.&quot; PMID:29287092
</body>
</html>
</notes>
......
<?xml version="1.0" encoding="UTF-8"?>
<sbml xmlns="http://www.sbml.org/sbml/level2/version4" xmlns:celldesigner="http://www.sbml.org/2001/ns/celldesigner" level="2" version="4">
<model metaid="untitled" id="untitled">
<notes>
<html xmlns="http://www.w3.org/1999/xhtml">
<head>
<title/>
</head>
<body>
Authors:
Jan Hasenauer, University of Bonn, Germany
Description:
Proteasome protein degradation, and its inhibition by the Orf10 of SARS-CoV-2
</body>
</html>
</notes>
<annotation>
<celldesigner:extension>
<celldesigner:modelVersion>4.0</celldesigner:modelVersion>
......@@ -7461,7 +7474,7 @@
<head>
<title/>
</head>
<body>Gene obtained by reverse transcription of viral mRNA
<body>Gene obtained by reverse transcription of viral mRNA
</body>
</html>
</notes>
......@@ -8392,7 +8405,7 @@ glycines (10.1126/science.aaw4912). For the complex including Orf10 this is uncl
<head>
<title/>
</head>
<body>Ref:
<body>Ref:
(1) Neddylation: https://doi.org/10.1182/blood-2018-02-829051
(2) Ordering of events (here neddylation before E2 binding): https://doi.org/10.1593/neo.06520
</body>
......
......@@ -6,9 +6,11 @@
<head>
<title/>
</head>
<body>Name: Marcio Acencio
Institution: Luxembourg Centre for Systens Biomedicine, University of Luxembourg
Description: Set of pathways encompassing the replication cycle of SARS-CoV-2: attachment, entry, translation, transcription, replication, assembly and release.
<body>
Author:
Marcio Acencio, Luxembourg Centre for Systens Biomedicine, University of Luxembourg
Description:
Set of pathways encompassing the replication cycle of SARS-CoV-2: attachment, entry, translation, transcription, replication, assembly and release.
</body>
</html>
</notes>
......
Markdown is supported
0% or .
You are about to add 0 people to the discussion. Proceed with caution.
Finish editing this message first!
Please register or to comment