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  1. Article ; Online: Keratins Modulate Cellular Reduction‒Oxidation Homeostasis and Mitochondrial Dynamics.

    Vetter, Alyssa / Beier, Laura-Sophie / Bouameur, Jamal-Eddine / Magin, Thomas M

    The Journal of investigative dermatology

    2021  Volume 142, Issue 8, Page(s) 2264–2267.e6

    MeSH term(s) Cytoskeletal Proteins ; Homeostasis ; Keratins/genetics ; Mitochondria ; Mitochondrial Dynamics
    Chemical Substances Cytoskeletal Proteins ; Keratins (68238-35-7)
    Language English
    Publishing date 2021-12-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1016/j.jid.2021.12.025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Claudin-Targeted Suicide Gene Therapy for Claudin-Overexpressing Tumor Cells by Using Modified Clostridium perfringens Enterotoxin (CPE).

    Beier, Laura-Sophie / Piontek, Jörg / Piontek, Anna / Protze, Jonas / Kobelt, Dennis / Walther, Wolfgang

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2521, Page(s) 173–188

    Abstract: Bacterial toxins gain growing attention as potential cancer treatment due to their potent cytotoxic effects. Among the very different toxins with diverse modes of action, the Clostridium perfringens enterotoxin (CPE) is in focus to treat solid cancers. ... ...

    Abstract Bacterial toxins gain growing attention as potential cancer treatment due to their potent cytotoxic effects. Among the very different toxins with diverse modes of action, the Clostridium perfringens enterotoxin (CPE) is in focus to treat solid cancers. This toxin targets the tight junction proteins claudin-3 and -4 (Cldn-3/4), which are frequently overexpressed in solid cancers. Binding to these claudins induces pore formation in the host cell plasma membrane leading to rapid oncoleaking cell death of tumor cells. Based on this, extending the targeting of CPE beyond Cldn-3/4 is of interest, since other claudins, such as claudin-1 or -5 are often overexpressed in various cancer entities such as non-small-cell lung cancer (NSCLC) or papillary thyroid carcinoma. In this chapter we describe the modification of a CPE-encoding vector by structure-directed mutagenesis to either preferentially target Cldn-1 and -5 or to expand targeting to Cldn1-9 for improved broadened cytotoxic targeting of claudin-overexpressing tumors such as but not limited to lung cancer via CPE gene transfer.
    MeSH term(s) Carcinoma, Non-Small-Cell Lung ; Claudins/genetics ; Claudins/metabolism ; Clostridium perfringens/genetics ; Clostridium perfringens/metabolism ; Enterotoxins/genetics ; Enterotoxins/metabolism ; Genetic Therapy ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/therapy
    Chemical Substances Claudins ; Enterotoxins ; enterotoxin, Clostridium
    Language English
    Publishing date 2022-06-23
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2441-8_9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Pro-inflammatory effects of DEHP in SGBS-derived adipocytes and THP-1 macrophages.

    Schaedlich, Kristina / Beier, Laura-Sophie / Kolbe, Judith / Wabitsch, Martin / Ernst, Jana

    Scientific reports

    2021  Volume 11, Issue 1, Page(s) 7928

    Abstract: In the member countries of the Organization for Economic Co-operation and Development (OECD), overweight and obesity affect the majority of the population. The use of environmental chemicals, such as the plasticizer DEHP, has largely increased ... ...

    Abstract In the member countries of the Organization for Economic Co-operation and Development (OECD), overweight and obesity affect the majority of the population. The use of environmental chemicals, such as the plasticizer DEHP, has largely increased simultaneously with this development. DEHP is an "obesogen" that interferes with normal adipocyte differentiation and energy homeostasis. Obesity in turn is accompanied by chronic low-grade adipose tissue inflammation, leading to metabolic disorders such as type II diabetes. The main actors in adipose tissue inflammation are adipocytes and macrophages. However, the impact of DEHP on adipose tissue inflammation and the crosstalk between adipocytes and macrophages are unknown and the subjects of the current study. The influence of DEHP on inflammation was investigated in human Simpson-Golabi-Behmel syndrome (SGBS)-derived adipocytes and human THP-1 macrophages. The proinflammatory markers IL8, MCP1, IL1β, TNFα and others were measured (qRT-PCR, ELISA) in SGBS-derived adipocytes treated with DEHP [day 0 (d0)-d4; 50 µg/ml] and THP-1 macrophages cultured with conditioned medium (CM) from DEHP-treated adipocytes (SGBS-CM) (from d4 and d8). DEHP exposure led to a proinflammatory state in SGBS-derived adipocytes (e.g., increased secretion of IL8 and MCP1). Surprisingly, exposure of THP-1 macrophages to SGBS-CM did not show DEHP-induced effects. However, we demonstrated that medium containing (pre)adipocyte-secreted factors had a significant impact on the expression and secretion of macrophage and inflammatory markers in THP-1 macrophages in general and led to the significantly increased accumulation of intracellular lipid droplets.
    MeSH term(s) Adipocytes/drug effects ; Adipocytes/metabolism ; Adipocytes/pathology ; Arrhythmias, Cardiac/pathology ; Chemokine CCL2/metabolism ; Culture Media, Conditioned/pharmacology ; Cytokines/metabolism ; Diethylhexyl Phthalate/toxicity ; Fluorescence ; Gene Expression Regulation/drug effects ; Genetic Diseases, X-Linked/pathology ; Gigantism/pathology ; Heart Defects, Congenital/pathology ; Humans ; Inflammation/genetics ; Inflammation/pathology ; Intellectual Disability/pathology ; Interleukin-8/metabolism ; Lipid Droplets/metabolism ; Macrophages/drug effects ; Macrophages/pathology ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; THP-1 Cells
    Chemical Substances CCL2 protein, human ; Chemokine CCL2 ; Culture Media, Conditioned ; Cytokines ; Interleukin-8 ; RNA, Messenger ; Diethylhexyl Phthalate (C42K0PH13C)
    Language English
    Publishing date 2021-04-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-85119-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Claudin targeting as an effective tool for directed barrier modulation of the viable epidermis.

    Beier, Laura-Sophie / Waldow, Ayk / Khomeijani Farahani, Saeed / Mannweiler, Roman / Vidal-Y-Sy, Sabine / Brandner, Johanna M / Piontek, Jörg / Günzel, Dorothee

    Annals of the New York Academy of Sciences

    2022  Volume 1517, Issue 1, Page(s) 251–265

    Abstract: Tight junction (TJ) formation is vital for epidermal barrier function. We aimed to specifically manipulate TJ barriers in the reconstructed human epidermis (RHE) by claudin-1 and -4 knockdown (KD) and by claudin-binding fusion proteins of glutathione S- ... ...

    Abstract Tight junction (TJ) formation is vital for epidermal barrier function. We aimed to specifically manipulate TJ barriers in the reconstructed human epidermis (RHE) by claudin-1 and -4 knockdown (KD) and by claudin-binding fusion proteins of glutathione S-transferase and modified C-terminal fragments of Clostridium perfringens enterotoxin (GST-cCPE). Impedance spectroscopy and tracer permeability imaging were employed for functional barrier assessment and investigation of claudin contribution. KD of claudin-1, but not claudin-4, impaired the paracellular barrier in vitro. Similarly, claudin-binding GST-cCPE variants weakened the paracellular but not the stratum corneum barrier. Combining both TJ targeting methods, we found that claudin-1 targeting by GST-cCPE after claudin-4 KD led to a marked decrease in paracellular barrier properties. Conversely, after claudin-1 KD, GST-cCPE did not further impair the barrier. Comparison of GST-cCPE variants with different claudin-1/claudin-4 affinities, NHS-fluorescein tracer detection, and immunostaining of RHE paraffin sections showed that GST-cCPE variants bind to extrajunctional claudin-1 and -4, which are differentially distributed along the stratum basale-stratum granulosum axis. GST-cCPE binding blocks these claudins, thereby specifically opening the paracellular barrier of RHE. The data indicate a critical role for claudin-1 in regulating paracellular permeability for ions and small molecules in the viable epidermis. Claudin targeting is presented as a proof-of-concept for precise barrier modulation.
    MeSH term(s) Humans ; Claudins/metabolism ; Claudin-1/metabolism ; Claudin-4/metabolism ; Epidermis/metabolism ; Permeability ; Tight Junctions/metabolism ; Claudin-5/metabolism
    Chemical Substances Claudins ; Claudin-1 ; Claudin-4 ; Claudin-5
    Language English
    Publishing date 2022-08-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 211003-9
    ISSN 1749-6632 ; 0077-8923
    ISSN (online) 1749-6632
    ISSN 0077-8923
    DOI 10.1111/nyas.14879
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: cCPE Fusion Proteins as Molecular Probes to Detect Claudins and Tight Junction Dysregulation in Gastrointestinal Cell Lines, Tissue Explants and Patient-Derived Organoids.

    Waldow, Ayk / Beier, Laura-Sophie / Arndt, Janine / Schallenberg, Simon / Vollbrecht, Claudia / Bischoff, Philip / Farrera-Sal, Martí / Loch, Florian N / Bojarski, Christian / Schumann, Michael / Winkler, Lars / Kamphues, Carsten / Ehlen, Lukas / Piontek, Jörg

    Pharmaceutics

    2023  Volume 15, Issue 7

    Abstract: Claudins regulate paracellular permeability, contribute to epithelial polarization and are dysregulated during inflammation and carcinogenesis. Variants of the claudin-binding domain ... ...

    Abstract Claudins regulate paracellular permeability, contribute to epithelial polarization and are dysregulated during inflammation and carcinogenesis. Variants of the claudin-binding domain of
    Language English
    Publishing date 2023-07-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527217-2
    ISSN 1999-4923
    ISSN 1999-4923
    DOI 10.3390/pharmaceutics15071980
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  6. Article ; Online: DEHP deregulates adipokine levels and impairs fatty acid storage in human SGBS-adipocytes.

    Schaedlich, Kristina / Gebauer, Scarlett / Hunger, Luise / Beier, Laura-Sophie / Koch, Holger M / Wabitsch, Martin / Fischer, Bernd / Ernst, Jana

    Scientific reports

    2018  Volume 8, Issue 1, Page(s) 3447

    Abstract: DEHP is a plasticizer which has been used in plastic products of everyday use for decades. Studies in mice and murine cell culture models identified DEHP as an endocrine disruptor that may also act as an obesogen. As this is of high concern in respect of ...

    Abstract DEHP is a plasticizer which has been used in plastic products of everyday use for decades. Studies in mice and murine cell culture models identified DEHP as an endocrine disruptor that may also act as an obesogen. As this is of high concern in respect of the worldwide obesity epidemic, our aim is the translation of these findings into a human model system. On the basis of DOHaD, we investigated the influence of an environmentally relevant dose of DEHP [50 µg/ml] on adipogenesis in the human cell culture model SGBS. Pre-adipocytes were exposed to DEHP and differentiated into mature adipocytes. At different stages of differentiation, markers of adipogenesis like GLUT4, FABP4, LPL and PPARs, and of signaling pathways like AMPK/ACC2, JAK/STAT and MAPK were analyzed. Functional markers like adipokine secretion and triglyceride content as well as ROS production were measured in mature adipocytes. We found significantly lower expression levels of adipogenic markers, a reduction in lipid accumulation, higher leptin- and reduced adiponectin levels in the supernatant of treated adipocytes. Moreover, ROS production was significantly elevated after DEHP-exposure. In conclusion, DEHP led to lower grade of adipogenic differentiation in human SGBS-adipocytes under the chosen conditions.
    MeSH term(s) Adipocytes/drug effects ; Adipocytes/metabolism ; Adipogenesis/drug effects ; Adiponectin/metabolism ; Arrhythmias, Cardiac/metabolism ; Cells, Cultured ; Diethylhexyl Phthalate/toxicity ; Fatty Acids/metabolism ; Genetic Diseases, X-Linked/metabolism ; Gigantism/metabolism ; Heart Defects, Congenital/metabolism ; Humans ; Intellectual Disability/metabolism ; Leptin/metabolism ; Plasticizers/toxicity ; Reactive Oxygen Species/metabolism ; Triglycerides/metabolism
    Chemical Substances Adiponectin ; Fatty Acids ; Leptin ; Plasticizers ; Reactive Oxygen Species ; Triglycerides ; Diethylhexyl Phthalate (C42K0PH13C)
    Language English
    Publishing date 2018-02-22
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-018-21800-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Targeting claudin-overexpressing thyroid and lung cancer by modified Clostridium perfringens enterotoxin.

    Piontek, Anna / Eichner, Miriam / Zwanziger, Denise / Beier, Laura-Sophie / Protze, Jonas / Walther, Wolfgang / Theurer, Sarah / Schmid, Kurt Werner / Führer-Sakel, Dagmar / Piontek, Jörg / Krause, Gerd

    Molecular oncology

    2020  Volume 14, Issue 2, Page(s) 261–276

    Abstract: Clostridium perfringens enterotoxin (CPE) can be used to eliminate carcinoma cells that overexpress on their cell surface CPE receptors - a subset of claudins (e.g., Cldn3 and Cldn4). However, CPE cannot target tumors expressing solely CPE-insensitive ... ...

    Abstract Clostridium perfringens enterotoxin (CPE) can be used to eliminate carcinoma cells that overexpress on their cell surface CPE receptors - a subset of claudins (e.g., Cldn3 and Cldn4). However, CPE cannot target tumors expressing solely CPE-insensitive claudins (such as Cldn1 and Cldn5). To overcome this limitation, structure-guided modifications were used to generate CPE variants that can strongly bind to Cldn1, Cldn2 and/or Cldn5, while maintaining the ability to bind Cldn3 and Cldn4. This enabled (a) targeting of the most frequent endocrine malignancy, namely, Cldn1-overexpressing thyroid cancer, and (b) improved targeting of the most common cancer type worldwide, non-small-cell lung cancer (NSCLC), which is characterized by high expression of several claudins, including Cldn1 and Cldn5. Different CPE variants, including the novel mutant CPE-Mut3 (S231R/S313H), were applied on thyroid cancer (K1 cells) and NSCLC (PC-9 cells) models. In vitro, CPE-Mut3, but not CPEwt, showed Cldn1-dependent binding and cytotoxicity toward K1 cells. For PC-9 cells, CPE-Mut3 improved claudin-dependent cytotoxic targeting, when compared to CPEwt. In vivo, intratumoral injection of CPE-Mut3 in xenograft models bearing K1 or PC-9 tumors induced necrosis and reduced the growth of both tumor types. Thus, directed modification of CPE enables eradication of tumor entities that cannot be targeted by CPEwt, for instance, Cldn1-overexpressing thyroid cancer by using the novel CPE-Mut3.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/therapy ; Cell Line, Tumor ; Cell Survival/drug effects ; Claudin-1/chemistry ; Claudin-1/genetics ; Claudin-1/metabolism ; Claudin-3/chemistry ; Claudin-3/genetics ; Claudin-3/metabolism ; Claudin-4/chemistry ; Claudin-4/genetics ; Claudin-4/metabolism ; Claudin-5/chemistry ; Claudin-5/genetics ; Claudin-5/metabolism ; Claudins/chemistry ; Claudins/genetics ; Claudins/metabolism ; Clostridium perfringens/metabolism ; Enterotoxins/chemistry ; Enterotoxins/pharmacology ; Enterotoxins/therapeutic use ; Female ; Humans ; Immunohistochemistry ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/therapy ; Mice ; Mutagenesis, Site-Directed ; Mutation ; Necrosis/chemically induced ; Protein Binding ; Recombinant Proteins ; Thyroid Neoplasms/drug therapy ; Thyroid Neoplasms/metabolism ; Thyroid Neoplasms/therapy ; Transfection ; Xenograft Model Antitumor Assays
    Chemical Substances Antineoplastic Agents ; CLDN1 protein, human ; CLDN3 protein, human ; CLDN4 protein, human ; CLDN5 protein, human ; Claudin-1 ; Claudin-3 ; Claudin-4 ; Claudin-5 ; Claudins ; Enterotoxins ; Recombinant Proteins ; enterotoxin, Clostridium
    Language English
    Publishing date 2020-01-08
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2415106-3
    ISSN 1878-0261 ; 1574-7891
    ISSN (online) 1878-0261
    ISSN 1574-7891
    DOI 10.1002/1878-0261.12615
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6637: Show issues Location:
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  8. Article ; Online: Use of Modified

    Beier, Laura-Sophie / Rossa, Jan / Woodhouse, Stephen / Bergmann, Sophia / Kramer, Holger B / Protze, Jonas / Eichner, Miriam / Piontek, Anna / Vidal-Y-Sy, Sabine / Brandner, Johanna M / Krause, Gerd / Zitzmann, Nicole / Piontek, Jörg

    International journal of molecular sciences

    2019  Volume 20, Issue 19

    Abstract: Claudins regulate paracellular permeability in different tissues. The claudin-binding domain ... ...

    Abstract Claudins regulate paracellular permeability in different tissues. The claudin-binding domain of
    MeSH term(s) Amino Acid Substitution ; Cell Line, Tumor ; Claudins/chemistry ; Claudins/metabolism ; Enterotoxins/chemistry ; Enterotoxins/metabolism ; Enterotoxins/pharmacology ; Epidermis/metabolism ; Hepacivirus/drug effects ; Hepacivirus/physiology ; Hepatitis C/metabolism ; Hepatitis C/virology ; Hepatocytes/metabolism ; Humans ; Models, Molecular ; Molecular Conformation ; Protein Binding ; Skin/cytology ; Skin/metabolism ; Virus Internalization/drug effects ; Virus Replication
    Chemical Substances Claudins ; Enterotoxins ; enterotoxin, Clostridium
    Language English
    Publishing date 2019-09-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms20194774
    Database MEDical Literature Analysis and Retrieval System OnLINE

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