Relevant bibliographies by topics / GATA4 Hypertrophie Herz

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Academic literature on the topic 'GATA4 Hypertrophie Herz'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

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Journal articles on the topic "GATA4 Hypertrophie Herz"

1

Liang, Qiangrong, Russell J. Wiese, Orlando F. Bueno, Yan-Shan Dai, Bruce E. Markham, and Jeffery D. Molkentin. "The Transcription Factor GATA4 Is Activated by Extracellular Signal-Regulated Kinase 1- and 2-Mediated Phosphorylation of Serine 105 in Cardiomyocytes." Molecular and Cellular Biology 21, no. 21 (2001): 7460–69. http://dx.doi.org/10.1128/mcb.21.21.7460-7469.2001.

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ABSTRACT The zinc finger-containing transcription factor GATA4 has been implicated as a critical regulator of multiple cardiac-expressed genes as well as a regulator of inducible gene expression in response to hypertrophic stimulation. Here we demonstrate that GATA4 is itself regulated by the mitogen-activated protein kinase signaling cascade through direct phosphorylation. Site-directed mutagenesis and phospho-specific GATA4 antiserum revealed serine 105 as the primary site involved in agonist-induced phosphorylation of GATA4. Infection of cultured cardiomyocytes with an activated MEK1-expres
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2

Ahmadvand, Shiva, Ali Osia, Anna Meyfour, and Sara Pahlavan. "Gender-specific characteristics of hypertrophic response in cardiomyocytes derived from human embryonic stem cells." Journal of Cardiovascular and Thoracic Research 13, no. 2 (2021): 146–55. http://dx.doi.org/10.34172/jcvtr.2021.32.

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Introduction: Gender-specific phenotypes of the heart were reported with respect to both physiology and pathology. While most differences were associated with the sex hormones, differential expression of genes received special attention, particularly X-Y chromosomes’ genes. Methods: Here, we compared cardiogenesis by gene expression analysis of lineage specific markers and X-Y chromosomes’ genes, during in vitro differentiation of XY and XX human embryonic stem cells (hESC), in a hormone-free setup. Results: Downregulation of pluripotency marker (NANOG) and upregulation of cardiac mesoderm and
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Lu, Chieh-Hsiang, Chia-Yao Shen, Dennis Jine-Yuan Hsieh, et al. "Deep ocean minerals inhibit IL-6 and IGFIIR hypertrophic signaling pathways to attenuate diabetes-induced hypertrophy in rat hearts." Journal of Applied Physiology 127, no. 2 (2019): 356–64. http://dx.doi.org/10.1152/japplphysiol.00184.2019.

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We previously reported that deep sea water (DSW) prolongs the life span of streptozotocin (STZ)-induced diabetic rats by the compensatory augmentation of the insulin like growth factor (IGF)-I survival signaling and inhibition of apoptosis. Here, we investigated the effects of DSW on cardiac hypertrophy in diabetic rats. Cardiac hypertrophy was induced in rats by using STZ (65 mg/kg) administered via IP injection. DSW was prepared by mixing DSW mineral extracts and desalinated water. Different dosages of DSW-1X (equivalent to 37 mg Mg2+·kg−1·day−1), 2X (equivalent to 74 mg Mg2+·kg−1·day−1) and
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4

Harrison, Brooke C., Charles R. Roberts, David B. Hood, et al. "The CRM1 Nuclear Export Receptor Controls Pathological Cardiac Gene Expression." Molecular and Cellular Biology 24, no. 24 (2004): 10636–49. http://dx.doi.org/10.1128/mcb.24.24.10636-10649.2004.

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ABSTRACT Diverse pathological insults trigger a cardiac remodeling process during which myocytes undergo hypertrophy, with consequent decline in cardiac function and eventual heart failure. Multiple transcriptional regulators of pathological cardiac hypertrophy are controlled at the level of subcellular distribution. For example, prohypertrophic transcription factors belonging to the nuclear factor of activated T cells (NFAT) and GATA families are subject to CRM1-dependent nuclear export but are rapidly relocalized to the nucleus in response to cues for hypertrophic growth. Here, we demonstrat
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5

Kim, Tae-gyun, Junqin Chen, Junich Sadoshima, and Youngsook Lee. "Jumonji Represses Atrial Natriuretic Factor Gene Expression by Inhibiting Transcriptional Activities of Cardiac Transcription Factors." Molecular and Cellular Biology 24, no. 23 (2004): 10151–60. http://dx.doi.org/10.1128/mcb.24.23.10151-10160.2004.

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ABSTRACT Mice with a homozygous knockout of the jumonji (jmj) gene showed abnormal heart development and defective regulation of cardiac-specific genes, including the atrial natriuretic factor (ANF). ANF is one of the earliest markers of cardiac differentiation and a hallmark for cardiac hypertrophy. Here, we show that JMJ represses ANF gene expression by inhibiting transcriptional activities of Nkx2.5 and GATA4. JMJ represses the Nkx2.5- or GATA4-dependent activation of the reporter genes containing the ANF promoter-enhancer or containing the Nkx2.5 or GATA4-binding consensus sequence. JMJ ph
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Oka, Toru, Yan-Shan Dai та Jeffery D. Molkentin. "Regulation of Calcineurin through Transcriptional Induction of the calcineurin Aβ Promoter In Vitro and In Vivo". Molecular and Cellular Biology 25, № 15 (2005): 6649–59. http://dx.doi.org/10.1128/mcb.25.15.6649-6659.2005.

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ABSTRACT The calcineurin-nuclear factor of activated T cells (NFAT) signaling pathway has been shown to be of critical importance in regulating the growth response of cardiac myocytes. We have previously demonstrated that calcineurin Aβ (CnAβ) mRNA and protein are increased in response to growth stimulation, although the precise regulatory mechanism underlying CnAβ upregulation is not clear. Here, we isolated the mouse CnAβ promoter and characterized its responsiveness to growth stimuli in vitro and in vivo. A 2.3-kb promoter fragment was strongly activated by phenylephrine and endothelin-1 st
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7

Panguluri, Siva K., Jared Tur, Jutaro Fukumoto, et al. "Hyperoxia-induced hypertrophy and ion channel remodeling in left ventricle." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 12 (2013): H1651—H1661. http://dx.doi.org/10.1152/ajpheart.00474.2012.

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Ventricular arrhythmias account for high mortality in cardiopulmonary patients in intensive care units. Cardiovascular alterations and molecular-level changes in response to the commonly used oxygen treatment remains unknown. In the present study we investigated cardiac hypertrophy and cardiac complications in mice subjected to hyperoxia. Results demonstrate that there is a significant increase in average heart weight to tibia length (22%) in mice subjected to hyperoxia treatment vs. normoxia. Functional assessment was performed in mice subjected to hyperoxic treatment, and results demonstrate
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8

Purcell, Nicole H., Dina Darwis, Orlando F. Bueno, Judith M. Müller, Roland Schüle, and Jeffery D. Molkentin. "Extracellular Signal-Regulated Kinase 2 Interacts with and Is Negatively Regulated by the LIM-Only Protein FHL2 in Cardiomyocytes." Molecular and Cellular Biology 24, no. 3 (2004): 1081–95. http://dx.doi.org/10.1128/mcb.24.3.1081-1095.2004.

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ABSTRACT The mitogen-activated protein kinase (MAPK) signaling pathway regulates diverse biologic functions including cell growth, differentiation, proliferation, and apoptosis. The extracellular signal-regulated kinases (ERKs) constitute one branch of the MAPK pathway that has been implicated in the regulation of cardiac differentiated growth, although the downstream mechanisms whereby ERK signaling affects this process are not well characterized. Here we performed a yeast two-hybrid screen with ERK2 bait and a cardiac cDNA library to identify novel proteins involved in regulating ERK signali
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9

Leigh, Robert S., and Bogac L. Kaynak. "Vitamin A as a Transcriptional Regulator of Cardiovascular Disease." Hearts 1, no. 2 (2020): 126–45. http://dx.doi.org/10.3390/hearts1020013.

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Vitamin A is a micronutrient and signaling molecule that regulates transcription, cellular differentiation, and organ homeostasis. Additionally, metabolites of Vitamin A are utilized as differentiation agents in the treatment of hematological cancers and skin disorders, necessitating further study into the effects of both nutrient deficiency and the exogenous delivery of Vitamin A and its metabolites on cardiovascular phenotypes. Though vitamin A/retinoids are well-known regulators of cardiac formation, recent evidence has emerged that supports their role as regulators of cardiac regeneration,
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10

Prakash, Ajay, Aaron M. Udager, David A. Saenz, and Deborah L. Gumucio. "Roles for Nkx2–5 and Gata3 in the ontogeny of the murine smooth muscle gastric ligaments." American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no. 4 (2014): G430—G436. http://dx.doi.org/10.1152/ajpgi.00360.2013.

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The gastric ligaments are superficial cord-like structures, located on the lesser curvature of the stomach, that extend from the pylorus to the esophagus. These ligaments have been documented in a wide variety of mammalian species, including humans, but their composition and ontogeny is unexplored. Here, we demonstrate that, during ontogeny, the gastric ligaments are first visible as extensions from a C-shaped domain of Gata3-expressing cells that surround the future pylorus; this domain will later give rise to the pyloric outer longitudinal muscle (OLM). The open ends of the C are located ven
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Dissertations / Theses on the topic "GATA4 Hypertrophie Herz"

1

Wilken, Andre. "Der Transkriptionsfaktor GATA4 und seine Rolle in der Entwicklung kardialer Hypertrophie." Doctoral thesis, 2016. http://hdl.handle.net/11858/00-1735-0000-002B-7C98-D.

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Die Rolle von GATA4 für die Entwicklung einer Hypertrophie und seine Regulation in Abhängigkeit von der Last sind im menschlichen Herzen im Gegensatz zu den zahlreichen tierexperimentellen Ansätzen bislang nicht gezielt untersucht worden. Die vorliegende Arbeit sollte zeigen, wie biomechanische Last im menschlichen Herzen die Expression von GATA4 und seine Phosphorylierung an einer aktivierenden Phosphorylierungsstelle (Serin-105) reguliert. Hierfür wurde der Einfluss eines chronischen Lastzustandes, hervorgerufen durch eine Aortenstenose, ebenso wie der eines akuten Lastzustandes durch Steig
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