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  1. Article ; Online: SLFN12 Over-expression Sensitizes Triple Negative Breast Cancer Cells to Chemotherapy Drugs and Radiotherapy.

    Raafat Elsayed, Ahmed Adham / Al-Marsoummi, Sarmad / Vomhof-Dekrey, Emilie E / Basson, Marc D

    Cancer genomics & proteomics

    2022  Volume 19, Issue 3, Page(s) 328–338

    Abstract: Background/aim: Schlafen 12 (SLFN12) expression correlates with survival in triple negative breast cancer (TNBC). SLFN12 slows TNBC proliferation and induces TNBC differentiation, but whether SLFN12 affects the tumoral response to chemotherapy or ... ...

    Abstract Background/aim: Schlafen 12 (SLFN12) expression correlates with survival in triple negative breast cancer (TNBC). SLFN12 slows TNBC proliferation and induces TNBC differentiation, but whether SLFN12 affects the tumoral response to chemotherapy or radiation is unknown.
    Materials and methods: We over-expressed SLFN12 in MDA-MB-231 cells using two different lentiviral vectors. We assessed viable cell numbers via crystal violet assay after treatment with carboplatin, paclitaxel, olaparib, zoledronic acid, camptothecin, or cesium irradiation. CHK1 and CHK2 phosphorylation was assessed by western blot and the effects of inhibiting CHK1/CHK2 by AZD7762 were examined. Key findings were confirmed in Hs578t and BT549 TNBC cells after adenoviral SLFN12 over-expression.
    Results: SLFN12 over-expression increased TNBC sensitivity to radiation, carboplatin, paclitaxel, zoledronic acid, and camptothecin, but not to olaparib. SLFN12 over-expression decreased CHK1 and CHK2 phosphorylation after treatment with the DNA damaging agent camptothecin (CPT). The CHK1/CHK2 inhibitor diminished the significant cytotoxicity difference between over-expression and baseline SLFN12 levels in response to carboplatin.
    Conclusion: SLFN12 increases TNBC sensitivity to DNA-damaging agents at least in part by reducing CHK1/2 phosphorylation. This may contribute to improved survival in patients whose TNBC over-expresses SLFN12. Therefore, SLFN12 levels may be used to customize or predict radiotherapy and chemotherapy effects in TNBC.
    MeSH term(s) Camptothecin/pharmacology ; Camptothecin/therapeutic use ; Carboplatin/pharmacology ; Cell Line, Tumor ; Cell Proliferation ; Checkpoint Kinase 1/genetics ; Humans ; Paclitaxel/pharmacology ; Protein Kinase Inhibitors/pharmacology ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/genetics ; Triple Negative Breast Neoplasms/radiotherapy ; Zoledronic Acid/pharmacology ; Zoledronic Acid/therapeutic use
    Chemical Substances Protein Kinase Inhibitors ; Zoledronic Acid (6XC1PAD3KF) ; Carboplatin (BG3F62OND5) ; Checkpoint Kinase 1 (EC 2.7.11.1) ; Paclitaxel (P88XT4IS4D) ; Camptothecin (XT3Z54Z28A)
    Language English
    Publishing date 2022-04-16
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 2144517-5
    ISSN 1790-6245 ; 1109-6535
    ISSN (online) 1790-6245
    ISSN 1109-6535
    DOI 10.21873/cgp.20323
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5873: Show issues Location:
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  2. Article: ZINC4085554 inhibits cancer cell adhesion by interfering with the interaction of Akt1 and FAK.

    More, Shyam K / Vomhof-Dekrey, Emilie E / Basson, Marc D

    Oncology letters

    2019  Volume 17, Issue 6, Page(s) 5251–5260

    Abstract: Perioperative or circulatory forces enhance disseminated cancer cell adhesiveness by modulating focal adhesion kinase (FAK)-Akt1 interaction. Selectively blocking FAK-Akt1 interaction by a peptide derived from the FAK-Four-point-one, ezrin, radixin, ... ...

    Abstract Perioperative or circulatory forces enhance disseminated cancer cell adhesiveness by modulating focal adhesion kinase (FAK)-Akt1 interaction. Selectively blocking FAK-Akt1 interaction by a peptide derived from the FAK-Four-point-one, ezrin, radixin, moesin (FERM) domain reduces colon cancer cell adhesion
    Language English
    Publishing date 2019-03-27
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 2573196-8
    ISSN 1792-1082 ; 1792-1074
    ISSN (online) 1792-1082
    ISSN 1792-1074
    DOI 10.3892/ol.2019.10192
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The Nrf2-antioxidant response element pathway: a target for regulating energy metabolism.

    Vomhof-Dekrey, Emilie E / Picklo, Matthew J

    The Journal of nutritional biochemistry

    2012  Volume 23, Issue 10, Page(s) 1201–1206

    Abstract: The nuclear factor E2-related factor 2 (Nrf2) is a transcription factor that responds to oxidative stress by binding to the antioxidant response element (ARE) in the promoter of genes coding for antioxidant enzymes like NAD(P)H:quinone oxidoreductase 1 ... ...

    Abstract The nuclear factor E2-related factor 2 (Nrf2) is a transcription factor that responds to oxidative stress by binding to the antioxidant response element (ARE) in the promoter of genes coding for antioxidant enzymes like NAD(P)H:quinone oxidoreductase 1 and proteins for glutathione synthesis. The Nrf2/ARE pathway has nutritional interest owing to its activation by phytochemicals such as sulforaphane. Recently, the Nrf2 pathway was identified as having regulatory functions in mitochondrial biogenesis, adipocyte differentiation and liver energy metabolism. Activation of Nrf2 increases energy metabolism and conversely suppresses lipid synthesis. Lard-based, but not soybean oil-based, high-fat diets reduce mRNA expression of Nrf2 and its downstream targets, suggesting a macronutrient influence on the activation of the Nrf2 pathway and susceptibility to oxidative stress. This review examines data revealing the Nrf2 pathway's regulatory role in energy metabolism at the molecular, cellular and whole animal levels. Understanding the relationship of Nrf2 and energy metabolism in cells, tissues and physiologic systems will provide novel insights for nutritional interventions for obesity and its comorbidities such as diabetes.
    MeSH term(s) Adipocytes/metabolism ; Animals ; Antioxidant Response Elements ; Cell Differentiation ; Cell Line ; Diet, High-Fat ; Energy Metabolism/genetics ; Gene Expression Regulation ; Humans ; Liver/metabolism ; Mitochondrial Turnover ; NAD(P)H Dehydrogenase (Quinone)/genetics ; NAD(P)H Dehydrogenase (Quinone)/metabolism ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress/genetics ; Signal Transduction
    Chemical Substances NF-E2-Related Factor 2 ; NAD(P)H Dehydrogenase (Quinone) (EC 1.6.5.2)
    Language English
    Publishing date 2012-10
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2012.03.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2838: Show issues Location:
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  4. Article: Gene expression profiling and network analysis of peripheral blood monocytes in a chronic model of allergic asthma.

    Dorsam, Glenn P / Hoselton, Scott A / Sandy, Ashley R / Samarasinghe, Amali E / Vomhof-Dekrey, Emilie E / Dorsam, Sheri T / Schuh, Jane M

    Microbiology and immunology

    2010  Volume 54, Issue 9, Page(s) 558–563

    Abstract: The Aspergillus fumigatus mouse model of asthma mimics the characteristics of human fungal asthma, including local and systemic inflammation. Monocyte/macrophage lineage cells direct innate immune responses and guide adaptive responses. To identify gene ... ...

    Abstract The Aspergillus fumigatus mouse model of asthma mimics the characteristics of human fungal asthma, including local and systemic inflammation. Monocyte/macrophage lineage cells direct innate immune responses and guide adaptive responses. To identify gene expression changes in peripheral blood monocytes in the context of fungal allergy, mice were exposed to systemic and intranasal inoculations of fungal antigen (sensitized), and naïve and sensitized animals were challenged intratracheally with live A. fumigatus conidia. Microarray analysis of blood monocytes from allergic versus non-allergic mice showed ≥ twofold modulation of 45 genes. Ingenuity pathway analysis revealed a network of these genes involved in antigen presentation, inflammation, and immune cell trafficking. These data show that allergen sensitization and challenge affects gene expression in peripheral monocytes.
    MeSH term(s) Animals ; Aspergillus fumigatus/immunology ; Asthma/genetics ; Chronic Disease ; Disease Models, Animal ; Gene Expression Profiling ; Gene Regulatory Networks ; Hypersensitivity/genetics ; Mice ; Mice, Inbred BALB C ; Monocytes/metabolism
    Language English
    Publishing date 2010-09-15
    Publishing country Australia
    Document type 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.
    ZDB-ID 224792-6
    ISSN 1348-0421 ; 0385-5600
    ISSN (online) 1348-0421
    ISSN 0385-5600
    DOI 10.1111/j.1348-0421.2010.00242.x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ud II Zs.204: Show issues Location:
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  5. Article ; Online: Regulatory iNKT cells lack expression of the transcription factor PLZF and control the homeostasis of T(reg) cells and macrophages in adipose tissue.

    Lynch, Lydia / Michelet, Xavier / Zhang, Sai / Brennan, Patrick J / Moseman, Ashley / Lester, Chantel / Besra, Gurdyal / Vomhof-Dekrey, Emilie E / Tighe, Mike / Koay, Hui-Fern / Godfrey, Dale I / Leadbetter, Elizabeth A / Sant'Angelo, Derek B / von Andrian, Ulrich / Brenner, Michael B

    Nature immunology

    2014  Volume 16, Issue 1, Page(s) 85–95

    Abstract: Invariant natural killer T cells (iNKT cells) are lipid-sensing innate T cells that are restricted by the antigen-presenting molecule CD1d and express the transcription factor PLZF. iNKT cells accumulate in adipose tissue, where they are anti- ... ...

    Abstract Invariant natural killer T cells (iNKT cells) are lipid-sensing innate T cells that are restricted by the antigen-presenting molecule CD1d and express the transcription factor PLZF. iNKT cells accumulate in adipose tissue, where they are anti-inflammatory, but the factors that contribute to their anti-inflammatory nature, as well as their targets in adipose tissue, are unknown. Here we found that iNKT cells in adipose tissue had a unique transcriptional program and produced interleukin 2 (IL-2) and IL-10. Unlike other iNKT cells, they lacked PLZF but expressed the transcription factor E4BP4, which controlled their IL-10 production. The adipose iNKT cells were a tissue-resident population that induced an anti-inflammatory phenotype in macrophages and, through the production of IL-2, controlled the number, proliferation and suppressor function of regulatory T cells (Treg cells) in adipose tissue. Thus, iNKT cells in adipose tissue are unique regulators of immunological homeostasis in this tissue.
    MeSH term(s) Adipose Tissue/cytology ; Adipose Tissue/immunology ; Animals ; Basic-Leucine Zipper Transcription Factors/genetics ; Basic-Leucine Zipper Transcription Factors/immunology ; Cell Growth Processes/immunology ; Female ; Flow Cytometry ; Gene Expression Regulation ; Homeostasis/immunology ; Interleukin-10/genetics ; Interleukin-10/immunology ; Interleukin-2/genetics ; Interleukin-2/immunology ; Kruppel-Like Transcription Factors/biosynthesis ; Kruppel-Like Transcription Factors/deficiency ; Kruppel-Like Transcription Factors/genetics ; Kruppel-Like Transcription Factors/immunology ; Macrophages/cytology ; Macrophages/immunology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Natural Killer T-Cells/cytology ; Natural Killer T-Cells/immunology ; Natural Killer T-Cells/metabolism ; Promyelocytic Leukemia Zinc Finger Protein ; Specific Pathogen-Free Organisms ; T-Lymphocytes, Regulatory/cytology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism
    Chemical Substances Basic-Leucine Zipper Transcription Factors ; Interleukin-2 ; Kruppel-Like Transcription Factors ; Nfil3 protein, mouse ; Promyelocytic Leukemia Zinc Finger Protein ; Zbtb16 protein, mouse ; Interleukin-10 (130068-27-8)
    Language English
    Publishing date 2014-12-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/ni.3047
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5294: Show issues Location:
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    Zs.MG 42: Show issues

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  6. Article ; Online: Characterization and use of a rabbit-anti-mouse VPAC1 antibody by flow cytometry.

    Hermann, Rebecca J / Van der Steen, Travis / Vomhof-Dekrey, Emilie E / Al-Badrani, Sejaa / Wanjara, Steve B / Failing, Jarrett J / Haring, Jodie S / Dorsam, Glenn P

    Journal of immunological methods

    2011  Volume 376, Issue 1-2, Page(s) 20–31

    Abstract: Vasoactive intestinal peptide receptor-1 signaling in lymphocytes has been shown to regulate chemotaxis, proliferation, apoptosis and differentiation. During T cell activation, VPAC1 mRNA is downregulated, but the effect on its protein levels is less ... ...

    Abstract Vasoactive intestinal peptide receptor-1 signaling in lymphocytes has been shown to regulate chemotaxis, proliferation, apoptosis and differentiation. During T cell activation, VPAC1 mRNA is downregulated, but the effect on its protein levels is less clear. A small number of studies have reported measurement of human VPAC1 by flow cytometry, but murine VPAC1 reagents are unavailable. Therefore, we set out to generate a reliable and highly specific α-mouse VPAC1 polyclonal antibody for use with flow cytometry. After successfully generating a rabbit α-VPAC1 polyclonal antibody (α-mVPAC1 pAb), we characterized its cross-reactivity and showed that it does not recognize other family receptors (mouse VPAC2 and PAC1, and human VPAC1, VPAC2 and PAC1) by flow cytometry. Partial purification of the rabbit α-VPAC1 sera increased the specific-activity of the α-mVPAC1 pAb by 20-fold, and immunofluorescence microscopy (IF) confirmed a plasma membrane subcellular localization for mouse VPAC1 protein. To test the usefulness of this specific α-mVPAC1 pAb, we showed that primary, resting mouse T cells express detectable levels of VPAC1 protein, with little detectable signal from activated T cells, or CD19 B cells. These data support our previously published data showing a downregulation of VPAC1 mRNA during T cell activation. Collectively, we have established a well-characterized, and highly species specific α-mVPAC1 pAb for VPAC1 surface measurement by IF and flow cytometry.
    MeSH term(s) Animals ; Antibodies/genetics ; Antibodies/immunology ; CHO Cells ; Cricetinae ; Flow Cytometry/methods ; Mice ; Microscopy, Fluorescence ; RNA/chemistry ; RNA/genetics ; Rabbits ; Receptors, Vasoactive Intestinal Polypeptide, Type I/genetics ; Receptors, Vasoactive Intestinal Polypeptide, Type I/immunology ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection/methods
    Chemical Substances Antibodies ; Receptors, Vasoactive Intestinal Polypeptide, Type I ; RNA (63231-63-0)
    Language English
    Publishing date 2011-11-04
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 120142-6
    ISSN 1872-7905 ; 0022-1759
    ISSN (online) 1872-7905
    ISSN 0022-1759
    DOI 10.1016/j.jim.2011.10.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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