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  1. Article ; Online: The ephrin signaling pathway regulates morphology and adhesion of mouse granulosa cells in vitro.

    Buensuceso, Adrian V / Deroo, Bonnie J

    Biology of reproduction

    2013  Volume 88, Issue 1, Page(s) 25

    Abstract: Follicle-stimulating hormone (FSH)-mediated changes in granulosa cell adhesion and morphology are essential for preovulatory follicle development, given the dramatic changes in follicle size and granulosa cell number that occur during this transition. ... ...

    Abstract Follicle-stimulating hormone (FSH)-mediated changes in granulosa cell adhesion and morphology are essential for preovulatory follicle development, given the dramatic changes in follicle size and granulosa cell number that occur during this transition. Members of the Eph-ephrin family of cell-positioning and adhesion molecules, a family that consists of ephrin ligands and their Ephrin (Eph) receptors, regulate cell location, adhesion, and migration during embryonic development and tumor growth. However, very little is known about ephrin signaling during folliculogenesis. We have found that FSH increases the expression of several members of the Eph-ephrin family and that this signaling regulates granulosa cell morphology and adhesion. FSH induced increased mRNA levels of the ephrin ligand, ephrin-A5 (Efna5), and its receptors, Eph receptors A3, A5, and A8 (Epha3, Epha5, and Epha8, respectively), in granulosa cells. Immunofluorescence studies indicated that EFNA5 and EPHA5 are located in the membrane of granulosa cells of developing mouse follicles. Eph-ephrin signaling directly affected granulosa cell morphology and adhesion. Recombinant EFNA5 reduced cell spreading and increased cell rounding in mouse primary granulosa cells and in a rat granulosa cell line, whereas EPHA5 reduced granulosa cell adhesion in both model systems. Both FSH and forskolin also increased Efna5 and Epha5 mRNA levels in rat and human granulosa cell lines, indicating that FSH regulates these genes via the cAMP-dependent protein kinase A pathway and that this regulation is conserved across different species. The present study identifies Eph-ephrin signaling as a novel FSH-mediated pathway regulating granulosa cell morphology and adhesion.
    MeSH term(s) Animals ; Cell Line ; Ephrins/genetics ; Ephrins/metabolism ; Female ; Follicle Stimulating Hormone/pharmacology ; Gene Expression Regulation/drug effects ; Granulosa Cells/physiology ; Humans ; Mice ; Multigene Family ; Rats ; Receptors, Eph Family/physiology ; Signal Transduction/physiology ; beta Catenin/genetics ; beta Catenin/metabolism
    Chemical Substances Ephrins ; beta Catenin ; Follicle Stimulating Hormone (9002-68-0) ; Receptors, Eph Family (EC 2.7.10.1)
    Language English
    Publishing date 2013-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1118-6
    ISSN 1529-7268 ; 0006-3363
    ISSN (online) 1529-7268
    ISSN 0006-3363
    DOI 10.1095/biolreprod.112.100123
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Minireview: Estrogen receptor-beta: mechanistic insights from recent studies.

    Deroo, Bonnie J / Buensuceso, Adrian V

    Molecular endocrinology (Baltimore, Md.)

    2010  Volume 24, Issue 9, Page(s) 1703–1714

    Abstract: The discovery of estrogen receptor-beta (ERbeta) in 1996 stimulated great interest in the physiological roles and molecular mechanisms of ERbeta action. We now know that ERbeta plays a major role in mediating estrogen action in several tissues and organ ... ...

    Abstract The discovery of estrogen receptor-beta (ERbeta) in 1996 stimulated great interest in the physiological roles and molecular mechanisms of ERbeta action. We now know that ERbeta plays a major role in mediating estrogen action in several tissues and organ systems, including the ovary, cardiovascular system, brain, and the immune system, and that ERbeta and ERalpha generally play distinct physiological roles in the body. Although significant progress has been made toward understanding the molecular mechanisms of ERbeta action, particularly in vitro, there remains a large gap in our understanding of the mechanisms by which ERbeta elicits its biological functions in a true physiological context.
    MeSH term(s) Animals ; Estrogen Receptor beta/metabolism ; Humans ; Ligands ; Receptor Cross-Talk ; Signal Transduction
    Chemical Substances Estrogen Receptor beta ; Ligands
    Language English
    Publishing date 2010-04-02
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 639167-9
    ISSN 1944-9917 ; 0888-8809
    ISSN (online) 1944-9917
    ISSN 0888-8809
    DOI 10.1210/me.2009-0288
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Expression of extracellular matrix components is disrupted in the immature and adult estrogen receptor β-null mouse ovary.

    Zalewski, Alexandra / Cecchini, Erin L / Deroo, Bonnie J

    PloS one

    2012  Volume 7, Issue 1, Page(s) e29937

    Abstract: Within the ovary, Estrogen Receptor β (ERβ) is localized to the granulosa cells of growing follicles. 17β-estradiol (E2) acting via ERβ augments the actions of follicle stimulating hormone in granulosa cells, leading to granulosa cell differentiation and ...

    Abstract Within the ovary, Estrogen Receptor β (ERβ) is localized to the granulosa cells of growing follicles. 17β-estradiol (E2) acting via ERβ augments the actions of follicle stimulating hormone in granulosa cells, leading to granulosa cell differentiation and formation of a preovulatory follicle. Adult ERβ-null females are subfertile and possess ovaries with reduced numbers of growing follicles and corpora lutea. Because the majority of E2 production by granulosa cells occurs once puberty is reached, a role for ERβ in the ovary prior to puberty has not been well examined. We now provide evidence that lack of ERβ disrupts gene expression as early as post-natal day (PND) 13, and in particular, we identify a number of genes of the extracellular matrix (ECM) that are significantly higher in ERβ-null follicles than in wildtype (WT) follicles. Considerable changes occur to the ECM occur during normal folliculogenesis to allow for the dramatic growth, cellular differentiation, and reorganization of the follicle from the primary to preovulatory stage. Using quantitative PCR and immunofluorescence, we now show that several ECM genes are aberrantly overexpressed in ERβ-null follicles. We find that Collagen11a1, a protein highly expressed in cartilage, is significantly higher in ERβ-null follicles than WT follicles as early as PND 13, and this heightened expression continues through PND 23-29 into adulthood. Similarly, Nidogen 2, a highly conserved basement membrane glycoprotein, is elevated in ERβ-null follicles at PND 13 into adulthood, and is elevated specifically in the ERβ-null focimatrix, a basal lamina-like matrix located between granulosa cells. Focimatrix laminin and Collagen IV expression were also higher in ERβ-null ovaries than in WT ovaries at various ages. Our findings suggest two novel observations: a) that ERβ regulates granulosa cell gene expression ovary prior to puberty, and b) that ERβ regulates expression of ECM components in the mouse ovary.
    MeSH term(s) Aging/genetics ; Aging/metabolism ; Animals ; Estrogen Receptor beta/deficiency ; Estrogen Receptor beta/metabolism ; Extracellular Matrix Proteins/genetics ; Extracellular Matrix Proteins/metabolism ; Female ; Gene Expression Regulation ; Male ; Mice ; Mice, Inbred C57BL ; Ovary/metabolism ; Ovary/pathology ; Protein Transport
    Chemical Substances Estrogen Receptor beta ; Extracellular Matrix Proteins
    Language English
    Publishing date 2012-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0029937
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Ephrin-A5 Is Required for Optimal Fertility and a Complete Ovulatory Response to Gonadotropins in the Female Mouse.

    Buensuceso, Adrian V / Son, Alexander I / Zhou, Renping / Paquet, Marilène / Withers, Benjamin M / Deroo, Bonnie J

    Endocrinology

    2016  Volume 157, Issue 2, Page(s) 942–955

    Abstract: Follicle growth and ovulation involve the coordinated expression of many genes, driven by FSH and LH. Reports indicate that Eph receptors and ephrins are expressed in the ovary, suggesting roles in follicle growth and/or ovulation. We previously reported ...

    Abstract Follicle growth and ovulation involve the coordinated expression of many genes, driven by FSH and LH. Reports indicate that Eph receptors and ephrins are expressed in the ovary, suggesting roles in follicle growth and/or ovulation. We previously reported FSH-induced expression of ephrin-A5 (EFNA5) and 4 of its cognate Eph receptors in mouse granulosa cells. We now report that female mice lacking EFNA5 are subfertile, exhibit a compromised response to LH, and display abnormal ovarian histology after superovulation. Efna5(-/-) females litters were 40% smaller than controls, although no difference in litter frequency was detected. The ovarian response to superovulation was also compromised in Efna5(-/-) females, with 37% fewer oocytes ovulated than controls. These results corresponded with a reduction in ovarian mRNA levels of several LH-responsive genes, including Pgr, Ptgs2, Tnfaip6, Ereg, Btc, and Adamts4, suggesting that Efna5(-/-) ovaries exhibit a partially attenuated response to LH. Histopathological analysis indicated that superovulated Efna5(-/-) females exhibited numerous ovarian defects, including intraovarian release of cumulus oocyte complexes, increased incidence of oocytes trapped within luteinized follicles, granulosa cell and follicular fluid emboli, fibrin thrombi, and interstitial hemorrhage. In addition, adult Efna5(-/-) ovaries exhibited a 4-fold increase in multioocyte follicles compared with controls, although no difference was detected in 3-week-old mice, suggesting the possibility of follicle merging. Our observations indicate that loss of EFNA5 in female mice results in subfertility and imply that Eph-ephrin signaling may also play a previously unidentified role in the regulation of fertility in women.
    MeSH term(s) ADAM Proteins/genetics ; ADAM Proteins/metabolism ; ADAMTS4 Protein ; Animals ; Betacellulin/genetics ; Betacellulin/metabolism ; Cell Adhesion Molecules/genetics ; Cell Adhesion Molecules/metabolism ; Corpus Luteum/pathology ; Cumulus Cells/pathology ; Cyclooxygenase 2/genetics ; Cyclooxygenase 2/metabolism ; Ephrin-A5/genetics ; Ephrin-A5/metabolism ; Epiregulin/genetics ; Epiregulin/metabolism ; Female ; Fertility/genetics ; Gonadotropins ; Granulosa Cells/pathology ; Infertility/genetics ; Luteinization ; Mice ; Mice, Knockout ; Ovarian Follicle/pathology ; Ovary/metabolism ; Ovary/pathology ; Ovulation/genetics ; Procollagen N-Endopeptidase/genetics ; Procollagen N-Endopeptidase/metabolism ; RNA, Messenger/metabolism ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Superovulation/genetics
    Chemical Substances Betacellulin ; Btc protein, mouse ; Cell Adhesion Molecules ; Ephrin-A5 ; Epiregulin ; Ereg protein, mouse ; Gonadotropins ; RNA, Messenger ; Tnfaip6 protein, mouse ; Ptgs2 protein, mouse (EC 1.14.99.-) ; Cyclooxygenase 2 (EC 1.14.99.1) ; ADAM Proteins (EC 3.4.24.-) ; Procollagen N-Endopeptidase (EC 3.4.24.14) ; ADAMTS4 Protein (EC 3.4.24.82) ; Adamts4 protein, mouse (EC 3.4.24.82)
    Language English
    Publishing date 2016-02
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 427856-2
    ISSN 1945-7170 ; 0013-7227
    ISSN (online) 1945-7170
    ISSN 0013-7227
    DOI 10.1210/en.2015-1216
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Evaluating the effectiveness of cancer drug sensitization in vitro and in vivo.

    Rytelewski, Mateusz / Buensuceso, Adrian / Leong, Hon S / Deroo, Bonnie J / Chambers, Ann F / Koropatnick, James

    Journal of visualized experiments : JoVE

    2015  , Issue 96

    Abstract: Due to the high level of heterogeneity and mutations inherent in human cancers, single agent therapies, or combination regimens which target the same pathway, are likely to fail. Emphasis must be placed upon the inhibition of pathways that are ... ...

    Abstract Due to the high level of heterogeneity and mutations inherent in human cancers, single agent therapies, or combination regimens which target the same pathway, are likely to fail. Emphasis must be placed upon the inhibition of pathways that are responsible for intrinsic and/or adaptive resistance to therapy. An active field of investigation is the development and testing of DNA repair inhibitors that promote the action of, and prevent resistance to, commonly used chemotherapy and radiotherapy. We used a novel protocol to evaluate the effectiveness of BRCA2 inhibition as a means to sensitize tumor cells to the DNA damaging drug cisplatin. Tumor cell metabolism (acidification and respiration) was monitored in real-time for a period of 72 hr to delineate treatment effectiveness on a minute by minute basis. In combination, we performed an assessment of metastatic frequency using a chicken embryo chorioallantoic membrane (CAM) model of extravasation and invasion. This protocol addresses some of the weaknesses of commonly used in vitro and in vivo methods to evaluate novel cancer therapy regimens. It can be used in addition to common methods such as cell proliferation assays, cell death assays, and in vivo murine xenograft studies, to more closely discriminate amongst candidate targets and agents, and select only the most promising candidates for further development.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; BRCA2 Protein/genetics ; Chick Embryo ; Chorioallantoic Membrane/drug effects ; Cisplatin/administration & dosage ; Cisplatin/pharmacology ; Drug Screening Assays, Antitumor/methods ; Drug Synergism ; Humans ; Mice ; Neoplasm Metastasis ; Neoplasms/drug therapy ; Neoplasms/pathology ; Oligonucleotides, Antisense/administration & dosage ; Oligonucleotides, Antisense/genetics ; Oligonucleotides, Antisense/pharmacology
    Chemical Substances Antineoplastic Agents ; BRCA2 Protein ; BRCA2 protein, human ; Oligonucleotides, Antisense ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2015-02-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
    ISSN 1940-087X
    ISSN (online) 1940-087X
    DOI 10.3791/52388
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Estrogen receptors and human disease.

    Deroo, Bonnie J / Korach, Kenneth S

    The Journal of clinical investigation

    2006  Volume 116, Issue 3, Page(s) 561–570

    Abstract: Estrogens influence many physiological processes in mammals, including but not limited to reproduction, cardiovascular health, bone integrity, cognition, and behavior. Given this widespread role for estrogen in human physiology, it is not surprising that ...

    Abstract Estrogens influence many physiological processes in mammals, including but not limited to reproduction, cardiovascular health, bone integrity, cognition, and behavior. Given this widespread role for estrogen in human physiology, it is not surprising that estrogen is also implicated in the development or progression of numerous diseases, which include but are not limited to various types of cancer (breast, ovarian, colorectal, prostate, endometrial), osteoporosis, neurodegenerative diseases, cardiovascular disease, insulin resistance, lupus erythematosus, endometriosis, and obesity. In many of these diseases, estrogen mediates its effects through the estrogen receptor (ER), which serves as the basis for many therapeutic interventions. This Review will describe diseases in which estrogen, through the ER, plays a role in the development or severity of disease.
    MeSH term(s) Animals ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/metabolism ; Obesity/metabolism ; Osteoporosis/genetics ; Osteoporosis/metabolism ; Receptors, Estrogen/chemistry ; Receptors, Estrogen/genetics ; Receptors, Estrogen/physiology
    Chemical Substances Receptors, Estrogen
    Language English
    Publishing date 2006-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Intramural ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI27987
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Expression of extracellular matrix components is disrupted in the immature and adult estrogen receptor β-null mouse ovary.

    Alexandra Zalewski / Erin L Cecchini / Bonnie J Deroo

    PLoS ONE, Vol 7, Iss 1, p e

    2012  Volume 29937

    Abstract: Within the ovary, Estrogen Receptor β (ERβ) is localized to the granulosa cells of growing follicles. 17β-estradiol (E2) acting via ERβ augments the actions of follicle stimulating hormone in granulosa cells, leading to granulosa cell differentiation and ...

    Abstract Within the ovary, Estrogen Receptor β (ERβ) is localized to the granulosa cells of growing follicles. 17β-estradiol (E2) acting via ERβ augments the actions of follicle stimulating hormone in granulosa cells, leading to granulosa cell differentiation and formation of a preovulatory follicle. Adult ERβ-null females are subfertile and possess ovaries with reduced numbers of growing follicles and corpora lutea. Because the majority of E2 production by granulosa cells occurs once puberty is reached, a role for ERβ in the ovary prior to puberty has not been well examined. We now provide evidence that lack of ERβ disrupts gene expression as early as post-natal day (PND) 13, and in particular, we identify a number of genes of the extracellular matrix (ECM) that are significantly higher in ERβ-null follicles than in wildtype (WT) follicles. Considerable changes occur to the ECM occur during normal folliculogenesis to allow for the dramatic growth, cellular differentiation, and reorganization of the follicle from the primary to preovulatory stage. Using quantitative PCR and immunofluorescence, we now show that several ECM genes are aberrantly overexpressed in ERβ-null follicles. We find that Collagen11a1, a protein highly expressed in cartilage, is significantly higher in ERβ-null follicles than WT follicles as early as PND 13, and this heightened expression continues through PND 23-29 into adulthood. Similarly, Nidogen 2, a highly conserved basement membrane glycoprotein, is elevated in ERβ-null follicles at PND 13 into adulthood, and is elevated specifically in the ERβ-null focimatrix, a basal lamina-like matrix located between granulosa cells. Focimatrix laminin and Collagen IV expression were also higher in ERβ-null ovaries than in WT ovaries at various ages. Our findings suggest two novel observations: a) that ERβ regulates granulosa cell gene expression ovary prior to puberty, and b) that ERβ regulates expression of ECM components in the mouse ovary.
    Keywords Medicine ; R ; Science ; Q
    Subject code 570
    Language English
    Publishing date 2012-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  8. Article: Proteasome inhibitors reduce luciferase and beta-galactosidase activity in tissue culture cells.

    Deroo, Bonnie J / Archer, Trevor K

    The Journal of biological chemistry

    2002  Volume 277, Issue 23, Page(s) 20120–20123

    Abstract: Reporter enzymes are commonly used in cell biology to study transcriptional activity of genes. Recently, reporter enzymes in combination with compounds that inhibit proteasome function have been used to study the effect of blocking transcription factor ... ...

    Abstract Reporter enzymes are commonly used in cell biology to study transcriptional activity of genes. Recently, reporter enzymes in combination with compounds that inhibit proteasome function have been used to study the effect of blocking transcription factor degradation on gene activation. While investigating the effect of proteasome inhibition on steroid receptor activation of the mouse mammary tumor virus (MMTV) promoter, we found that treatment with proteasome inhibitors enhanced glucocorticoid activation of the promoter attached to a chloramphenicol acetyltransferase (CAT) reporter, but inhibited activation of MMTV attached to a firefly luciferase or beta-galactosidase reporter. MMTV RNA levels under these conditions correlated with the promoter activity observed using the CAT reporter, suggesting that proteasome inhibitor treatment interfered with luciferase or beta-galactosidase reporter assays. Washout experiments demonstrated that the majority of luciferase activity was lost if the proteasome inhibitor was added at the same time luciferase was produced, not once the functional protein was made, suggesting that proteasome inhibition interferes with production of luciferase protein. Indeed, we found that proteasome inhibitor treatment dramatically reduced the levels of luciferase and beta-galactosidase protein produced, as determined by Western blot. Thus, treatment with proteasome inhibitors interferes with luciferase and beta-galactosidase reporter assays, possibly by inhibiting production of a functional reporter protein.
    MeSH term(s) Cysteine Endopeptidases/drug effects ; Cysteine Proteinase Inhibitors/pharmacology ; Genes, Reporter ; Luciferases/genetics ; Multienzyme Complexes/drug effects ; Proteasome Endopeptidase Complex ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Cells, Cultured ; beta-Galactosidase/genetics
    Chemical Substances Cysteine Proteinase Inhibitors ; Multienzyme Complexes ; Luciferases (EC 1.13.12.-) ; beta-Galactosidase (EC 3.2.1.23) ; Cysteine Endopeptidases (EC 3.4.22.-) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
    Language English
    Publishing date 2002-04-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.C200173200
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: Differential activation of the IkappaBalpha and mouse mammary tumor virus promoters by progesterone and glucocorticoid receptors.

    Deroo, Bonnie J / Archer, Trevor K

    The Journal of steroid biochemistry and molecular biology

    2002  Volume 81, Issue 4-5, Page(s) 309–317

    Abstract: The glucocorticoid and progesterone receptors (GR and PR) are structurally homologous and bind a common hormone response element (HRE). The mechanisms by which receptors activate specific promoters when multiple steroids are present in a cell is a ... ...

    Abstract The glucocorticoid and progesterone receptors (GR and PR) are structurally homologous and bind a common hormone response element (HRE). The mechanisms by which receptors activate specific promoters when multiple steroids are present in a cell is a critical question in endocrinology. To investigate how co-existing steroid receptors regulate gene transcription, we have compared two hormone-responsive promoters in T47D/A1-2 human breast cancer cells expressing both the GR and PR. The promoters chosen were those for the mouse mammary tumor virus (MMTV) and the gene for IkappaBalpha, the inhibitor of the ubiquitous transcription factor, nuclear factor kappa B (NFkappaB). Several differences between glucocorticoid and progestin activation of the IkappaBalpha and MMTV promoters were revealed. Both steroids activated the endogenous IkappaBalpha promoter, while only glucocorticoids activated a stably integrated MMTV promoter. In combination, progestins enhanced glucocorticoid activation of IkappaBalpha, but antagonized glucocorticoid activation of MMTV. These differences in steroid receptor competition were further demonstrated when levels of the PR were reduced by prolonged treatment with progestin. Under these conditions, the PR no longer competes effectively with the GR for activation of the MMTV promoter. However, on the IkappaBalpha promoter, the GR and PR still activate the promoter in a cooperative fashion. Another difference between the two promoters is their chromatin structure. In this cell line, the MMTV promoter chromatin is "closed" and insensitive to restriction enzyme cleavage, while the IkappaBalpha promoter is "open." Using PR antagonists, we demonstrate that at least one cofactor complex, the BRG-1 chromatin remodeling complex, differentially contributes to activation of both promoters.
    MeSH term(s) Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Chloramphenicol O-Acetyltransferase/metabolism ; Chromatin/genetics ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Dexamethasone/pharmacology ; Estrenes/pharmacology ; Furans/pharmacology ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; I-kappa B Proteins ; Mammary Tumor Virus, Mouse/genetics ; Mammary Tumor Virus, Mouse/metabolism ; Mice ; NF-KappaB Inhibitor alpha ; NF-kappa B/antagonists & inhibitors ; NF-kappa B/genetics ; Plasmids/genetics ; Polymerase Chain Reaction ; Progestins/pharmacology ; RNA, Viral/metabolism ; Receptors, Glucocorticoid/antagonists & inhibitors ; Receptors, Glucocorticoid/metabolism ; Receptors, Progesterone/antagonists & inhibitors ; Receptors, Progesterone/metabolism ; Regulatory Sequences, Nucleic Acid ; Transcriptional Activation ; Transfection ; Tumor Cells, Cultured
    Chemical Substances Chromatin ; DNA-Binding Proteins ; Estrenes ; Furans ; I-kappa B Proteins ; NF-kappa B ; NFKBIA protein, human ; Nfkbia protein, mouse ; Progestins ; RNA, Viral ; Receptors, Glucocorticoid ; Receptors, Progesterone ; Org 31710 (118968-41-5) ; NF-KappaB Inhibitor alpha (139874-52-5) ; Dexamethasone (7S5I7G3JQL) ; Chloramphenicol O-Acetyltransferase (EC 2.3.1.28)
    Language English
    Publishing date 2002-10-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1049188-0
    ISSN 1879-1220 ; 0960-0760
    ISSN (online) 1879-1220
    ISSN 0960-0760
    DOI 10.1016/s0960-0760(02)00072-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Signal transduction. A new mediator for an old hormone?

    Hewitt, Sylvia Curtis / Deroo, Bonnie J / Korach, Kenneth S

    Science (New York, N.Y.)

    2005  Volume 307, Issue 5715, Page(s) 1572–1573

    MeSH term(s) Cell Membrane/metabolism ; Endoplasmic Reticulum/metabolism ; Estradiol/analogs & derivatives ; Estradiol/metabolism ; Estrogen Receptor alpha/metabolism ; Estrogens/metabolism ; Fulvestrant ; Gene Expression Regulation ; Humans ; Models, Biological ; Receptors, Estrogen/chemistry ; Receptors, Estrogen/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction ; Tamoxifen/metabolism ; Time Factors
    Chemical Substances Estrogen Receptor alpha ; Estrogens ; GPER1 protein, human ; Receptors, Estrogen ; Receptors, G-Protein-Coupled ; Tamoxifen (094ZI81Y45) ; Fulvestrant (22X328QOC4) ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2005-03-10
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.1110345
    Database MEDical Literature Analysis and Retrieval System OnLINE

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