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  1. AU="Csályi, Kitti"
  2. AU="Orobello, Nicklas C"
  3. AU=Kim Chang H.
  4. AU="Livingston, Abel"
  5. AU="DeKoven, Mitchell P"
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  1. Book ; Online ; Thesis: Identification of molecular mechanisms of Wnt11 non-canonical signaling in regulation of L-type calcium channel

    Csályi, Kitti Dóra [Verfasser]

    2018  

    Author's details Kitti Dóra Csályi
    Keywords Biowissenschaften, Biologie ; Life Science, Biology
    Subject code sg570
    Language English
    Publisher Freie Universität Berlin
    Publishing place Berlin
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  2. Article: Tissue-Specific Requirement for the GINS Complex During Zebrafish Development.

    Varga, Máté / Csályi, Kitti / Bertyák, István / Menyhárd, Dóra K / Poole, Richard J / Cerveny, Kara L / Kövesdi, Dorottya / Barátki, Balázs / Rouse, Hannah / Vad, Zsuzsa / Hawkins, Thomas A / Stickney, Heather L / Cavodeassi, Florencia / Schwarz, Quenten / Young, Rodrigo M / Wilson, Stephen W

    Frontiers in cell and developmental biology

    2020  Volume 8, Page(s) 373

    Abstract: Efficient and accurate DNA replication is particularly critical in stem and progenitor cells for successful proliferation and survival. The replisome, an amalgam of protein complexes, is responsible for binding potential origins of replication, unwinding ...

    Abstract Efficient and accurate DNA replication is particularly critical in stem and progenitor cells for successful proliferation and survival. The replisome, an amalgam of protein complexes, is responsible for binding potential origins of replication, unwinding the double helix, and then synthesizing complimentary strands of DNA. According to current models, the initial steps of DNA unwinding and opening are facilitated by the CMG complex, which is composed of a GINS heterotetramer that connects Cdc45 with the mini-chromosome maintenance (Mcm) helicase. In this work, we provide evidence that in the absence of GINS function DNA replication is cell autonomously impaired, and we also show that
    Language English
    Publishing date 2020-05-28
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2020.00373
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Ninjurin1 regulates striated muscle growth and differentiation.

    Kny, Melanie / Csályi, Kitti D / Klaeske, Kristin / Busch, Katharina / Meyer, Alexander M / Merks, Anne M / Darm, Katrin / Dworatzek, Elke / Fliegner, Daniela / Baczko, Istvan / Regitz-Zagrosek, Vera / Butter, Christian / Luft, Friedrich C / Panáková, Daniela / Fielitz, Jens

    PloS one

    2019  Volume 14, Issue 5, Page(s) e0216987

    Abstract: Chronic pressure overload due to aortic valve stenosis leads to pathological cardiac hypertrophy and heart failure. Hypertrophy is accompanied by an increase in myocyte surface area, which requires a proportional increase in the number of cell-cell and ... ...

    Abstract Chronic pressure overload due to aortic valve stenosis leads to pathological cardiac hypertrophy and heart failure. Hypertrophy is accompanied by an increase in myocyte surface area, which requires a proportional increase in the number of cell-cell and cell-matrix contacts to withstand enhanced workload. In a proteomic analysis we identified nerve injury-induced protein 1 (Ninjurin1), a 16kDa transmembrane cell-surface protein involved in cell adhesion and nerve repair, to be increased in hypertrophic hearts from patients with aortic stenosis. We hypothesised that Ninjurin1 is involved in myocyte hypertrophy. We analyzed cardiac biopsies from aortic-stenosis patients and control patients undergoing elective heart surgery. We studied cardiac hypertrophy in mice after transverse aortic constriction and angiotensin II infusions, and performed mechanistic analyses in cultured myocytes. We assessed the physiological role of ninjurin1 in zebrafish during heart and skeletal muscle development. Ninjurin1 was increased in hearts of aortic stenosis patients, compared to controls, as well as in hearts from mice with cardiac hypertrophy. Besides the 16kDa Ninjurin1 (Ninjurin1-16) we detected a 24kDa variant of Ninjurin1 (Ninjurin1-24), which was predominantly expressed during myocyte hypertrophy. We disclosed that the higher molecular weight of Ninjurin1-24 was caused by N-glycosylation. Ninjurin1-16 was contained in the cytoplasm of myocytes where it colocalized with stress-fibers. In contrast, Ninjurin1-24 was localized at myocyte membranes. Gain and loss-of-function experiments showed that Ninjurin1-24 plays a role in myocyte hypertrophy and myogenic differentiation in vitro. Reduced levels of ninjurin1 impaired cardiac and skeletal muscle development in zebrafish. We conclude that Ninjurin1 contributes to myocyte growth and differentiation, and that these effects are mainly mediated by N-glycosylated Ninjurin1-24.
    MeSH term(s) Animals ; Aortic Valve Stenosis/genetics ; Aortic Valve Stenosis/pathology ; Cardiomegaly/genetics ; Cardiomegaly/pathology ; Cell Adhesion Molecules, Neuronal/genetics ; Cell Differentiation/genetics ; Disease Models, Animal ; Female ; Humans ; Loss of Function Mutation/genetics ; Male ; Mice ; Muscle Development/genetics ; Muscle, Striated/growth & development ; Muscle, Striated/metabolism ; Muscle, Striated/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Nerve Growth Factors/genetics ; Signal Transduction/genetics ; Zebrafish
    Chemical Substances Cell Adhesion Molecules, Neuronal ; NINJ1 protein, human ; Nerve Growth Factors ; Ninj1 protein, mouse
    Language English
    Publishing date 2019-05-15
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0216987
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: SignaLink3: a multi-layered resource to uncover tissue-specific signaling networks.

    Csabai, Luca / Fazekas, Dávid / Kadlecsik, Tamás / Szalay-Bekő, Máté / Bohár, Balázs / Madgwick, Matthew / Módos, Dezső / Ölbei, Márton / Gul, Lejla / Sudhakar, Padhmanand / Kubisch, János / Oyeyemi, Oyebode James / Liska, Orsolya / Ari, Eszter / Hotzi, Bernadette / Billes, Viktor A / Molnár, Eszter / Földvári-Nagy, László / Csályi, Kitti /
    Demeter, Amanda / Pápai, Nóra / Koltai, Mihály / Varga, Máté / Lenti, Katalin / Farkas, Illés J / Türei, Dénes / Csermely, Péter / Vellai, Tibor / Korcsmáros, Tamás

    Nucleic acids research

    2021  Volume 50, Issue D1, Page(s) D701–D709

    Abstract: Signaling networks represent the molecular mechanisms controlling a cell's response to various internal or external stimuli. Most currently available signaling databases contain only a part of the complex network of intertwining pathways, leaving out key ...

    Abstract Signaling networks represent the molecular mechanisms controlling a cell's response to various internal or external stimuli. Most currently available signaling databases contain only a part of the complex network of intertwining pathways, leaving out key interactions or processes. Hence, we have developed SignaLink3 (http://signalink.org/), a value-added knowledge-base that provides manually curated data on signaling pathways and integrated data from several types of databases (interaction, regulation, localisation, disease, etc.) for humans, and three major animal model organisms. SignaLink3 contains over 400 000 newly added human protein-protein interactions resulting in a total of 700 000 interactions for Homo sapiens, making it one of the largest integrated signaling network resources. Next to H. sapiens, SignaLink3 is the only current signaling network resource to provide regulatory information for the model species Caenorhabditis elegans and Danio rerio, and the largest resource for Drosophila melanogaster. Compared to previous versions, we have integrated gene expression data as well as subcellular localization of the interactors, therefore uniquely allowing tissue-, or compartment-specific pathway interaction analysis to create more accurate models. Data is freely available for download in widely used formats, including CSV, PSI-MI TAB or SQL.
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Databases, Genetic ; Drosophila melanogaster/genetics ; Gene Regulatory Networks/genetics ; Humans ; Protein Interaction Maps/genetics ; Signal Transduction/genetics ; Zebrafish/genetics
    Language English
    Publishing date 2021-10-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkab909
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  5. Article ; Online: SignaFish: A Zebrafish-Specific Signaling Pathway Resource.

    Csályi, Kitti / Fazekas, Dávid / Kadlecsik, Tamás / Türei, Dénes / Gul, Leila / Horváth, Balázs / Módos, Dezső / Demeter, Amanda / Pápai, Nóra / Lenti, Katalin / Csermely, Péter / Vellai, Tibor / Korcsmáros, Tamás / Varga, Máté

    Zebrafish

    2016  Volume 13, Issue 6, Page(s) 541–544

    Abstract: Understanding living systems requires an in-depth knowledge of the signaling networks that drive cellular homeostasis, regulate intercellular communication, and contribute to cell fates during development. Several resources exist to provide high- ... ...

    Abstract Understanding living systems requires an in-depth knowledge of the signaling networks that drive cellular homeostasis, regulate intercellular communication, and contribute to cell fates during development. Several resources exist to provide high-throughput data sets or manually curated interaction information from human or invertebrate model organisms. We previously developed SignaLink, a uniformly curated, multi-layered signaling resource containing information for human and for the model organisms nematode Caenorhabditis elegans and fruit fly Drosophila melanogaster. Until now, the use of the SignaLink database for zebrafish pathway analysis was limited. To overcome this limitation, we created SignaFish ( http://signafish.org ), a fish-specific signaling resource, built using the concept of SignaLink. SignaFish contains more than 200 curation-based signaling interactions, 132 further interactions listed in other resources, and it also lists potential miRNA-based regulatory connections for seven major signaling pathways. From the SignaFish website, users can reach other web resources, such as ZFIN. SignaFish provides signaling or signaling-related interactions that can be examined for each gene or downloaded for each signaling pathway. We believe that the SignaFish resource will serve as a novel navigating point for experimental design and evaluation for the zebrafish community and for researchers focusing on nonmodel fish species, such as cyclids.
    MeSH term(s) Animals ; Databases, Genetic ; Gene Regulatory Networks ; Internet ; Signal Transduction ; Zebrafish/genetics
    Language English
    Publishing date 2016-12
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2156020-1
    ISSN 1557-8542 ; 1545-8547
    ISSN (online) 1557-8542
    ISSN 1545-8547
    DOI 10.1089/zeb.2016.1277
    Database MEDical Literature Analysis and Retrieval System OnLINE

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