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  • 1
    Online Resource
    Online Resource
    Ant nests in tank bromeliads — an example of non-specific interaction
    Springer Science and Business Media LLC ; 2000
    In:  Insectes Sociaux Vol. 47, No. 4 ( 2000-11), p. 313-316
    Details
    In: Insectes Sociaux, Springer Science and Business Media LLC, Vol. 47, No. 4 ( 2000-11), p. 313-316
    Type of Medium: Online Resource
    ISSN: 0020-1812
    URL: Article
    DOI: 10.1007/PL00001722
    RVK:
    WA 15000
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2000
    detail.hit.zdb_id: 1463941-5
    SSG: 12
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  • 2
    Online Resource
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    Complement activation induces excessive T cell cytotoxicity in severe COVID-19
    Elsevier BV ; 2022
    In:  Cell Vol. 185, No. 3 ( 2022-02), p. 493-512.e25
    Details
    In: Cell, Elsevier BV, Vol. 185, No. 3 ( 2022-02), p. 493-512.e25
    Type of Medium: Online Resource
    ISSN: 0092-8674
    URL: Article
    DOI: 10.1016/j.cell.2021.12.040
    RVK:
    XA 36269
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 187009-9
    detail.hit.zdb_id: 2001951-8
    SSG: 12
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  • 3
    Online Resource
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    Systems analysis of MAPK signal transduction
    Portland Press Ltd. ; 2008
    In:  Essays in Biochemistry Vol. 45 ( 2008-09-30), p. 95-108
    Details
    In: Essays in Biochemistry, Portland Press Ltd., Vol. 45 ( 2008-09-30), p. 95-108
    Abstract: For more than a decade, the MAPK (mitogen-activated protein kinase) cascade has been studied using mathematical modelling and quantitative experimentation [1]. The MAPK cascade relays the presence of extracellular stimuli such as growth hormones to the nucleus and controls the expression of hundreds of genes. MAPKs control major cell fate decisions such as proliferation, differentiation and apoptosis, mainly by inducing alterations in gene expression. In this chapter, we discuss how systems biology analysis provides insights into the functioning of this cascade. We show how this pathway assists the cell in responding properly to extracellular cues by filtering out sub-threshold stimuli, while efficiently transmitting physiologically relevant inputs. Several different receptors signal through the MAPK pathway even though they elicit opposite biological responses, thus raising the question of how specificity is achieved in MAPK signalling. Experimental studies revealed that specific biological responses are encoded by quantitative aspects of the MAPK signal such as amplitude or duration. We discuss mechanisms that enable the pathway to generate quantitatively different signals, and also explain how different signals are interpreted by the downstream gene expression machinery.
    Type of Medium: Online Resource
    ISSN: 0071-1365 , 1744-1358
    URL: Article
    DOI: 10.1042/bse045095
    RVK:
    WD 1002
    RVK:
    WD 4010
    RVK:
    WD 4000
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2008
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Oncogenic signaling is coupled to colorectal cancer cell differentiation state
    Rockefeller University Press ; 2023
    In:  Journal of Cell Biology Vol. 222, No. 6 ( 2023-06-05)
    Details
    In: Journal of Cell Biology, Rockefeller University Press, Vol. 222, No. 6 ( 2023-06-05)
    Abstract: Colorectal cancer progression is intrinsically linked to stepwise deregulation of the intestinal differentiation trajectory. In this process, sequential mutations of APC, KRAS, TP53, and SMAD4 enable oncogenic signaling and establish the hallmarks of cancer. Here, we use mass cytometry of isogenic human colon organoids and patient-derived cancer organoids to capture oncogenic signaling, cell phenotypes, and differentiation states in a high-dimensional single-cell map. We define a differentiation axis in all tumor progression states from normal to cancer. Our data show that colorectal cancer driver mutations shape the distribution of cells along the differentiation axis. In this regard, subsequent mutations can have stem cell promoting or restricting effects. Individual nodes of the cancer cell signaling network remain coupled to the differentiation state, regardless of the presence of driver mutations. We use single-cell RNA sequencing to link the (phospho-)protein signaling network to transcriptomic states with biological and clinical relevance. Our work highlights how oncogenes gradually shape signaling and transcriptomes during tumor progression.
    Type of Medium: Online Resource
    ISSN: 0021-9525 , 1540-8140
    URL: Article
    DOI: 10.1083/jcb.202204001
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2023
    detail.hit.zdb_id: 1421310-2
    SSG: 12
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  • 5
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    Online Resource
    Oncogenic β-catenin and PIK3CA instruct network states and cancer phenotypes in intestinal organoids
    Rockefeller University Press ; 2017
    In:  Journal of Cell Biology Vol. 216, No. 6 ( 2017-06-05), p. 1567-1577
    Details
    In: Journal of Cell Biology, Rockefeller University Press, Vol. 216, No. 6 ( 2017-06-05), p. 1567-1577
    Abstract: Colorectal cancer is driven by cooperating oncogenic mutations. In this study, we use organotypic cultures derived from transgenic mice inducibly expressing oncogenic β-catenin and/or PIK3CAH1047R to follow sequential changes in cancer-related signaling networks, intestinal cell metabolism, and physiology in a three-dimensional environment mimicking tissue architecture. Activation of β-catenin alone results in the formation of highly clonogenic cells that are nonmotile and prone to undergo apoptosis. In contrast, coexpression of stabilized β-catenin and PIK3CAH1047R gives rise to intestinal cells that are apoptosis-resistant, proliferative, stem cell–like, and motile. Systematic inhibitor treatments of organoids followed by quantitative phenotyping and phosphoprotein analyses uncover key changes in the signaling network topology of intestinal cells after induction of stabilized β-catenin and PIK3CAH1047R. We find that survival and motility of organoid cells are associated with 4EBP1 and AKT phosphorylation, respectively. Our work defines phenotypes, signaling network states, and vulnerabilities of transgenic intestinal organoids as a novel approach to understanding oncogene activities and guiding the development of targeted therapies.
    Type of Medium: Online Resource
    ISSN: 0021-9525 , 1540-8140
    URL: Article
    DOI: 10.1083/jcb.201610058
    RVK:
    WA 15000
    Language: English
    Publisher: Rockefeller University Press
    Publication Date: 2017
    detail.hit.zdb_id: 1421310-2
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Kinetic modeling of stem cell transcriptome dynamics to identify regulatory modules of normal and disturbed neuroectodermal differentiation
    Oxford University Press (OUP) ; 2020
    In:  Nucleic Acids Research Vol. 48, No. 22 ( 2020-12-16), p. 12577-12592
    Details
    In: Nucleic Acids Research, Oxford University Press (OUP), Vol. 48, No. 22 ( 2020-12-16), p. 12577-12592
    Abstract: Thousands of transcriptome data sets are available, but approaches for their use in dynamic cell response modelling are few, especially for processes affected simultaneously by two orthogonal influencing variables. We approached this problem for neuroepithelial development of human pluripotent stem cells (differentiation variable), in the presence or absence of valproic acid (signaling variable). Using few basic assumptions (sequential differentiation states of cells; discrete on/off states for individual genes in these states), and time-resolved transcriptome data, a comprehensive model of spontaneous and perturbed gene expression dynamics was developed. The model made reliable predictions (average correlation of 0.85 between predicted and subsequently tested expression values). Even regulations predicted to be non-monotonic were successfully validated by PCR in new sets of experiments. Transient patterns of gene regulation were identified from model predictions. They pointed towards activation of Wnt signaling as a candidate pathway leading to a redirection of differentiation away from neuroepithelial cells towards neural crest. Intervention experiments, using a Wnt/beta-catenin antagonist, led to a phenotypic rescue of this disturbed differentiation. Thus, our broadly applicable model allows the analysis of transcriptome changes in complex time/perturbation matrices.
    Type of Medium: Online Resource
    ISSN: 0305-1048 , 1362-4962
    URL: Article
    DOI: 10.1093/nar/gkaa1089
    RVK:
    WA 15000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 1472175-2
    SSG: 12
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  • 7
    Online Resource
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    A compendium of ERK targets
    Wiley ; 2017
    In:  FEBS Letters Vol. 591, No. 17 ( 2017-09), p. 2607-2615
    Details
    In: FEBS Letters, Wiley, Vol. 591, No. 17 ( 2017-09), p. 2607-2615
    Abstract: The RAF‐MEK‐ERK cascade is one of the most studied signaling pathways as it controls many vital cellular programs. There has been an immense amount of effort to determine ERK target proteins involved in regulating these programs. Classical biochemical and genetic approaches have elicited hundreds of direct ERK substrates, and with the advent of phospho‐proteomic technologies, numerous studies have expanded the number of ERK target proteins. Here, we compile a comprehensive ERK target phospho‐site archive, in which we gathered information from various research studies, and we provide this archive as an online database to form a searchable compendium of ERK targets.
    Type of Medium: Online Resource
    ISSN: 0014-5793 , 1873-3468
    URL: Issue
    URL: Article
    DOI: 10.1002/feb2.2017.591.issue-17
    DOI: 10.1002/1873-3468.12740
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 1460391-3
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    MicroRNA control of protein expression noise
    American Association for the Advancement of Science (AAAS) ; 2015
    In:  Science Vol. 348, No. 6230 ( 2015-04-03), p. 128-132
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 348, No. 6230 ( 2015-04-03), p. 128-132
    Abstract: MicroRNAs (miRNAs) repress the expression of many genes in metazoans by accelerating messenger RNA degradation and inhibiting translation, thereby reducing the level of protein. However, miRNAs only slightly reduce the mean expression of most targeted proteins, leading to speculation about their role in the variability, or noise, of protein expression. We used mathematical modeling and single-cell reporter assays to show that miRNAs, in conjunction with increased transcription, decrease protein expression noise for lowly expressed genes but increase noise for highly expressed genes. Genes that are regulated by multiple miRNAs show more-pronounced noise reduction. We estimate that hundreds of (lowly expressed) genes in mouse embryonic stem cells have reduced noise due to substantial miRNA regulation. Our findings suggest that miRNAs confer precision to protein expression and thus offer plausible explanations for the commonly observed combinatorial targeting of endogenous genes by multiple miRNAs, as well as the preferential targeting of lowly expressed genes.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aaa1738
    RVK:
    TA 1000
    RVK:
    WA 15000
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2015
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
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  • 9
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    The gene regulatory network of mESC differentiation: a benchmark for reverse engineering methods
    The Royal Society ; 2018
    In:  Philosophical Transactions of the Royal Society B: Biological Sciences Vol. 373, No. 1750 ( 2018-07-05), p. 20170222-
    Details
    In: Philosophical Transactions of the Royal Society B: Biological Sciences, The Royal Society, Vol. 373, No. 1750 ( 2018-07-05), p. 20170222-
    Abstract: A large body of data have accumulated that characterize the gene regulatory network of stem cells. Yet, a comprehensive and integrative understanding of this complex network is lacking. Network reverse engineering methods that use transcriptome data to derive these networks may help to uncover the topology in an unbiased way. Many methods exist that use co-expression to reconstruct networks. However, it remains unclear how these methods perform in the context of stem cell differentiation, as most systematic assessments have been made for regulatory networks of unicellular organisms. Here, we report a systematic benchmark of different reverse engineering methods against functional data. We show that network pruning is critical for reconstruction performance. We also find that performance is similar for algorithms that use different co-expression measures, i.e. mutual information or correlation. In addition, different methods yield very different network topologies, highlighting the challenge of interpreting these resulting networks as a whole. This article is part of the theme issue ‘Designer human tissue: coming to a lab near you’.
    Type of Medium: Online Resource
    ISSN: 0962-8436 , 1471-2970
    URL: Article
    DOI: 10.1098/rstb.2017.0222
    RVK:
    WA 15000
    Language: English
    Publisher: The Royal Society
    Publication Date: 2018
    detail.hit.zdb_id: 1462620-2
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Assessment of stem cell differentiation based on genome-wide expression profiles
    The Royal Society ; 2018
    In:  Philosophical Transactions of the Royal Society B: Biological Sciences Vol. 373, No. 1750 ( 2018-07-05), p. 20170221-
    Details
    In: Philosophical Transactions of the Royal Society B: Biological Sciences, The Royal Society, Vol. 373, No. 1750 ( 2018-07-05), p. 20170221-
    Abstract: In recent years, protocols have been established to differentiate stem and precursor cells into more mature cell types. However, progress in this field has been hampered by difficulties to assess the differentiation status of stem cell-derived cells in an unbiased manner. Here, we present an analysis pipeline based on published data and methods to quantify the degree of differentiation and to identify transcriptional control factors explaining differences from the intended target cells or tissues. The pipeline requires RNA-Seq or gene array data of the stem cell starting population, derived ‘mature’ cells and primary target cells or tissue. It consists of a principal component analysis to represent global expression changes and to identify possible problems of the dataset that require special attention, such as: batch effects; clustering techniques to identify gene groups with similar features; over-representation analysis to characterize biological motifs and transcriptional control factors of the identified gene clusters; and metagenes as well as gene regulatory networks for quantitative cell-type assessment and identification of influential transcription factors. Possibilities and limitations of the analysis pipeline are illustrated using the example of human embryonic stem cell and human induced pluripotent cells to generate ‘hepatocyte-like cells'. The pipeline quantifies the degree of incomplete differentiation as well as remaining stemness and identifies unwanted features, such as colon- and fibroblast-associated gene clusters that are absent in real hepatocytes but typically induced by currently available differentiation protocols. Finally, transcription factors responsible for incomplete and unwanted differentiation are identified. The proposed method is widely applicable and allows an unbiased and quantitative assessment of stem cell-derived cells. This article is part of the theme issue ‘Designer human tissue: coming to a lab near you’.
    Type of Medium: Online Resource
    ISSN: 0962-8436 , 1471-2970
    URL: Article
    DOI: 10.1098/rstb.2017.0221
    RVK:
    WA 15000
    Language: English
    Publisher: The Royal Society
    Publication Date: 2018
    detail.hit.zdb_id: 1462620-2
    SSG: 12
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