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  1. Article: Genes & cells: Drug candidate may stop MERS: Chemical disrupts assembly centers of coronaviruses.

    Rosen, Meghan

    Science news

    2014  Volume 185, Issue 13, Page(s) 10–11

    Keywords covid19
    Language English
    Publishing date 2014-06-17
    Publishing country United States
    Document type News
    ZDB-ID 2023570-7
    ISSN 1943-0930 ; 0036-8423
    ISSN (online) 1943-0930
    ISSN 0036-8423
    DOI 10.1002/scin.5591851308
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Thyroid hormone receptor mutations in cancer and resistance to thyroid hormone: perspective and prognosis.

    Rosen, Meghan D / Privalsky, Martin L

    Journal of thyroid research

    2011  Volume 2011, Page(s) 361304

    Abstract: Thyroid hormone, operating through its receptors, plays crucial roles in the control of normal human physiology and development; deviations from the norm can give rise to disease. Clinical endocrinologists often must confront and correct the consequences ...

    Abstract Thyroid hormone, operating through its receptors, plays crucial roles in the control of normal human physiology and development; deviations from the norm can give rise to disease. Clinical endocrinologists often must confront and correct the consequences of inappropriately high or low thyroid hormone synthesis. Although more rare, disruptions in thyroid hormone endocrinology due to aberrations in the receptor also have severe medical consequences. This review will focus on the afflictions that are caused by, or are closely associated with, mutated thyroid hormone receptors. These include Resistance to Thyroid Hormone Syndrome, erythroleukemia, hepatocellular carcinoma, renal clear cell carcinoma, and thyroid cancer. We will describe current views on the molecular bases of these diseases, and what distinguishes the neoplastic from the non-neoplastic. We will also touch on studies that implicate alterations in receptor expression, and thyroid hormone levels, in certain oncogenic processes.
    Language English
    Publishing date 2011-06-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2549014-X
    ISSN 2042-0072 ; 2042-0072
    ISSN (online) 2042-0072
    ISSN 2042-0072
    DOI 10.4061/2011/361304
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Thyroid hormone receptor mutations found in renal clear cell carcinomas alter corepressor release and reveal helix 12 as key determinant of corepressor specificity.

    Rosen, Meghan D / Privalsky, Martin L

    Molecular endocrinology (Baltimore, Md.)

    2009  Volume 23, Issue 8, Page(s) 1183–1192

    Abstract: Thyroid hormone receptors (TRs) regulate multiple normal physiological and developmental pathways, whereas mutations in TRs can result in endocrine and neoplastic disease. A particularly high rate of TR mutations has been found in human renal clear cell ... ...

    Abstract Thyroid hormone receptors (TRs) regulate multiple normal physiological and developmental pathways, whereas mutations in TRs can result in endocrine and neoplastic disease. A particularly high rate of TR mutations has been found in human renal clear cell carcinomas (RCCCs). We report here that the majority of these RCCC TR mutants tested are defective for transcriptional activation and behave as dominant-negative inhibitors of wild-type receptor function. Although several of the dominant-negative RCCC TR mutants are impaired for hormone binding, all fail to release from corepressors appropriately in response to T(3), a trait that closely correlates with their defective transcriptional properties. Notably, many of these mutants exhibit additional changes in their specificity for different corepressor splice forms that may further contribute to the disease phenotype. Mapping of the relevant mutations reveals that the C-terminal receptor helix 12 is not simply a hormone-operated switch that either permits or prevents all corepressor binding, but is instead a selective gatekeeper that actively discriminates between different forms of corepressor even in the absence of T(3).
    MeSH term(s) Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/metabolism ; Cell Line, Tumor ; Cloning, Molecular ; Gene Expression Regulation, Neoplastic ; Genes, Dominant ; Hormones/metabolism ; Humans ; Kidney Neoplasms/genetics ; Kidney Neoplasms/metabolism ; Mutation ; Phenotype ; Protein Binding ; Protein Structure, Tertiary ; Receptors, Thyroid Hormone/genetics ; Repressor Proteins/metabolism ; Transcriptional Activation
    Chemical Substances Hormones ; Receptors, Thyroid Hormone ; Repressor Proteins
    Language English
    Publishing date 2009-04-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 639167-9
    ISSN 1944-9917 ; 0888-8809
    ISSN (online) 1944-9917
    ISSN 0888-8809
    DOI 10.1210/me.2009-0126
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2261: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Mutant thyroid hormone receptors (TRs) isolated from distinct cancer types display distinct target gene specificities: a unique regulatory repertoire associated with two renal clear cell carcinomas.

    Rosen, Meghan D / Chan, Ivan H / Privalsky, Martin L

    Molecular endocrinology (Baltimore, Md.)

    2011  Volume 25, Issue 8, Page(s) 1311–1325

    Abstract: Thyroid hormone receptors (TRs) are hormone-regulated transcription factors that regulate a diverse array of biological activities, including metabolism, homeostasis, and development. TRs also serve as tumor suppressors, and aberrant TR function (via ... ...

    Abstract Thyroid hormone receptors (TRs) are hormone-regulated transcription factors that regulate a diverse array of biological activities, including metabolism, homeostasis, and development. TRs also serve as tumor suppressors, and aberrant TR function (via mutation, deletion, or altered expression) is associated with a spectrum of both neoplastic and endocrine diseases. A particularly high frequency of TR mutations has been reported in renal clear cell carcinoma (RCCC) and in hepatocellular carcinoma (HCC). We have shown that HCC-TR mutants regulate only a fraction of the genes targeted by wild-type TRs but have gained the ability to regulate other, unique, targets. We have suggested that this altered gene recognition may contribute to the neoplastic phenotype. Here, to determine the generality of this phenomenon, we examined a distinct set of TR mutants associated with RCCC. We report that two different TR mutants, isolated from independent RCCC tumors, possess greatly expanded target gene specificities that extensively overlap one another, but only minimally overlap that of the wild-type TRs, or those of two HCC-TR mutants. Many of the genes targeted by either or both RCCC-TR mutants have been previously implicated in RCCC and include a series of metallothioneins, solute carriers, and genes involved in glycolysis and energy metabolism. We propose as a hypothesis that TR mutations from RCCC and HCC may play tissue-specific roles in carcinogenesis, and that the divergent target gene recognition patterns of TR mutants isolated from the two different types of tumors may arise from different selective pressures during development of RCCC vs. HCC.
    MeSH term(s) Carcinoma, Hepatocellular/metabolism ; Carcinoma, Renal Cell/genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/drug effects ; Genes, Neoplasm/genetics ; Hep G2 Cells ; Humans ; Kidney Neoplasms/genetics ; Liver Neoplasms/metabolism ; Mutant Proteins/isolation & purification ; Mutant Proteins/metabolism ; Receptors, Thyroid Hormone/metabolism ; Repressor Proteins/metabolism ; Transcription, Genetic/drug effects ; Transcriptional Activation/drug effects ; Transcriptional Activation/genetics ; Triiodothyronine/pharmacology
    Chemical Substances Mutant Proteins ; Receptors, Thyroid Hormone ; Repressor Proteins ; Triiodothyronine (06LU7C9H1V)
    Language English
    Publishing date 2011-05-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 639167-9
    ISSN 1944-9917 ; 0888-8809
    ISSN (online) 1944-9917
    ISSN 0888-8809
    DOI 10.1210/me.2010-0420
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2261: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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