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  1. AU=Ratner Nancy
  2. AU="Lynch, Jeremy"
  3. AU=Krieger Nancy
  4. AU="Castro, Andrea"
  5. AU="de Souza, H Vieira"
  6. AU="Shou-Hsia Cheng" AU="Shou-Hsia Cheng"
  7. AU="Nawrocki, Eric P."
  8. AU="Su, Bo"
  9. AU="Silva, Carla G Bueno"
  10. AU="Paredes-Vazquez, Jose Gildardo"
  11. AU=Cen Gengyu AU=Cen Gengyu
  12. AU="Gosavi, Suresh"
  13. AU="Cheng, Canhong H"
  14. AU="Sakharkar, Amul"
  15. AU=Liu Bai
  16. AU=Baumeister A
  17. AU="Vasconcellos, Silvio A"
  18. AU="Etenko, A."
  19. AU="Gianluca Dini"
  20. AU="Pabon, Jonathan"
  21. AU="Samalantin, K M"
  22. AU="Babin, Patrick J"
  23. AU="Sesti, Giorgio"

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  1. Artikel: A Farewell Toast to Outgoing Co-Editor in Chief Nancy Helm-Estabrooks

    Ratner, Nan Bernstein

    Seminars in Speech and Language

    (Perseveration in Neurogenic Communication Disorders)

    2004  Band 26, Heft 04, Seite(n) 287–287

    Serientitel Perseveration in Neurogenic Communication Disorders
    Sprache Englisch
    Erscheinungsdatum 2004-01-01
    Erscheinungsort Stuttgart ; New York
    Dokumenttyp Artikel
    ZDB-ID 604960-6
    ISSN 1098-9056 ; 0734-0478
    ISSN (online) 1098-9056
    ISSN 0734-0478
    DOI 10.1055/s-2004-837240
    Datenquelle Thieme Verlag

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  2. Artikel ; Online: Shedding New Light: Novel Therapies for Common Disorders in Children with Neurofibromatosis Type I.

    Pillay-Smiley, Natasha / Fletcher, Jonathan S / de Blank, Peter / Ratner, Nancy

    Pediatric clinics of North America

    2023  Band 70, Heft 5, Seite(n) 937–950

    Abstract: Neurofibromatosis type I (NF1) is a common dominantly inherited disorder, and one of the most common of the RASopathies. Most individuals with NF1 develop plexiform neurofibromas and cutaneous neurofibromas, nerve tumors caused by NF1 loss of function in ...

    Abstract Neurofibromatosis type I (NF1) is a common dominantly inherited disorder, and one of the most common of the RASopathies. Most individuals with NF1 develop plexiform neurofibromas and cutaneous neurofibromas, nerve tumors caused by NF1 loss of function in Schwann cells. Cell culture models and mouse models of NF1 are being used to test drug efficacy in preclinical trials, which led to Food and Drug Administration approval for use of MEK inhibitors to shrink most inoperable plexiform neurofibromas. This article details methods used for testing in preclinical models, and outlines newer models that may identify additional, curative, strategies.
    Mesh-Begriff(e) United States ; Humans ; Animals ; Mice ; Child ; Neurofibromatosis 1/complications ; Neurofibromatosis 1/diagnosis ; Neurofibromatosis 1/drug therapy ; Neurofibroma, Plexiform/complications ; Neurofibroma, Plexiform/drug therapy
    Sprache Englisch
    Erscheinungsdatum 2023-07-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 215711-1
    ISSN 1557-8240 ; 0031-3955
    ISSN (online) 1557-8240
    ISSN 0031-3955
    DOI 10.1016/j.pcl.2023.05.007
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Merlin tumor suppressor function is regulated by PIP2-mediated dimerization.

    Hennigan, Robert F / Thomson, Craig S / Stachowski, Kye / Nassar, Nicolas / Ratner, Nancy

    PloS one

    2023  Band 18, Heft 2, Seite(n) e0281876

    Abstract: Neurofibromatosis Type 2 is an inherited disease characterized by Schwann cell tumors of cranial and peripheral nerves. The NF2 gene encodes Merlin, a member of the ERM family consisting of an N-terminal FERM domain, a central α-helical region, and a C- ... ...

    Abstract Neurofibromatosis Type 2 is an inherited disease characterized by Schwann cell tumors of cranial and peripheral nerves. The NF2 gene encodes Merlin, a member of the ERM family consisting of an N-terminal FERM domain, a central α-helical region, and a C-terminal domain. Changes in the intermolecular FERM-CTD interaction allow Merlin to transition between an open, FERM accessible conformation and a closed, FERM-inaccessible conformation, modulating Merlin activity. Merlin has been shown to dimerize, but the regulation and function Merlin dimerization is not clear. We used a nanobody based binding assay to show that Merlin dimerizes via a FERM-FERM interaction, orientated with each C-terminus close to each other. Patient derived and structural mutants show that dimerization controls interactions with specific binding partners, including HIPPO pathway components, and correlates with tumor suppressor activity. Gel filtration experiments showed that dimerization occurs after a PIP2 mediated transition from closed to open conformation monomers. This process requires the first 18 amino acids of the FERM domain and is inhibited by phosphorylation at serine 518. The discovery that active, open conformation Merlin is a dimer represents a new paradigm for Merlin function with implications for the development of therapies designed to compensate for Merlin loss.
    Mesh-Begriff(e) Humans ; Dimerization ; Genes, Neurofibromatosis 2 ; Genes, Tumor Suppressor ; Neurofibromin 2/genetics ; Protein Structure, Tertiary ; Protein Multimerization
    Chemische Substanzen Neurofibromin 2
    Sprache Englisch
    Erscheinungsdatum 2023-02-21
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0281876
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: The Need for New Treatments Targeting MPNST: The Potential of Strategies Combining MEK Inhibitors with Antiangiogenic Agents.

    González-Muñoz, Teresa / Kim, AeRang / Ratner, Nancy / Peinado, Héctor

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2022  Band 28, Heft 15, Seite(n) 3185–3195

    Abstract: Malignant peripheral nerve sheath tumors (MPNST) are aggressive soft-tissue sarcomas that represent an important clinical challenge, particularly given their strong tendency to relapse and metastasize and their relatively poor response to conventional ... ...

    Abstract Malignant peripheral nerve sheath tumors (MPNST) are aggressive soft-tissue sarcomas that represent an important clinical challenge, particularly given their strong tendency to relapse and metastasize and their relatively poor response to conventional therapies. To date, targeted, noncytotoxic treatments have demonstrated limited clinical success with MPNSTs, highlighting the need to explore other key pathways to find novel, improved therapeutic approaches. Here, we review evidence supporting the crucial role of the RAS/MEK/ERK pathway and angiogenesis in MPNST pathogenesis, and we focus on the potential of therapies targeting these pathways to treat this disease. We also present works suggesting that the combination of MEK inhibitors and antiangiogenic agents could represent a promising therapeutic strategy to manage MPNSTs. In support of this notion, we discuss the preclinical rational and clinical benefits of this combination therapy in other solid tumor types. Finally, we describe other emerging therapeutic approaches that could improve patient outcomes in MPNSTs, such as immune-based therapies.
    Mesh-Begriff(e) Angiogenesis Inhibitors/pharmacology ; Angiogenesis Inhibitors/therapeutic use ; Humans ; Mitogen-Activated Protein Kinase Kinases ; Neoplasm Recurrence, Local/drug therapy ; Nerve Sheath Neoplasms/drug therapy ; Neurofibrosarcoma/drug therapy ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use
    Chemische Substanzen Angiogenesis Inhibitors ; Protein Kinase Inhibitors ; Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2)
    Sprache Englisch
    Erscheinungsdatum 2022-04-20
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-21-3760
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 4223: Hefte anzeigen Standort:
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    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
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  5. Artikel ; Online: iGEAK: an interactive gene expression analysis kit for seamless workflow using the R/shiny platform.

    Choi, Kwangmin / Ratner, Nancy

    BMC genomics

    2019  Band 20, Heft 1, Seite(n) 177

    Abstract: Background: The use of microarrays and RNA-seq technologies is ubiquitous for transcriptome analyses in modern biology. With proper analysis tools, the differential gene expression analysis process can be significantly accelerated. Many open-source ... ...

    Abstract Background: The use of microarrays and RNA-seq technologies is ubiquitous for transcriptome analyses in modern biology. With proper analysis tools, the differential gene expression analysis process can be significantly accelerated. Many open-source programs provide cutting-edge techniques, but these often require programming skills and lack intuitive and interactive or graphical user interfaces. To avoid bottlenecks impeding seamless analysis processing, we have developed an Interactive Gene Expression Analysis Kit, we term iGEAK, focusing on usability and interactivity. iGEAK is designed to be a simple, intuitive, light-weight that contrasts with heavy-duty programs.
    Results: iGEAK is an R/Shiny-based client-side desktop application, providing an interactive gene expression data analysis pipeline for microarray and RNA-seq data. Gene expression data can be intuitively explored using a seamless analysis pipeline consisting of sample selection, differentially expressed gene prediction, protein-protein interaction, and gene set enrichment analyses. For each analysis step, users can easily alter parameters to mine more relevant biological information.
    Conclusion: iGEAK is the outcome of close collaboration with wet-bench biologists who are eager to easily explore, mine, and analyze new or public microarray and RNA-seq data. We designed iGEAK as a gene expression analysis pipeline tool to provide essential analysis steps and a user-friendly interactive graphical user interface. iGEAK enables users without programing knowledge to comfortably perform differential gene expression predictions and downstream analyses. iGEAK packages, manuals, tutorials, sample datasets are available at the iGEAK project homepage ( https://sites.google.com/view/iGEAK ).
    Mesh-Begriff(e) Gene Expression Profiling/methods ; Oligonucleotide Array Sequence Analysis ; Sequence Analysis, RNA ; Workflow
    Sprache Englisch
    Erscheinungsdatum 2019-03-06
    Erscheinungsland England
    Dokumenttyp Journal Article
    ISSN 1471-2164
    ISSN (online) 1471-2164
    DOI 10.1186/s12864-019-5548-x
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Merlin tumor suppressor function is regulated by PIP2-mediated dimerization.

    Robert F Hennigan / Craig S Thomson / Kye Stachowski / Nicolas Nassar / Nancy Ratner

    PLoS ONE, Vol 18, Iss 2, p e

    2023  Band 0281876

    Abstract: Neurofibromatosis Type 2 is an inherited disease characterized by Schwann cell tumors of cranial and peripheral nerves. The NF2 gene encodes Merlin, a member of the ERM family consisting of an N-terminal FERM domain, a central α-helical region, and a C- ... ...

    Abstract Neurofibromatosis Type 2 is an inherited disease characterized by Schwann cell tumors of cranial and peripheral nerves. The NF2 gene encodes Merlin, a member of the ERM family consisting of an N-terminal FERM domain, a central α-helical region, and a C-terminal domain. Changes in the intermolecular FERM-CTD interaction allow Merlin to transition between an open, FERM accessible conformation and a closed, FERM-inaccessible conformation, modulating Merlin activity. Merlin has been shown to dimerize, but the regulation and function Merlin dimerization is not clear. We used a nanobody based binding assay to show that Merlin dimerizes via a FERM-FERM interaction, orientated with each C-terminus close to each other. Patient derived and structural mutants show that dimerization controls interactions with specific binding partners, including HIPPO pathway components, and correlates with tumor suppressor activity. Gel filtration experiments showed that dimerization occurs after a PIP2 mediated transition from closed to open conformation monomers. This process requires the first 18 amino acids of the FERM domain and is inhibited by phosphorylation at serine 518. The discovery that active, open conformation Merlin is a dimer represents a new paradigm for Merlin function with implications for the development of therapies designed to compensate for Merlin loss.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: C5aR plus MEK inhibition durably targets the tumor milieu and reveals tumor cell phagocytosis.

    Perrino, Melissa R / Ahmari, Niousha / Hall, Ashley / Jackson, Mark / Na, Youjin / Pundavela, Jay / Szabo, Sara / Woodruff, Trent M / Dombi, Eva / Kim, Mi-Ok / Köhl, Jörg / Wu, Jianqiang / Ratner, Nancy

    Life science alliance

    2024  Band 7, Heft 5

    Abstract: Plexiform neurofibromas (PNFs) are nerve tumors caused by loss ... ...

    Abstract Plexiform neurofibromas (PNFs) are nerve tumors caused by loss of
    Mesh-Begriff(e) Humans ; Cytophagocytosis ; Macrophages/pathology ; Mitogen-Activated Protein Kinase Kinases ; Neurofibroma, Plexiform/pathology ; Signal Transduction ; Tumor Microenvironment
    Chemische Substanzen Mitogen-Activated Protein Kinase Kinases (EC 2.7.12.2) ; C5AR1 protein, human
    Sprache Englisch
    Erscheinungsdatum 2024-03-08
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 2575-1077
    ISSN (online) 2575-1077
    DOI 10.26508/lsa.202302229
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel: Pharmacogenomic synthetic lethal screens reveal hidden vulnerabilities and new therapeutic approaches for treatment of NF1-associated tumors.

    Williams, Kyle B / Larsson, Alex T / Keller, Bryant J / Chaney, Katherine E / Williams, Rory L / Bhunia, Minu M / Draper, Garrett M / Jubenville, Tyler A / Rathe, Sue K / Moertel, Christopher L / Ratner, Nancy / Largaespada, David A

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Neurofibromatosis Type 1 (NF1) is a common cancer predisposition syndrome, caused by heterozygous loss of function mutations in the tumor suppressor ... ...

    Abstract Neurofibromatosis Type 1 (NF1) is a common cancer predisposition syndrome, caused by heterozygous loss of function mutations in the tumor suppressor gene
    Sprache Englisch
    Erscheinungsdatum 2024-03-25
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2024.03.25.585959
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: After

    Fletcher, Jonathan S / Pundavela, Jay / Ratner, Nancy

    Neuro-oncology advances

    2019  Band 2, Heft Suppl 1, Seite(n) i23–i32

    Abstract: Plexiform neurofibromas (PNF) are peripheral nerve tumors caused by bi-allelic loss ... ...

    Abstract Plexiform neurofibromas (PNF) are peripheral nerve tumors caused by bi-allelic loss of
    Sprache Englisch
    Erscheinungsdatum 2019-11-22
    Erscheinungsland England
    Dokumenttyp Journal Article ; Review
    ZDB-ID 3009682-0
    ISSN 2632-2498 ; 2632-2498
    ISSN (online) 2632-2498
    ISSN 2632-2498
    DOI 10.1093/noajnl/vdz045
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Purinergic signaling in peripheral nervous system glial cells.

    Patritti-Cram, Jennifer / Coover, Robert A / Jankowski, Michael P / Ratner, Nancy

    Glia

    2021  Band 69, Heft 8, Seite(n) 1837–1851

    Abstract: To facilitate analyses of purinergic signaling in peripheral nerve glia, we review recent literature and catalog purinergic receptor mRNA expression in cultured mouse Schwann cells (SCs). Purinergic signaling can decrease developmental SC proliferation, ... ...

    Abstract To facilitate analyses of purinergic signaling in peripheral nerve glia, we review recent literature and catalog purinergic receptor mRNA expression in cultured mouse Schwann cells (SCs). Purinergic signaling can decrease developmental SC proliferation, and promote SC differentiation. The purinergic receptors P2RY2 and P2RX7 are implicated in nerve development and in the ratio of Remak SCs to myelinating SCs in differentiated peripheral nerve. P2RY2, P2RX7, and other receptors are also implicated in peripheral neuropathies and SC tumors. In SC tumors lacking the tumor suppressor NF1, the SC pathway that suppresses SC growth through P2RY2-driven β-arrestin-mediated AKT signaling is aberrant. SC-released purinergic agonists acting through SC and/or neuronal purinergic receptors activate pain responses. In all these settings, purinergic receptor activation can result in calcium-independent and calcium-dependent release of SC ATP and UDP, growth factors, and cytokines that may contribute to disease and nerve repair. Thus, current research suggests that purinergic agonists and/or antagonists might have the potential to modulate peripheral glia function in development and in disease.
    Mesh-Begriff(e) Animals ; Mice ; Neuroglia/metabolism ; Peripheral Nervous System Diseases/metabolism ; Receptors, Purinergic/metabolism ; Schwann Cells/metabolism ; Signal Transduction/physiology
    Chemische Substanzen Receptors, Purinergic
    Sprache Englisch
    Erscheinungsdatum 2021-01-28
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 639414-0
    ISSN 1098-1136 ; 0894-1491
    ISSN (online) 1098-1136
    ISSN 0894-1491
    DOI 10.1002/glia.23969
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2345: Hefte anzeigen Standort:
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