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  1. Article ; Online: AP-1 Subunit JUNB Promotes Invasive Phenotypes in Endometriosis.

    Wilson, Mike R / Reske, Jake J / Chandler, Ronald L

    Reproductive sciences (Thousand Oaks, Calif.)

    2022  Volume 29, Issue 11, Page(s) 3266–3277

    Abstract: Endometriosis is a disease defined by the presence of abnormal endometrium at ectopic sites, causing pain and infertility in 10% of women. Mutations in the chromatin remodeling protein ARID1A (AT-rich interactive domain-containing protein 1A) have been ... ...

    Abstract Endometriosis is a disease defined by the presence of abnormal endometrium at ectopic sites, causing pain and infertility in 10% of women. Mutations in the chromatin remodeling protein ARID1A (AT-rich interactive domain-containing protein 1A) have been identified in endometriosis, particularly in the more severe deep infiltrating endometriosis and ovarian endometrioma subtypes. ARID1A has been shown to regulate chromatin at binding sites of the Activator Protein 1 (AP-1) transcription factor, and AP-1 expression has been shown in multiple endometriosis models. Here, we describe a role for AP-1 subunit JUNB in promoting invasive phenotypes in endometriosis. Through a series of knockdown experiments in the 12Z endometriosis cell line, we show that JUNB expression in endometriosis promotes the expression of epithelial-to-mesenchymal transition genes co-regulated by ARID1A including transcription factors SNAI1 and SNAI2, cell adhesion molecules ICAM1 and VCAM1, and extracellular matrix remodelers LOX and LOXL2. In highly invasive ARID1A-deficient endometriotic cells, co-knockdown of JUNB is sufficient to suppress invasion. These results suggest that AP-1 plays an important role in the progression of invasive endometriosis, and that therapeutic inhibition of AP-1 could prevent the occurrence of deep infiltrating endometriosis.
    MeSH term(s) Humans ; Female ; Endometriosis/genetics ; Endometriosis/metabolism ; Transcription Factor AP-1/metabolism ; Endometrium/metabolism ; Epithelial-Mesenchymal Transition ; Phenotype ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Transcription Factor AP-1 ; JunB protein, human ; Transcription Factors
    Language English
    Publishing date 2022-05-26
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2276411-2
    ISSN 1933-7205 ; 1933-7191
    ISSN (online) 1933-7205
    ISSN 1933-7191
    DOI 10.1007/s43032-022-00974-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: WHO Insulin Access Workshop 21-25 September 2020 - Joint IDF, JDRF and NCDA statement.

    Colagiuri, Stephen / Wilson, Mike

    Diabetes research and clinical practice

    2020  Volume 170, Page(s) 108594

    Language English
    Publishing date 2020-12-11
    Publishing country Ireland
    Document type Editorial
    ZDB-ID 632523-3
    ISSN 1872-8227 ; 0168-8227
    ISSN (online) 1872-8227
    ISSN 0168-8227
    DOI 10.1016/j.diabres.2020.108594
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  3. Article ; Online: ATAC-seq normalization method can significantly affect differential accessibility analysis and interpretation.

    Reske, Jake J / Wilson, Mike R / Chandler, Ronald L

    Epigenetics & chromatin

    2020  Volume 13, Issue 1, Page(s) 22

    Abstract: Background: Chromatin dysregulation is associated with developmental disorders and cancer. Numerous methods for measuring genome-wide chromatin accessibility have been developed in the genomic era to interrogate the function of chromatin regulators. A ... ...

    Abstract Background: Chromatin dysregulation is associated with developmental disorders and cancer. Numerous methods for measuring genome-wide chromatin accessibility have been developed in the genomic era to interrogate the function of chromatin regulators. A recent technique which has gained widespread use due to speed and low input requirements with native chromatin is the Assay for Transposase-Accessible Chromatin, or ATAC-seq. Biologists have since used this method to compare chromatin accessibility between two cellular conditions. However, approaches for calculating differential accessibility can yield conflicting results, and little emphasis is placed on choice of normalization method during differential ATAC-seq analysis, especially when global chromatin alterations might be expected.
    Results: Using an in vivo ATAC-seq data set generated in our recent report, we observed differences in chromatin accessibility patterns depending on the data normalization method used to calculate differential accessibility. This observation was further verified on published ATAC-seq data from yeast. We propose a generalized workflow for differential accessibility analysis using ATAC-seq data. We further show this workflow identifies sites of differential chromatin accessibility that correlate with gene expression and is sensitive to differential analysis using negative controls.
    Conclusions: We argue that researchers should systematically compare multiple normalization methods before continuing with differential accessibility analysis. ATAC-seq users should be aware of the interpretations of potential bias within experimental data and the assumptions of the normalization method implemented.
    MeSH term(s) Algorithms ; Chromatin/chemistry ; Chromatin/genetics ; Chromatin Immunoprecipitation Sequencing/methods ; Chromatin Immunoprecipitation Sequencing/standards ; Data Interpretation, Statistical ; Genome, Fungal ; Saccharomyces cerevisiae
    Chemical Substances Chromatin
    Language English
    Publishing date 2020-04-22
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2462129-8
    ISSN 1756-8935 ; 1756-8935
    ISSN (online) 1756-8935
    ISSN 1756-8935
    DOI 10.1186/s13072-020-00342-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: PIK3CA mutation in endometriotic epithelial cells promotes viperin-dependent inflammatory response to insulin.

    Wilson, Mike R / Harkins, Shannon / Reske, Jake J / Siwicki, Rebecca A / Adams, Marie / Bae-Jump, Victoria L / Teixeira, Jose M / Chandler, Ronald L

    Reproductive biology and endocrinology : RB&E

    2023  Volume 21, Issue 1, Page(s) 43

    Abstract: Endometrial epithelia are known to harbor cancer driver mutations in the absence of any pathologies, including mutations in PIK3CA. Insulin plays an important role in regulating uterine metabolism during pregnancy, and hyperinsulinemia is associated with ...

    Abstract Endometrial epithelia are known to harbor cancer driver mutations in the absence of any pathologies, including mutations in PIK3CA. Insulin plays an important role in regulating uterine metabolism during pregnancy, and hyperinsulinemia is associated with conditions impacting fertility. Hyperinsulinemia also promotes cancer, but the direct action of insulin on mutated endometrial epithelial cells is unknown. Here, we treated 12Z endometriotic epithelial cells carrying the PIK3CA
    MeSH term(s) Female ; Humans ; Class I Phosphatidylinositol 3-Kinases/genetics ; Class I Phosphatidylinositol 3-Kinases/metabolism ; Epithelial Cells/metabolism ; Hyperinsulinism ; Insulin/pharmacology ; Insulin/genetics ; Interferons/genetics ; Mutation ; Neoplasms ; Endometrium/metabolism
    Chemical Substances Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; Insulin ; Interferons (9008-11-1) ; PIK3CA protein, human (EC 2.7.1.137)
    Language English
    Publishing date 2023-05-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 2119215-7
    ISSN 1477-7827 ; 1477-7827
    ISSN (online) 1477-7827
    ISSN 1477-7827
    DOI 10.1186/s12958-023-01094-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: A mouse model of endometriosis mimicking the natural spread of invasive endometrium.

    Wilson, Mike R / Holladay, Jeanne / Chandler, Ronald L

    Human reproduction (Oxford, England)

    2019  Volume 35, Issue 1, Page(s) 58–69

    Abstract: Study question: Is it possible to establish a genetically engineered mouse model (GEMM) of endometriosis that mimics the natural spread of invasive endometrium?: Summary answer: Endometriosis occurs in an ARID1A (AT-rich interactive domain-containing ...

    Abstract Study question: Is it possible to establish a genetically engineered mouse model (GEMM) of endometriosis that mimics the natural spread of invasive endometrium?
    Summary answer: Endometriosis occurs in an ARID1A (AT-rich interactive domain-containing protein 1A) and PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha) mutant GEMM of endometrial dysfunction following salpingectomy.
    What is known already: Although mouse models of endometriosis have long been established, most models rely on intraperitoneal injection of uterine fragments, steroid hormone treatments or the use of immune-compromised mice.
    Study design, size, duration: Mice harboring the lactotransferrin-Cre (LtfCre0/+), Arid1afl, (Gt)R26Pik3ca*H1047R and (Gt)R26mTmG alleles were subject to unilateral salpingectomies at 6 weeks of age. Control (n = 9), LtfCre0/+; (Gt)R26Pik3ca*H1047R; Arid1afl/+ (n = 8) and LtfCre0/+; (Gt)R26Pik3ca*H1047R; Arid1afl/fl (n = 9) were used for the study. The (Gt)R26mTmG allele was used for the purpose of fluorescent lineage tracing of endometrial epithelium. LtfCre0/+; (Gt)R26mTmG (n = 3) and LtfCre0/+; (Gt)R26Pik3ca*H1047R/mTmG; Arid1afl/fl (n = 4) were used for this purpose. Mice were followed until the endpoint of vaginal bleeding at an average time of 17 weeks of age.
    Participants/materials, setting, methods: At 6 weeks of age, mice were subjected to salpingectomy surgery. Mice were followed until the time point of vaginal bleeding (average 17 weeks), or aged for 1 year in the case of control mice. At time of sacrifice, endometriotic lesions, ovaries and uterus were collected for the purpose of histochemical and immunohistochemical analyses. Samples were analyzed for markers of the endometriotic tissue and other relevant biomarkers.
    Main results and the role of chance: Following salpingectomy, LtfCre0/+; (Gt)R26Pik3ca*H1047R/mTmG; Arid1afl/fl mice developed endometriotic lesions, including lesions on the ovary, omentum and abdominal wall. Epithelial glands within lesions were negative for ARID1A and positive for phospho-S6 staining, indicating ARID1A-PIK3CA co-mutation status, and expressed EGFP (enhanced green fluorescent protein), indicating endometrial origins.
    Large-scale data: N/A.
    Limitations, reasons for caution: LtfCre0/+; (Gt)R26Pik3ca*H1047R; Arid1afl/fl mice develop vaginal bleeding as a result of endometrial dysfunction at an average age of 17 weeks and must be sacrificed. Furthermore, while this model mimics the natural spread of endometriotic tissue directly from the uterus to the peritoneum, the data presented do not reject current hypotheses on endometriosis pathogenesis.
    Wider implications of the findings: The idea that endometriosis is the result of abnormal endometrial tissue colonizing the peritoneum via retrograde menstruation has gained widespread support over the past century. However, most models of endometriosis take for granted this possibility, relying on the surgical removal of bulk uterine tissue and subsequent transplantation into the peritoneum. Growing evidence suggests that somatic mutations in ARID1A and PIK3CA are present in the endometrial epithelium. The establishment of a GEMM which mimics the natural spread of endometrium and subsequent lesion formation supports the hypothesis that endometriosis is derived from mutant endometrial epithelium with invasive properties.
    Study funding/competing interest(s): This research was supported by the American Cancer Society PF-17-163-02-DDC (M.R.W.), the Mary Kay Foundation 026-16 (R.L.C.) and the Ovarian Cancer Research Fund Alliance 457446 (R.L.C.). The authors declare no competing interests.
    MeSH term(s) Aged ; Animals ; Disease Models, Animal ; Endometriosis ; Endometrium ; Female ; Humans ; Menstruation Disturbances ; Mice ; Peritoneum
    Language English
    Publishing date 2019-11-29
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 632776-x
    ISSN 1460-2350 ; 0268-1161 ; 1477-741X
    ISSN (online) 1460-2350
    ISSN 0268-1161 ; 1477-741X
    DOI 10.1093/humrep/dez253
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    Zs.B 2892: Show issues Location:
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  6. Book: Poverty

    Wilson, Mike

    (Introducing issues with opposing viewpoints)

    2009  

    Author's details Mike Wilson, book ed
    Series title Introducing issues with opposing viewpoints
    Keywords Poverty ; Armut ; Armutsbekämpfung ; USA ; Welt
    Language English
    Size 152 S., Ill., graph. Darst., Kt.
    Publisher Greenhaven Press
    Publishing place Farminton Hills, Mich
    Document type Book
    Note Includes bibliographical references and index. - Enth. 17 Beitr.
    ISBN 9780737743401 ; 0737743409
    Database ECONomics Information System

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  7. Article ; Online: RunBioSimulations: an extensible web application that simulates a wide range of computational modeling frameworks, algorithms, and formats.

    Shaikh, Bilal / Marupilla, Gnaneswara / Wilson, Mike / Blinov, Michael L / Moraru, Ion I / Karr, Jonathan R

    Nucleic acids research

    2021  Volume 49, Issue W1, Page(s) W597–W602

    Abstract: Comprehensive, predictive computational models have significant potential for science, bioengineering, and medicine. One promising way to achieve more predictive models is to combine submodels of multiple subsystems. To capture the multiple scales of ... ...

    Abstract Comprehensive, predictive computational models have significant potential for science, bioengineering, and medicine. One promising way to achieve more predictive models is to combine submodels of multiple subsystems. To capture the multiple scales of biology, these submodels will likely require multiple modeling frameworks and simulation algorithms. Several community resources are already available for working with many of these frameworks and algorithms. However, the variety and sheer number of these resources make it challenging to find and use appropriate tools for each model, especially for novice modelers and experimentalists. To make these resources easier to use, we developed RunBioSimulations (https://run.biosimulations.org), a single web application for executing a broad range of models. RunBioSimulations leverages community resources, including BioSimulators, a new open registry of simulation tools. These resources currently enable RunBioSimulations to execute nine frameworks and 44 algorithms, and they make RunBioSimulations extensible to additional frameworks and algorithms. RunBioSimulations also provides features for sharing simulations and interactively visualizing their results. We anticipate that RunBioSimulations will foster reproducibility, stimulate collaboration, and ultimately facilitate the creation of more predictive models.
    MeSH term(s) Algorithms ; Computational Biology ; Computer Simulation ; Internet ; Models, Biological ; Software
    Language English
    Publishing date 2021-06-16
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    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/gkab411
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  8. Article ; Online: SWI/SNF Antagonism of PRC2 Mediates Estrogen-Induced Progesterone Receptor Expression.

    Wilson, Mike R / Reske, Jake J / Koeman, Julie / Adams, Marie / Joshi, Niraj R / Fazleabas, Asgerally T / Chandler, Ronald L

    Cells

    2022  Volume 11, Issue 6

    Abstract: Endometrial cancer (EC) is characterized by high estrogen levels unopposed by progesterone. Treatment with progestins is standard for early EC, but the response to progestins is dependent on progesterone receptor (PGR) expression. Here, we show that the ... ...

    Abstract Endometrial cancer (EC) is characterized by high estrogen levels unopposed by progesterone. Treatment with progestins is standard for early EC, but the response to progestins is dependent on progesterone receptor (PGR) expression. Here, we show that the expression of PGR in endometrial epithelial cells is dependent on ARID1A, a DNA-binding subunit of the SWI/SNF chromatin-remodeling complex that is commonly mutated in EC. In endometrial epithelial cells with estrogen receptor overexpression, we find that ARID1A promotes estrogen signaling and regulates common gene expression programs. Normally, endometrial epithelial cells expressing estrogen receptors respond to estrogen by upregulating the PGR. However, when ARID1A expression is lost, upregulation of PGR expression is significantly reduced. This phenomenon can also occur following the loss of the SWI/SNF subunit BRG1, suggesting a role for ARID1A- and BRG1-containing complexes in PGR regulation. We find that PGR is regulated by a bivalent promoter, which harbors both H3K4me3 and H3K27me3 histone tail modifications. H3K27me3 is deposited by EZH2, and inhibition of EZH2 in the context of ARID1A loss results in restoration of estrogen-induced PGR expression. Our results suggest a role for ARID1A deficiency in the loss of PGR in late-stage EC and a therapeutic utility for EZH2 inhibitors in this disease.
    MeSH term(s) Estrogens/pharmacology ; Female ; Histones ; Humans ; Nuclear Proteins/metabolism ; Progestins/pharmacology ; Receptors, Progesterone/metabolism
    Chemical Substances Estrogens ; Histones ; Nuclear Proteins ; Progestins ; Receptors, Progesterone
    Language English
    Publishing date 2022-03-15
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; 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/cells11061000
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Book: Democracy

    Wilson, Mike

    opposing viewpoints

    (Opposing viewpoints series)

    2006  

    Author's details Mike Wilson, book editor
    Series title Opposing viewpoints series
    Keywords Wahlsystem ; Demokratie ; USA
    Language English
    Size 239 S, graph. Darst, 23 cm
    Publisher Greenhaven Press/Thomson Gale
    Publishing place Farmington Hills, MI
    Document type Book
    Note Includes bibliographical references (p. 231-233) and index ; What is the state of democracy? Democracy and freedom are spreading worldwide / David Lowe -- Spread of democracy does not always result in more freedom / Fareed Zakaria -- Spread of democracy benefits developing nations / Carl Gershman -- Spread of democracy causes ethnic strife in developing nations / Amy Chua -- Corporations threaten democracy / Lee Drutman, Charlie Cray -- Corporations can foster democracy / Daniel T. Griswold -- What should be the relationship between religion and democracy? Democracy is based on secular principles / Clark Moeller -- Democracy is based on religious principles / Bill O'Reilly -- Politicians should voice their religious convictions / Jordan Ballor -- Politicians should not voice their religious convictions / Cathy Young -- Islam and democracy are compatible / Fawaz A. Gerges -- Islam and democracy are incompatible / Amir Taheri -- Should U.S. elections be reformed? Electoral college should be abolished / Bradford Plumer -- Electoral college should not be abolished / Tara Ross -- Campaign finance laws should be reformed / Noreena Hertz -- Campaign finance laws should not be reformed / John J. Coleman -- Some felons should be allowed to vote / Steven Carbo et al. -- Felons should not be allowed to vote / Edward Feser -- Should democracy be fostered worldwide? Fostering democracy worldwide will help prevent terrorism / Jennifer L. Windsor -- Democracy alone will not prevent terrorism / F. Gregory Gause III -- Democracy is best for all countries / Natan Sharanksy, interviewed by Jamie Glazov -- Democracy is not best for all countries / James L. Payne -- Democracy will succeed in Iraq / George W. Bush -- Democracy will fail in Iraq / Edwin Black
    ISBN 0737733152 ; 0737733160 ; 9780737733150 ; 9780737733167
    Database Former special subject collection: coastal and deep sea fishing

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  10. Article ; Online: SWI/SNF inactivation in the endometrial epithelium leads to loss of epithelial integrity.

    Reske, Jake J / Wilson, Mike R / Holladay, Jeanne / Wegener, Marc / Adams, Marie / Chandler, Ronald L

    Human molecular genetics

    2020  Volume 29, Issue 20, Page(s) 3412–3430

    Abstract: Although ARID1A mutations are a hallmark feature, mutations in other SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling subunits are also observed in endometrial neoplasms. Here, we interrogated the roles of Brahma/SWI2-related gene 1 (BRG1, ... ...

    Abstract Although ARID1A mutations are a hallmark feature, mutations in other SWI/SNF (SWItch/Sucrose Non-Fermentable) chromatin remodeling subunits are also observed in endometrial neoplasms. Here, we interrogated the roles of Brahma/SWI2-related gene 1 (BRG1, SMARCA4), the SWI/SNF catalytic subunit, in the endometrial epithelium. BRG1 loss affects more than one-third of all active genes and highly overlaps with the ARID1A gene regulatory network. Chromatin immunoprecipitation studies revealed widespread subunit-specific differences in transcriptional regulation, as BRG1 promoter interactions are associated with gene activation, while ARID1A binding is associated with gene repression. However, we identified a physiologically relevant subset of BRG1 and ARID1A co-regulated epithelial identity genes. Mice were genetically engineered to inactivate BRG1 specifically in the endometrial epithelium. Endometrial glands were observed embedded in uterine myometrium, indicating adenomyosis-like phenotypes. Molecular similarities were observed between BRG1 and ARID1A mutant endometrial cells in vivo, including loss of epithelial cell adhesion and junction genes. Collectively, these studies illustrate overlapping contributions of multiple SWI/SNF subunit mutations in the translocation of endometrium to distal sites, with loss of cell integrity being a common feature in SWI/SNF mutant endometrial epithelia.
    MeSH term(s) Animals ; Chromatin Assembly and Disassembly ; DNA Helicases/physiology ; DNA-Binding Proteins/physiology ; Endometrium/metabolism ; Endometrium/pathology ; Epithelium/metabolism ; Epithelium/pathology ; Female ; Gene Expression Regulation ; Mice ; Mice, Knockout ; Mutation ; Nuclear Proteins/physiology ; Transcription Factors/physiology
    Chemical Substances Arid1a protein, mouse ; DNA-Binding Proteins ; Nuclear Proteins ; Transcription Factors ; Smarca4 protein, mouse (EC 3.6.1.-) ; DNA Helicases (EC 3.6.4.-)
    Language English
    Publishing date 2020-10-19
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1108742-0
    ISSN 1460-2083 ; 0964-6906
    ISSN (online) 1460-2083
    ISSN 0964-6906
    DOI 10.1093/hmg/ddaa227
    Database MEDical Literature Analysis and Retrieval System OnLINE

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