MSK-Mediated Phosphorylation of Histone H3 Ser28 Couples MAPK Signalling with Early Gene Induction and Cardiac Hypertrophy

Robinson, Emma; Drawnel, Faye; Mehdi, Saher; Archer, Caroline; Liu, Wei; Okkenhaug, Hanneke; Alkass, Kanar; Aronsen, Jan Magnus; Nagaraju, Chandan K.; Sjaastad, Ivar; Sipido, Karin R.; Bergmann, Olaf; Arthur, J. Simon C.; Wang, Xin; Roderick, H. Llewelyn

doi:10.3390/cells11040604

Cited by 8 publications

(3 citation statements)

References 78 publications

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“…ET-1 is an endothelium-derived pluripotent factor that is fundamental in developing pathological hypertrophic remodeling ( 112 ). In line with this, Emma L. Robinson et al found that the mitogen and stress-activated protein kinase/Brg1/immediate early gene (MSK/Brg1/IEG) axis mediated ET-1 initiated cardiac hypertrophy ( 113 ). In addition, Brg1 and Brm could be the upstream factors of ET-1, promoting its expression in a time-dependent manner ( 112 ).…”

Section: Role Of Sfⅱ Helicases In Cardiac Remodeling and Hfmentioning

confidence: 84%

Superfamily II helicases: the potential therapeutic target for cardiovascular diseases

Fang,

Wang,

Huangfu

2023

Front. Cardiovasc. Med.

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Cardiovascular diseases (CVDs) still maintain high morbidity and mortality globally. Helicases, a unique class of enzymes, are extensively implicated in the processes of nucleic acid (NA) metabolism across various organisms. They play a pivotal role in gene expression, inflammatory response, lipid metabolism, and so forth. However, abnormal helicase expression has been associated with immune response, cancer, and intellectual disability in humans. Superfamily II (SFII) is one of the largest and most diverse of the helicase superfamilies. Increasing evidence has implicated SFⅡ helicases in the pathogenesis of multiple CVDs. In this review, we comprehensively review the regulation mechanism of SFⅡ helicases in CVDs including atherosclerosis, myocardial infarction, cardiomyopathies, and heart failure, which will contribute to the investigation of ideal therapeutic targets for CVDs.

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Section: Role Of Sfⅱ Helicases In Cardiac Remodeling and Hfmentioning

confidence: 84%

Superfamily II helicases: the potential therapeutic target for cardiovascular diseases

Fang,

Wang,

Huangfu

2023

Front. Cardiovasc. Med.

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“…In addition, RKIP is regulated by feedback of KRAS-ERK pathway. At the same time, P-ERK can undergo self-phosphorylation, thereby activating downstream substrates such as Elk1, mitogen-and stress-activated protein Kinase, c-myc, etc [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Raf kinase inhibitor protein combined with phosphorylated extracellular signal-regulated kinase offers valuable prognosis in gastrointestinal stromal tumor

Qu¹,

Wang²,

Chen³

et al. 2023

World J Gastroenterol

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Coronavirus disease 2019 (COVID-19) has several extrapulmonary symptoms. Gastrointestinal (GI) symptoms are among the most frequent clinical manifestations of COVID-19, with severe consequences reported in elderly patients. Furthermore, the impact of COVID-19 on patients with pre-existing digestive diseases still needs to be fully elucidated, particularly in the older population. This review aimed to investigate the impact of COVID-19 on the GI tract, liver, and pancreas in individuals with and without previous digestive diseases, with a particular focus on the elderly, highlighting the distinctive characteristics observed in this population. Finally, the effectiveness and adverse events of the anti-COVID-19 vaccination in patients with digestive disorders and the peculiarities found in the elderly are discussed.

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“…Accordingly, the cardiomyocyte hypertrophic response is characterized by increases in cardiomyocyte size, RNA concentration, and protein synthesis as well as expression of fetal genes including atrial natriuretic factor (ANF) [ 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 ] due to the activation of several transcription factors [ 14 , 15 ]. Furthermore, a transient activation of the c-Fos and c-Jun complex (AP-1) also occurs in the early response to hypertrophic stimuli [ 14 , 16 ]. In fact, cumulative evidence has determined that both AP-1 complex and ANF induce the activation of several hypertrophic genes [ 14 , 17 , 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of Phospholipase C Gene Expression Due to Norepinephrine-Induced Hypertrophic Response

Tappia

Dhalla

2022

Cells

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The activation of phospholipase C (PLC) is thought to have a key role in the cardiomyocyte response to several different hypertrophic agents such as norepinephrine, angiotensin II and endothelin-1. PLC activity results in the generation of diacylglycerol and inositol trisphosphate, which are downstream signal transducers for the expression of fetal genes, increased protein synthesis, and subsequent cardiomyocyte growth. In this article, we describe the signal transduction elements that regulate PLC gene expression. The discussion is focused on the norepinephrine- α1-adrenoceptor signaling pathway and downstream signaling processes that mediate an upregulation of PLC isozyme gene expression. Evidence is also indicated to demonstrate that PLC activities self-regulate the expression of PLC isozymes with the suggestion that PLC activities may be part of a coordinated signaling process for the perpetuation of cardiac hypertrophy. Accordingly, from the information provided, it is plausible that specific PLC isozymes could be targeted for the mitigation of cardiac hypertrophy.

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MSK-Mediated Phosphorylation of Histone H3 Ser28 Couples MAPK Signalling with Early Gene Induction and Cardiac Hypertrophy

Cited by 8 publications

References 78 publications

Superfamily II helicases: the potential therapeutic target for cardiovascular diseases

Superfamily II helicases: the potential therapeutic target for cardiovascular diseases

Raf kinase inhibitor protein combined with phosphorylated extracellular signal-regulated kinase offers valuable prognosis in gastrointestinal stromal tumor

Upregulation of Phospholipase C Gene Expression Due to Norepinephrine-Induced Hypertrophic Response

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