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  1. Book: Mouse as a model organism

    Brakebusch, Cord / Pihlajaniemi, Taina

    from animals to cells

    2011  

    Author's details Cord Brakebusch ; Taina Pihlajaniemi eds
    Language English
    Size XIV, 165 S. : Ill.
    Publisher Springer
    Publishing place Dordrecht u.a.
    Publishing country Netherlands
    Document type Book
    HBZ-ID HT016793494
    ISBN 978-94-007-0749-8 ; 94-007-0749-5 ; 9789400707504 ; 9400707509
    Database Catalogue ZB MED Medicine, Health

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  2. Article ; Online: Rho GTPase Signaling in Health and Disease: A Complex Signaling Network.

    Brakebusch, Cord

    Cells

    2021  Volume 10, Issue 2

    Abstract: Rho GTPases are a family of small G-proteins of the Ras superfamily [ ... ]. ...

    Abstract Rho GTPases are a family of small G-proteins of the Ras superfamily [...].
    MeSH term(s) Animals ; Disease ; Health ; Humans ; RNA, Untranslated/genetics ; RNA, Untranslated/metabolism ; Signal Transduction ; cdc42 GTP-Binding Protein/metabolism ; rho GTP-Binding Proteins/metabolism
    Chemical Substances RNA, Untranslated ; cdc42 GTP-Binding Protein (EC 3.6.5.2) ; rho GTP-Binding Proteins (EC 3.6.5.2)
    Language English
    Publishing date 2021-02-16
    Publishing country Switzerland
    Document type Editorial ; Introductory Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10020401
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: CRISPR Genome Editing: How to Make a Fantastic Method Even Better.

    Brakebusch, Cord

    Cells

    2021  Volume 10, Issue 2

    Abstract: CRISPR genome editing describes targeted mutagenesis involving a programmable DNA scissor consisting of a protein (Cas9) bound to a short RNA [ ... ]. ...

    Abstract CRISPR genome editing describes targeted mutagenesis involving a programmable DNA scissor consisting of a protein (Cas9) bound to a short RNA [...].
    MeSH term(s) Animals ; CRISPR-Cas Systems/genetics ; Gene Editing/methods ; Humans
    Language English
    Publishing date 2021-02-16
    Publishing country Switzerland
    Document type Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10020408
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: A RhoA-mediated biomechanical response in Schwann cells modulates peripheral nerve myelination.

    Seixas, Ana I / Morais, Miguel R G / Brakebusch, Cord / Relvas, João B

    Progress in neurobiology

    2023  Volume 227, Page(s) 102481

    Abstract: Myelin improves axonal conduction velocity and is essential for nerve development and regeneration. In peripheral nerves, Schwann cells depend on bidirectional mechanical and biochemical signaling to form the myelin sheath but the mechanism underlying ... ...

    Abstract Myelin improves axonal conduction velocity and is essential for nerve development and regeneration. In peripheral nerves, Schwann cells depend on bidirectional mechanical and biochemical signaling to form the myelin sheath but the mechanism underlying this process is not understood. Rho GTPases are integrators of "outside-in" signaling that link cytoskeletal dynamics with cellular architecture to regulate morphology and adhesion. Using Schwann cell-specific gene inactivation in the mouse, we discovered that RhoA promotes the initiation of myelination, and is required to both drive and terminate myelin growth at different stages of peripheral myelination, suggesting developmentally-specific modes of action. In Schwann cells, RhoA targets actin filament turnover, via Cofilin 1, actomyosin contractility and cortical actin-membrane attachments. This mechanism couples actin cortex mechanics with the molecular organization of the cell boundary to target specific signaling networks that regulate axon-Schwann cell interaction/adhesion and myelin growth. This work shows that RhoA is a key component of a biomechanical response required to control Schwann cell state transitions for proper myelination of peripheral nerves.
    MeSH term(s) Mice ; Animals ; Actins ; Schwann Cells ; Myelin Sheath/physiology ; Peripheral Nerves/physiology ; Axons
    Chemical Substances Actins
    Language English
    Publishing date 2023-06-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 185535-9
    ISSN 1873-5118 ; 0301-0082
    ISSN (online) 1873-5118
    ISSN 0301-0082
    DOI 10.1016/j.pneurobio.2023.102481
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Analyzing skin tumor development in mice by the DMBA/TPA model.

    Li, Hui / Brakebusch, Cord

    Methods in cell biology

    2020  Volume 163, Page(s) 113–121

    Abstract: Mice are the most important animals to model tumor formation and malignant progression in humans. Chemical induction of skin tumors in mice by treatment with DMBA and TPA is a well-studied tumor induction model that is easy to use and directly applicable ...

    Abstract Mice are the most important animals to model tumor formation and malignant progression in humans. Chemical induction of skin tumors in mice by treatment with DMBA and TPA is a well-studied tumor induction model that is easy to use and directly applicable to genetically modified mice without any mandatory crossing with mice carrying mutations in oncogenes and tumorsuppressors. This article describes the basic protocol for DMBA/TPA induced skin tumor formation and discusses the advantages and limitations of this model, in particular the translatability of results obtained in this system to human cancer patients.
    MeSH term(s) 9,10-Dimethyl-1,2-benzanthracene/toxicity ; Animals ; Humans ; Mice ; Skin Neoplasms/chemically induced ; Skin Neoplasms/genetics ; Tetradecanoylphorbol Acetate
    Chemical Substances 9,10-Dimethyl-1,2-benzanthracene (57-97-6) ; Tetradecanoylphorbol Acetate (NI40JAQ945)
    Language English
    Publishing date 2020-10-03
    Publishing country United States
    Document type Journal Article
    ISSN 0091-679X
    ISSN 0091-679X
    DOI 10.1016/bs.mcb.2020.08.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Senescence regulation by nuclear N-WASP: a role in cancer?

    Li, Hui / Brakebusch, Cord

    Oncoscience

    2019  Volume 6, Issue 7-8, Page(s) 354–356

    Language English
    Publishing date 2019-08-23
    Publishing country United States
    Document type Journal Article
    ISSN 2331-4737
    ISSN 2331-4737
    DOI 10.18632/oncoscience.487
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Rho GTPases in cancer: friend or foe?

    Svensmark, Julius H / Brakebusch, Cord

    Oncogene

    2019  Volume 38, Issue 50, Page(s) 7447–7456

    Abstract: The Rho GTPases RhoA, Rac1, and Cdc42 are important regulators of cytoskeletal dynamics. Although many in vitro and in vivo data indicate tumor-promoting effects of activated Rho GTPases, also tumor suppressive functions have been described, suggesting ... ...

    Abstract The Rho GTPases RhoA, Rac1, and Cdc42 are important regulators of cytoskeletal dynamics. Although many in vitro and in vivo data indicate tumor-promoting effects of activated Rho GTPases, also tumor suppressive functions have been described, suggesting either highly cell-type-specific functions for Rho GTPases in cancer or insufficient cancer models. The availability of a large number of cancer genome-sequencing data by The Cancer Genome Atlas (TCGA) allows for the investigation of Rho GTPase function in human cancers in silico. This information should be used to improve our in vitro and in vivo cancer models, which are essential for a molecular understanding of Rho GTPase function in malignant tumors and for the potential development of cancer drugs targeting Rho GTPase signaling.
    MeSH term(s) Antineoplastic Agents/therapeutic use ; Cytoskeleton/genetics ; Genes, Tumor Suppressor ; Genome, Human/genetics ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Oncogenes/genetics ; Signal Transduction/genetics ; cdc42 GTP-Binding Protein/genetics ; rac1 GTP-Binding Protein/genetics ; rho GTP-Binding Proteins/genetics ; rhoA GTP-Binding Protein/genetics
    Chemical Substances Antineoplastic Agents ; RAC1 protein, human ; RHOA protein, human (124671-05-2) ; cdc42 GTP-Binding Protein (EC 3.6.5.2) ; rac1 GTP-Binding Protein (EC 3.6.5.2) ; rho GTP-Binding Proteins (EC 3.6.5.2) ; rhoA GTP-Binding Protein (EC 3.6.5.2)
    Language English
    Publishing date 2019-08-19
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 639046-8
    ISSN 1476-5594 ; 0950-9232
    ISSN (online) 1476-5594
    ISSN 0950-9232
    DOI 10.1038/s41388-019-0963-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Two Transient Receptor Potential Channels at Focal Adhesions.

    Mitsou, Ioli / Carlson, Cathrine Rein / Multhaupt, Hinke A B / Brakebusch, Cord / Couchman, John R

    The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society

    2023  Volume 71, Issue 9, Page(s) 495–508

    Abstract: Recently there have been reports that identify two transient receptor potential channels in cell-matrix junctions known as focal adhesions. These are the calcium channel TRP canonical 7 and the calcium-activated monovalent ion channel, TRP melastatin ( ... ...

    Abstract Recently there have been reports that identify two transient receptor potential channels in cell-matrix junctions known as focal adhesions. These are the calcium channel TRP canonical 7 and the calcium-activated monovalent ion channel, TRP melastatin (TRPM) 4. Here, we report on the occurrence of TRPM4 in focal adhesions of fibroblasts. Of three commercial antibodies recognizing this channel, only one yielded focal adhesion staining, while the other two did not. The epitope recognized by the focal adhesion-localizing antibody was mapped to the extreme C-terminus of the TRPM4 protein. The other two antibodies bind to N-terminal regions of the TRPM4 proteins. Deletion of the
    MeSH term(s) Humans ; Focal Adhesions ; Antibodies ; Cardiovascular Diseases ; Epitopes ; Fibroblasts
    Chemical Substances Antibodies ; Epitopes
    Language English
    Publishing date 2023-08-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 218208-7
    ISSN 1551-5044 ; 0022-1554
    ISSN (online) 1551-5044
    ISSN 0022-1554
    DOI 10.1369/00221554231194119
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Improving Precise CRISPR Genome Editing by Small Molecules: Is there a Magic Potion?

    Bischoff, Nadja / Wimberger, Sandra / Maresca, Marcello / Brakebusch, Cord

    Cells

    2020  Volume 9, Issue 5

    Abstract: Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) genome editing has become a standard method in molecular biology, for the establishment of genetically modified cellular and animal models, for the identification and validation of drug ... ...

    Abstract Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) genome editing has become a standard method in molecular biology, for the establishment of genetically modified cellular and animal models, for the identification and validation of drug targets in animals, and is heavily tested for use in gene therapy of humans. While the efficiency of CRISPR mediated gene targeting is much higher than of classical targeted mutagenesis, the efficiency of CRISPR genome editing to introduce defined changes into the genome is still low. Overcoming this problem will have a great impact on the use of CRISPR genome editing in academic and industrial research and the clinic. This review will present efforts to achieve this goal by small molecules, which modify the DNA repair mechanisms to facilitate the precise alteration of the genome.
    MeSH term(s) Animals ; CRISPR-Cas Systems/genetics ; Cell Cycle/genetics ; DNA Damage/genetics ; DNA Repair/genetics ; Gene Editing ; Humans ; Small Molecule Libraries/metabolism
    Chemical Substances Small Molecule Libraries
    Language English
    Publishing date 2020-05-25
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells9051318
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: ACK1 is dispensable for development, skin tumor formation, and breast cancer cell proliferation.

    Brandao, Rafael / Kwa, Mei Qi / Yarden, Yossi / Brakebusch, Cord

    FEBS open bio

    2021  Volume 11, Issue 6, Page(s) 1579–1592

    Abstract: Activated Cdc42-associated kinase 1 (ACK1), a widely expressed nonreceptor tyrosine kinase, is often amplified in cancer and has been shown to interact with Cell division cycle 42 (Cdc42), Epidermal growth factor receptor (EGFR), and several other cancer- ...

    Abstract Activated Cdc42-associated kinase 1 (ACK1), a widely expressed nonreceptor tyrosine kinase, is often amplified in cancer and has been shown to interact with Cell division cycle 42 (Cdc42), Epidermal growth factor receptor (EGFR), and several other cancer-relevant molecules, suggesting a possible role for ACK1 in development and tumor formation. To directly address this scenario, we generated mice lacking a functional ACK1 gene (ACK1 ko) using CRISPR genome editing. ACK1 ko mice developed normally, displayed no obvious defect in tissue maintenance, and were fertile. Primary ACK1-null keratinocytes showed normal phosphorylation of EGFR, but a tendency toward reduced activation of AKT serine/threonine kinase 1 (Akt) and Mitogen-activated protein kinase 1 (Erk). DMBA/TPA-induced skin tumor formation did not reveal significant differences between ACK1 ko and control mice. Deletion of the ACK1 gene in the breast cancer cell lines MDA-MB-231, 67NR, MCF7, 4T1, and T47D caused no differences in growth. Furthermore, EGF-induced phosphorylation kinetics of Erk, Akt, and p130Cas were not detectably altered in T47D cells by the loss of ACK1. Finally, loss of ACK1 in MDA-MB-231 and T47D breast cancer cells had a very limited or no effect on directed cell migration. These data do not support a major role for ACK1 in Cdc42 and EGFR signaling, development, or tumor formation.
    MeSH term(s) Animals ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Movement ; Cell Proliferation ; Female ; Mice ; Mice, Knockout ; Protein-Tyrosine Kinases/deficiency ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/metabolism ; Tumor Cells, Cultured
    Chemical Substances Tnk2 protein, mouse (EC 2.7.1.-) ; Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2021-05-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2651702-4
    ISSN 2211-5463 ; 2211-5463
    ISSN (online) 2211-5463
    ISSN 2211-5463
    DOI 10.1002/2211-5463.13149
    Database MEDical Literature Analysis and Retrieval System OnLINE

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