The progesterone receptor coactivator Hic-5 is involved in the pathophysiology of endometriosis.
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Endometrial biomarkers for the non-invasive diagnosis of endometriosisA systems-level integrative framework for genome-wide DNA methylation and gene expression data identifies differential gene expression modules under epigenetic control.The protein kinase A pathway-regulated transcriptome of endometrial stromal fibroblasts reveals compromised differentiation and persistent proliferative potential in endometriosisThe dynamics of nuclear receptors and nuclear receptor coregulators in the pathogenesis of endometriosis.A murine uterine transcriptome, responsive to steroid receptor coactivator-2, reveals transcription factor 23 as essential for decidualization of human endometrial stromal cells.The bone marrow-derived human mesenchymal stem cell: potential progenitor of the endometrial stromal fibroblast.VDR activity is differentially affected by Hic-5 in prostate cancer and stromal cells.Endometrial gene expression reveals compromised progesterone signaling in women refractory to embryo implantation.Advances in the genetics of endometriosisRole of nuclear progesterone receptor isoforms in uterine pathophysiology.Unique transcriptome, pathways, and networks in the human endometrial fibroblast response to progesterone in endometriosis.Decreased Notch pathway signaling in the endometrium of women with endometriosis impairs decidualization.Selective coregulator function and restriction of steroid receptor chromatin occupancy by Hic-5.Transforming growth factor-β1-induced transcript 1 protein, a novel marker for smooth muscle contractile phenotype, is regulated by serum response factor/myocardin proteinKrüppel-like factor 9 and progesterone receptor coregulation of decidualizing endometrial stromal cells: implications for the pathogenesis of endometriosis.Nuclear receptor, coregulator signaling, and chromatin remodeling pathways suggest involvement of the epigenome in the steroid hormone response of endometrium and abnormalities in endometriosis.Induction of endometriosis alters the peripheral and endometrial regulatory T cell population in the non-human primate.Progesterone Alleviates Endometriosis via Inhibition of Uterine Cell Proliferation, Inflammation and Angiogenesis in an Immunocompetent Mouse Model.Krüppel-Like Factor 13 Deficiency in Uterine Endometrial Cells Contributes to Defective Steroid Hormone Receptor Signaling but Not Lesion Establishment in a Mouse Model of EndometriosisHuman Endometrial Fibroblasts Derived from Mesenchymal Progenitors Inherit Progesterone Resistance and Acquire an Inflammatory Phenotype in the Endometrial Niche in Endometriosis.Oestrogen and progesterone action on endometrium: a translational approach to understanding endometrial receptivity.The non-human primate model of endometriosis: research and implications for fecundity.Connexin expression pattern in the endometrium of baboons is influenced by hormonal changes and the presence of endometriotic lesions.Extracellular matrix metalloproteinase inducer expression in the baboon endometrium: menstrual cycle and endometriosis.Possible involvement of CD10 in the development of endometriosis due to its inhibitory effects on CD44-dependent cell adhesion.Epigenetics of endometriosis.Reduced connexin 43 in eutopic endometrium and cultured endometrial stromal cells from subjects with endometriosis.Krüppel-like factor 9 deficiency in uterine endometrial cells promotes ectopic lesion establishment associated with activated notch and hedgehog signaling in a mouse model of endometriosis.Hic-5 is a transcription coregulator that acts before and/or after glucocorticoid receptor genome occupancy in a gene-selective manner.Lessons learned from the preclinical drug discovery of asoprisnil and ulipristal for non-surgical treatment of uterine leiomyomas.KRAS Activation and over-expression of SIRT1/BCL6 Contributes to the Pathogenesis of Endometriosis and Progesterone Resistance.Glucocorticoid receptor binding to chromatin is selectively controlled by the coregulator Hic-5 and chromatin remodeling enzymes.Progesterone resistance in endometriosis: origins, consequences and interventions.Different chromatin and DNA sequence characteristics define glucocorticoid receptor binding sites that are blocked or not blocked by coregulator Hic-5.The Endometriotic Tumor Microenvironment in Ovarian Cancer
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P2860
The progesterone receptor coactivator Hic-5 is involved in the pathophysiology of endometriosis.
description
article científic
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article scientifique
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articolo scientifico
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artigo científico
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bilimsel makale
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scientific article published on 23 April 2009
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vedecký článok
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vetenskaplig artikel
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videnskabelig artikel
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vědecký článek
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name
The progesterone receptor coac ...... hophysiology of endometriosis.
@en
The progesterone receptor coac ...... hophysiology of endometriosis.
@nl
type
label
The progesterone receptor coac ...... hophysiology of endometriosis.
@en
The progesterone receptor coac ...... hophysiology of endometriosis.
@nl
prefLabel
The progesterone receptor coac ...... hophysiology of endometriosis.
@en
The progesterone receptor coac ...... hophysiology of endometriosis.
@nl
P2093
P2860
P356
P1433
P1476
The progesterone receptor coac ...... hophysiology of endometriosis.
@en
P2093
Linda C Giudice
Lusine Aghajanova
Michael C Velarde
P2860
P304
P356
10.1210/EN.2009-0008
P407
P577
2009-04-23T00:00:00Z