1. Home
  2. Projects Index
  3. LiSyM network

LiSyM network

Overview

This comprises the whole LiSyM network

SEEK ID: https://seek.lisym.org/projects/13

Public web page: http://www.lisym.org

Organisms: Rattus norvegicus, Rattus rattus, Mus musculus, Homo sapiens

FAIRDOM PALs: Max Lüdemann, Matthias König, Vincent Moser, Matthias Reichert, Lutz Brusch, Christian Hudert, Janine Koehncke, Madlen Matz-Soja

Project created: 8th Jun 2017

Related items

Claire Barbieux

Projects: Chronic Liver Disease Progression (LiSyM-DP - Pillar II), Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF - Pillar III), LiSyM network

Institutions: Deutsches Krebsforschungszentrum

Richa Batra

Projects: Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF - Pillar III), LiSyM network

Institutions: Helmholtz Zentrum München - Institute of Computational Biology

https://orcid.org/0000-0003-3708-0086
Johannes Bausch

Projects: LiSyM Core Infrastructure and Management (LiSyM-PD), Chronic Liver Disease Progression (LiSyM-DP - Pillar II), Early Metabolic Injury (LiSyM-EMI - Pillar I), Liver Function Diagnostics (LiSyM-LiFuDi - Pillar IV), Model Guided Pharmacotherapy In Chronic Liver Disease (LiSyM-MGP), Molecular Steatosis - Imaging & Modeling (LiSyM-MSIM), Multi-Scale Models for Personalized Liver Function Tests (LiSyM-MM-PLF), Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF - Pillar III), The Hedgehog Signalling Pathway (LiSyM-JGMMS), LiSyM network, LiSyM Scientific Leadership Team

Institutions: University of Freiburg - Institute of Physics, LiSyM programme directorate

https://orcid.org/0000-0002-1003-1682
Ann-Kristin Becker

Projects: Early Metabolic Injury (LiSyM-EMI - Pillar I), LiSyM network

Institutions: University Medicine Greifswald - Institute of Bioinformatics

Nikolaus Berndt

Projects: LiSyM-Krebs Partnering, LiSyM network, Liver Function Diagnostics (LiSyM-LiFuDi - Pillar IV)

Institutions: Charité - Universitätsmedizin Berlin, Institute of Biochemistry, Computational Systems Biochemistry Group

1 hidden item
1 hidden item
SBMC 2018 Book of Abstracts
LiSyM network
No description specified

Creators: None

Contributor: Martin Golebiewski

Download
LPS stimulated BMDM (ELISA analysis TNF-alpha)
LiSyM network
No description specified

Creator: Sonja Kleeschulte

Contributor: Sonja Kleeschulte

Download
Key Visual SBMC 2018 Bremen
LiSyM network
No description specified

Creator: Johannes Bausch

Contributor: Johannes Bausch

Download
Logo SBMC 2018 Bremen
LiSyM network
No description specified

Creator: Johannes Bausch

Contributor: Johannes Bausch

Download
Banner SBMC 2018 Bremen
LiSyM network
No description specified

Creator: Johannes Bausch

Contributor: Johannes Bausch

Download
15 hidden items
Spatio-temporal model of YAP activation during liver regeneration
Early Metabolic Injury (LiSyM-EMI - Pillar I), LiSyM network

For the spatio-temporal dynamics of bile transport, bile canalicular dilation, mechanical stimulation and transduction of YAP signaling during liver regeneration see the open access publication and its appendix:
Meyer et al. (2020) Bile canaliculi remodeling activates YAP via the actin cytoskeleton during liver regeneration. Molecular Systems Biology 16:e8985. https://doi.org/10.15252/msb.20198985

The model format is MorpheusML that can readily be loaded and run in the free and open source software
...

Creator: Lutz Brusch

Contributor: Lutz Brusch

Download
SOP for the exchange of clinical samples and corresponding data between collaboration partners in LiSyM
LiSyM network

The purpose of this document is to define procedures to follow for exchanging the following items between collaboration partners within the LiSyM network:
a) Exchanging samples of human origin obtained from a natural person (i.e. a patient or other human subject).
b) Exchanging material derived from samples of human origin as defined in a).
c) Exchanging associated data describing samples of human origin and derived material as defined in a) and b).
d) Exchanging data derived from samples of human
...

Creators: Martin Golebiewski, Frank Lammert, Wolfgang Müller

Contributor: Martin Golebiewski

Protein modification with ISG15 blocks coxsackievirus pathology by antiviral and metabolic reprogramming.
LiSyM network

Abstract (Expand)

Protein modification with ISG15 (ISGylation) represents a major type I IFN-induced antimicrobial system. Common mechanisms of action and species-specific aspects of ISGylation, however, are still ill … defined and controversial. We used a multiphasic coxsackievirus B3 (CV) infection model with a first wave resulting in hepatic injury of the liver, followed by a second wave culminating in cardiac damage. This study shows that ISGylation sets nonhematopoietic cells into a resistant state, being indispensable for CV control, which is accomplished by synergistic activity of ISG15 on antiviral IFIT1/3 proteins. Concurrent with altered energy demands, ISG15 also adapts liver metabolism during infection. Shotgun proteomics, in combination with metabolic network modeling, revealed that ISG15 increases the oxidative capacity and promotes gluconeogenesis in liver cells. Cells lacking the activity of the ISG15-specific protease USP18 exhibit increased resistance to clinically relevant CV strains, therefore suggesting that stabilizing ISGylation by inhibiting USP18 could be exploited for CV-associated human pathologies.

Authors: M. Kespohl, C. Bredow, K. Klingel, M. Voss, A. Paeschke, M. Zickler, W. Poller, Z. Kaya, Johannes Eckstein, H. Fechner, J. Spranger, M. Fahling, E. K. Wirth, L. Radoshevich, F. Thery, F. Impens, Nikolaus Berndt, K. P. Knobeloch, A. Beling

Date Published: 21st Mar 2020

Journal: Sci Adv

Liver Fibrosis and Metabolic Alterations in Adults With alpha-1-antitrypsin Deficiency Caused by the Pi*ZZ Mutation.
Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF - Pillar III), LiSyM network

Abstract (Expand)

BACKGROUND & AIMS: Alpha-1 antitrypsin deficiency (AATD) is among the most common genetic disorders. Severe AATD is caused by a homozygous mutation in the SERPINA1 gene that encodes the Glu342Lys … substitution (called the Pi*Z mutation, Pi*ZZ genotype). Pi*ZZ carriers may develop lung and liver diseases. Mutation-associated lung disorders have been well studied, but less is known about the effects in liver. We assessed the liver disease burden and associated features in adults with this form of AATD. METHODS: We collected data from 554 Pi*ZZ adults (403 in an exploratory cohort, 151 in a confirmatory cohort), in 9 European countries, with AATD who were homozygous for the Pi*Z mutation, and 234 adults without the Pi*Z mutation (controls), all without pre-existing liver disease. We collected data on demographic parameters, comorbidities, lung- and liver-related health, and blood samples for laboratory analysis. Liver fibrosis was assessed non-invasively via the serum tests Aspartate Aminotransferase to Platelet Ratio Index and HepaScore and via transient elastography. Liver steatosis was determined via transient elastography-based controlled attenuation parameter. We performed histologic analyses of livers from transgenic mice that overexpress the AATD-associated Pi*Z variant. RESULTS: Serum levels of liver enzymes were significantly higher in Pi*ZZ carriers vs controls. Based on non-invasive tests for liver fibrosis, significant fibrosis was suspected in 20%-36% of Pi*ZZ carriers, whereas signs of advanced fibrosis were 9- to 20-fold more common in Pi*ZZ carriers compared to non-carriers. Male sex; age older than 50 years; increased levels of alanine aminotransferase, aspartate aminotransferase, or gamma-glutamyl transferase; and low numbers of platelets were associated with higher liver fibrosis burden. We did not find evidence for a relationship between lung function and liver fibrosis. Controlled attenuation parameter >/=280 dB/m, suggesting severe steatosis, was detected in 39% of Pi*ZZ carriers vs 31% of controls. Carriers of Pi*ZZ had lower serum concentrations of triglyceride and low- and very-low-density lipoprotein cholesterol than controls, suggesting impaired hepatic secretion of lipid. Livers from Pi*Z-overexpressing mice had steatosis and down-regulation of genes involved in lipid secretion. CONCLUSIONS: In studies of AATD adults with the Pi*ZZ mutation, and of Pi*Z-overexpressing mice, we found evidence of liver steatosis and impaired lipid secretion. We identified factors associated with significant liver fibrosis in patients, which could facilitate hepatologic assessment and counseling of individuals who carry the Pi*ZZ mutation. ClinicalTrials.gov Number NCT02929940.

Authors: K. Hamesch, M. Mandorfer, V. M. Pereira, L. S. Moeller, M. Pons, G. E. Dolman, Matthias Reichert, Annika Schneider, V. Woditsch, J. Voss, C. Lindhauer, M. Fromme, I. Spivak, N. Guldiken, B. Zhou, A. Arslanow, B. Schaefer, H. Zoller, E. Aigner, T. Reiberger, M. Wetzel, B. Siegmund, C. Simoes, R. Gaspar, L. Maia, D. Costa, M. Bento-Miranda, J. van Helden, E. Yagmur, D. Bzdok, J. Stolk, W. Gleiber, V. Knipel, W. Windisch, R. Mahadeva, R. Bals, R. Koczulla, M. Barrecheguren, M. Miravitlles, S. Janciauskiene, F. Stickel, Frank Lammert, R. Liberal, J. Genesca, W. J. Griffiths, M. Trauner, A. Krag, Christian Trautwein, P. Strnad

Date Published: 24th May 2019

Journal: Gastroenterology

Robustness and applicability of transcription factor and pathway analysis tools on single-cell RNA-seq data
Chronic Liver Disease Progression (LiSyM-DP - Pillar II), LiSyM network

Abstract (Expand)

Background Many functional analysis tools have been developed to extract functional and mechanistic insight from bulk transcriptome data. With the advent of single-cell RNA sequencing (scRNA-seq), it … is in principle possible to do such an analysis for single cells. However, scRNA-seq data has characteristics such as drop-out events and low library sizes. It is thus not clear if functional TF and pathway analysis tools established for bulk sequencing can be applied to scRNA-seq in a meaningful way. Results To address this question, we perform benchmark studies on simulated and real scRNA-seq data. We include the bulk-RNA tools PROGENy, GO enrichment, and DoRothEA that estimate pathway and transcription factor (TF) activities, respectively, and compare them against the tools SCENIC/AUCell and metaVIPER, designed for scRNA-seq. For the in silico study, we simulate single cells from TF/pathway perturbation bulk RNA-seq experiments. We complement the simulated data with real scRNA-seq data upon CRISPR-mediated knock-out. Our benchmarks on simulated and real data reveal comparable performance to the original bulk data. Additionally, we show that the TF and pathway activities preserve cell type-specific variability by analyzing a mixture sample sequenced with 13 scRNA-seq protocols. We also provide the benchmark data for further use by the community. Conclusions Our analyses suggest that bulk-based functional analysis tools that use manually curated footprint gene sets can be applied to scRNA-seq data, partially outperforming dedicated single-cell tools. Furthermore, we find that the performance of functional analysis tools is more sensitive to the gene sets than to the statistic used.

Authors: Christian Holland, Jovan Tanevski, Javier Perales-Patón, Jan Gleixner, Manu P. Kumar, Elisabetta Mereu, Brian A. Joughin, Oliver Stegle, Douglas A. Lauffenburger, Holger Heyn, Bence Szalai, Julio Saez-Rodriguez

Date Published: 1st Dec 2020

Journal: Genome Biol

Transfer of regulatory knowledge from human to mouse for functional genomics analysis
Chronic Liver Disease Progression (LiSyM-DP - Pillar II), LiSyM network

Abstract (Expand)

Transcriptome profiling followed by differential gene expression analysis often leads to lists of genes that are hard to analyze and interpret. Functional genomics tools are powerful approaches for … downstream analysis, as they summarize the large and noisy gene expression space into a smaller number of biological meaningful features. In particular, methods that estimate the activity of processes by mapping transcripts level to process members are popular. However, footprints of either a pathway or transcription factor (TF) on gene expression show superior performance over mapping-based gene sets. These footprints are largely developed for humans and their usability in the broadly-used model organism Mus musculus is uncertain. Evolutionary conservation of the gene regulatory system suggests that footprints of human pathways and TFs can functionally characterize mice data. In this paper we analyze this hypothesis. We perform a comprehensive benchmark study exploiting two state-of-the-art footprint methods, DoRothEA and an extended version of PROGENy. These methods infer TF and pathway activity, respectively. Our results show that both can recover mouse perturbations, confirming our hypothesis that footprints are conserved between mice and humans. Subsequently, we illustrate the usability of PROGENy and DoRothEA by recovering pathway/TF-disease associations from newly generated disease sets. Additionally, we provide pathway and TF activity scores for a large collection of human and mouse perturbation and disease experiments (2374). We believe that this resource, available for interactive exploration and download (https://saezlab.shinyapps.io/footprint_scores/), can have broad applications including the study of diseases and therapeutics.

Authors: Christian Holland, Bence Szalai, Julio Saez-Rodriguez

Date Published: 1st Sep 2019

Journal: Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms

Editorial: Systems Biology and Bioinformatics in Gastroenterology and Hepatology
LiSyM network

Abstract

Not specified

Authors: Peter Jansen, Kai Breuhahn, Andreas Teufel, Steven Dooley

Date Published: 22nd Nov 2019

Journal: Front. Physiol.

Robustness and applicability of functional genomic tools on scRNA-seq data
Chronic Liver Disease Progression (LiSyM-DP - Pillar II), LiSyM network
No description specified

Creator: Christian Holland

Contributor: Christian Holland

Download
Social media for Academics
LiSyM network

Workshop from LiSyM retreat in January 2020. Additional slides devoted to Social Media for Academics. Developed by Peter Krinenberg from https://naturalscience.careers/

Creator: Olga Vvedenskaya

Contributor: Olga Vvedenskaya

Download
Pathway modeling with SBML (LiSyM modeling workshop)
Multi-Scale Models for Personalized Liver Function Tests (LiSyM-MM-PLF), LiSyM network

We face a reproducibility crisis and computational science, with most published models neither being accessible nor reproducible.
The Systems Biology Markup Language (SBML) is the de facto standard format for encoding pathway based models, which provides a means for exchanging process based models between researchers and tools.
The talk gives an overview of SBML and SBML-based tools.

Creator: Matthias König

Contributor: Matthias König

Download
Participant Abstracts LiSyM Retreat 2020
LiSyM network
No description specified

Creator: Nachiket Vartak

Contributor: Nachiket Vartak

Download
Hedgehog around the clock
The Hedgehog Signalling Pathway (LiSyM-JGMMS), LiSyM PALs, LiSyM network
No description specified

Creator: Madlen Matz-Soja

Contributor: Madlen Matz-Soja

Download
46 hidden items
Systems Biology of Mammalian Cells 2020 (SBMC) - postponed to May 2021

SBMC 2020 was postponed to 10th - 12th of May 2021. Further information will follow soon.

Start Date: 10th May 2021

End Date: 12th May 2021

Event Website: https://sbmc2020.bioquant.uni-heidelberg.de

Country:  DE

City: Heidelberg

21st International Conference on Systems Biology (ICSB) - POSTPONED to 2021

ICSB is one of the largest international conferences on systems biology. Since the first conference in Tokyo in 2000, which was organized by Dr. Hiroaki Kitano, it has been held annually in different countries.

Start Date: 9th Oct 2021

End Date: 14th Oct 2021

Event Website: http://icsb2020.bioscience-ct.net/

Country:  US

City: Hartford, Connecticut

COMBINE 2020 (Computational Modeling in Biology Network Meeting) - VIRTUAL MEETING

The "Computational Modeling in Biology" Network (COMBINE) is an initiative to coordinate the development of the various community standards and formats in systems biology, systems medicine, synthetic biology and related fields. COMBINE 2020 will be a workshop-style event with invited lectures, oral presentations and posters, but also reserving enough time for afternoon breakout sessions to discuss topics around data and model standardization and integration, as well as harmonization and further
...

Start Date: 6th Oct 2020

End Date: 9th Oct 2020

Event Website: http://co.mbine.org/events

Country:  US

City: virtual

HARMONY 2020 (Hackathon on Resources for Modeling in Biology)

The Computational Modeling in Biology Network (COMBINE) is an initiative to coordinate the development of the various community standards and formats in systems biology, synthetic biology and related fields. HARMONY is a codefest-type meeting, with a focus on development of the standards, interoperability and infrastructure. There are generally not many general discussions or oral presentations during HARMONY; instead, the time is devoted to allowing hands-on hacking and interaction between people
...

Start Date: 9th Mar 2020

End Date: 13th Mar 2020

Event Website: http://co.mbine.org/events/HARMONY_2020

Country:  GB

City: Hinxton, Cambridge

LiSyM Jamboree 2020

Registration: https://docs.google.com/document/d/1ZokiSDgj-ekNpzqHnnEl4OMqX57w6LtuB56EEnCMpng/edit

60 Poster boards will be prepared for your poster presentation. Please register your poster in the following link:
https://docs.google.com/document/d/1ej2Mf_5Hkz28xDYEQiYA9cqWAztfmxO2KQn7AB1C-Y8/edit

Start Date: 4th Mar 2020

End Date: 5th Mar 2020

Event Website: Not specified

Country:  DE

City: Berlin

2 hidden items
Poster - Identifying alterations of proliferation signaling in chronic liver disease
Regeneration and Repair in Acute-on-Chronic Liver Failure (LiSyM-ACLF - Pillar III), LiSyM network

Poster for the PhD retreat in Hofgeismar - Svenja Kemmer

Creator: Svenja Kemmer

Contributor: Svenja Kemmer

12 hidden items
Powered by
 (v.1.9.0)
About FAIRDOM | LiSyM | Funding and Programmes | Credits | Imprint
Copyright © 2008 - 2019 The University of Manchester and HITS gGmbH