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  1. AU="Orozco, Paola"
  2. AU="Zirwas, Matt"

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  1. Article ; Online: RAS and beyond: the many faces of the neurofibromatosis type 1 protein.

    Anastasaki, Corina / Orozco, Paola / Gutmann, David H

    Disease models & mechanisms

    2022  Volume 15, Issue 2

    Abstract: Neurofibromatosis type 1 is a rare neurogenetic syndrome, characterized by pigmentary abnormalities, learning and social deficits, and a predisposition for benign and malignant tumor formation caused by germline mutations in the NF1 gene. With the ... ...

    Abstract Neurofibromatosis type 1 is a rare neurogenetic syndrome, characterized by pigmentary abnormalities, learning and social deficits, and a predisposition for benign and malignant tumor formation caused by germline mutations in the NF1 gene. With the cloning of the NF1 gene and the recognition that the encoded protein, neurofibromin, largely functions as a negative regulator of RAS activity, attention has mainly focused on RAS and canonical RAS effector pathway signaling relevant to disease pathogenesis and treatment. However, as neurofibromin is a large cytoplasmic protein the RAS regulatory domain of which occupies only 10% of its entire coding sequence, both canonical and non-canonical RAS pathway modulation, as well as the existence of potential non-RAS functions, are becoming apparent. In this Special article, we discuss our current understanding of neurofibromin function.
    MeSH term(s) Genes, Neurofibromatosis 1 ; Humans ; Neurofibromatosis 1/genetics ; Neurofibromin 1/genetics ; Proteins ; Signal Transduction/genetics
    Chemical Substances Neurofibromin 1 ; Proteins
    Language English
    Publishing date 2022-02-21
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2451104-3
    ISSN 1754-8411 ; 1754-8403
    ISSN (online) 1754-8411
    ISSN 1754-8403
    DOI 10.1242/dmm.049362
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Development of endomyocardial fibrosis model using a cell patterning technique: In vitro interaction of cell coculture of 3T3 fibroblasts and RL-14 cardiomyocytes.

    Orozco, Paola / Montoya, Yuliet / Bustamante, John

    PloS one

    2020  Volume 15, Issue 2, Page(s) e0229158

    Abstract: Cardiac functions can be altered by changes in the microstructure of the heart, i.e., remodeling of the cardiac tissue, which may activate pathologies such as hypertrophy, dilation, or cardiac fibrosis. Cardiac fibrosis can develop due to an excessive ... ...

    Abstract Cardiac functions can be altered by changes in the microstructure of the heart, i.e., remodeling of the cardiac tissue, which may activate pathologies such as hypertrophy, dilation, or cardiac fibrosis. Cardiac fibrosis can develop due to an excessive deposition of extracellular matrix proteins, which are products of the activation of fibroblasts. In this context, the anatomical-histological change may interfere with the functioning of the cardiac tissue, which requires specialized cells for its operation. The purpose of the present study was to determine the cellular interactions and morphological changes in cocultures of 3T3 fibroblasts and RL-14 cardiomyocytes via the generation of a platform an in vitro model. For this purpose, a platform emulating the biological characteristics of endomyocardial fibrosis was generated using a cell patterning technique to study morphological cellular changes in compact and irregular patterns of fibrosis. It was found that cellular patterns emulating the geometrical distributions of endomyocardial fibrosis generated morphological changes after interaction of the RL-14 cardiomyocytes with the 3T3 fibroblasts. Through this study, it was possible to evaluate biological characteristics such as cell proliferation, adhesion, and spatial distribution, which are directly related to the type of emulated endomyocardial fibrosis. This research concluded that fibroblasts inhibited the proliferation of cardiomyocytes via their interaction with specific microarchitectures. This behavior is consistent with the histopathological distribution of cardiac fibrosis; therefore, the platform developed in this research could be useful for the in vitro assessment of cellular microdomains. This would allow for the experimental determination of interactions with drugs, substrates, or biomaterials within the engineering of cardiac tissues.
    MeSH term(s) 3T3 Cells ; Animals ; Cell Adhesion ; Cell Communication ; Cell Line ; Cell Proliferation ; Coculture Techniques/methods ; Endomyocardial Fibrosis/etiology ; Endomyocardial Fibrosis/pathology ; Fibroblasts/pathology ; Humans ; Mice ; Models, Biological ; Myocytes, Cardiac/pathology
    Language English
    Publishing date 2020-02-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2267670-3
    ISSN 1932-6203 ; 1932-6203
    ISSN (online) 1932-6203
    ISSN 1932-6203
    DOI 10.1371/journal.pone.0229158
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The role of enhancer RNAs in epigenetic regulation of gene expression.

    Rahnamoun, Homa / Orozco, Paola / Lauberth, Shannon M

    Transcription

    2019  Volume 11, Issue 1, Page(s) 19–25

    Abstract: Since the discovery that enhancers can support transcription, the roles of enhancer RNAs have remained largely elusive. We identified that enhancer RNAs interact with and augment bromodomain engagement with acetylated chromatin. Here, we discuss our ... ...

    Abstract Since the discovery that enhancers can support transcription, the roles of enhancer RNAs have remained largely elusive. We identified that enhancer RNAs interact with and augment bromodomain engagement with acetylated chromatin. Here, we discuss our recent findings and the potential mechanisms underlying the regulation and functions of enhancer RNA-bromodomain associations.
    MeSH term(s) Animals ; Enhancer Elements, Genetic/genetics ; Epigenesis, Genetic/genetics ; Gene Expression Regulation/genetics ; Humans ; RNA/genetics
    Chemical Substances RNA (63231-63-0)
    Language English
    Publishing date 2019-12-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2646974-1
    ISSN 2154-1272 ; 2154-1264
    ISSN (online) 2154-1272
    ISSN 2154-1264
    DOI 10.1080/21541264.2019.1698934
    Database MEDical Literature Analysis and Retrieval System OnLINE

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