The promoter sequences of lettuce cis-prenyltransferase and its binding protein specify gene expression in laticifers

RNA binding proteins fulfil a wide number of roles in gene expression. Multiple mechanisms of RNA binding protein dysregulation have been implicated in the pathomechanisms of several neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Oxidative stress and mitochondrial dysfunction also play important roles in these diseases. In this review, we highlight the mechanistic interplay between RNA binding protein dysregulation, oxidative stress and mitochondrial dysfunction in ALS. We also discuss different potential therapeutic strategies targeting these pathways.

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RNA–Binding Protein HuD as a Versatile Factor in Neuronal and Non–Neuronal Systems

Biology ◽

10.3390/biology10050361 ◽

2021 ◽

Vol 10 (5) ◽

pp. 361

Author(s):

Myeongwoo Jung ◽

Eun-Kyung Lee

Keyword(s):

Gene Expression ◽

Neural Plasticity ◽

Molecular Mechanisms ◽

Neuronal Development ◽

Rna Binding ◽

Binding Protein ◽

Rna Binding Protein ◽

Novel Treatments ◽

Target Mrnas ◽

Neuronal Systems

HuD (also known as ELAVL4) is an RNA–binding protein belonging to the human antigen (Hu) family that regulates stability, translation, splicing, and adenylation of target mRNAs. Unlike ubiquitously distributed HuR, HuD is only expressed in certain types of tissues, mainly in neuronal systems. Numerous studies have shown that HuD plays essential roles in neuronal development, differentiation, neurogenesis, dendritic maturation, neural plasticity, and synaptic transmission by regulating the metabolism of target mRNAs. However, growing evidence suggests that HuD also functions as a pivotal regulator of gene expression in non–neuronal systems and its malfunction is implicated in disease pathogenesis. Comprehensive knowledge of HuD expression, abundance, molecular targets, and regulatory mechanisms will broaden our understanding of its role as a versatile regulator of gene expression, thus enabling novel treatments for diseases with aberrant HuD expression. This review focuses on recent advances investigating the emerging role of HuD, its molecular mechanisms of target gene regulation, and its disease relevance in both neuronal and non–neuronal systems.

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Adhesion Behaviour of Primary Human Osteoblasts and Fibroblasts on Polyether Ether Ketone Compared with Titanium under In Vitro Lipopolysaccharide Incubation

Materials ◽

10.3390/ma12172739 ◽

2019 ◽

Vol 12 (17) ◽

pp. 2739 ◽

Cited By ~ 1

Author(s):

Korbinian Benz ◽

Andreas Schöbel ◽

Marisa Dietz ◽

Peter Maurer ◽

Jochen Jackowski

Keyword(s):

Gene Expression ◽

Protein Level ◽

Binding Protein ◽

Sem Images ◽

Human Osteoblasts ◽

Polyether Ether Ketone ◽

Primary Human Osteoblasts ◽

Titanium Surfaces ◽

Ether Ketone

The aim of this in vitro pilot study was to analyse the adhesion behaviour of human osteoblasts and fibroblasts on polyether ether ketone (PEEK) when compared with titanium surfaces in an inflammatory environment under lipopolysaccharide (LPS) incubation. Scanning electron microscopy (SEM) images of primary human osteoblasts/fibroblasts on titanium/PEEK samples were created. The gene expression of the LPS-binding protein (LBP) and the LPS receptor (toll-like receptor 4; TLR4) was measured by real-time polymerase chain reaction (PCR). Immunocytochemistry was used to obtain evidence for the distribution of LBP/TLR4 at the protein level of the extra-cellular-matrix-binding protein vinculin and the actin cytoskeleton. SEM images revealed that the osteoblasts and fibroblasts on the PEEK surfaces had adhesion characteristics comparable to those of titanium. The osteoblasts contracted under LPS incubation and a significantly increased LBP gene expression were detected. This was discernible at the protein level on all the materials. Whereas no increase of TLR4 was detected with regard to mRNA concentrations, a considerable increase in the antibody reaction was detected on all the materials. As is the case with titanium, the colonisation of human osteoblasts and fibroblasts on PEEK samples is possible under pro-inflammatory environmental conditions and the cellular inflammation behaviour towards PEEK is lower than that of titanium.

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Neuropeptide and calcium-binding protein gene expression profiles predict neuronal anatomical type in the juvenile rat

The Journal of Physiology ◽

10.1113/jphysiol.2005.089250 ◽

2005 ◽

Vol 567 (2) ◽

pp. 401-413 ◽

Cited By ~ 58

Author(s):

Maria Toledo-Rodriguez ◽

Philip Goodman ◽

Milena Illic ◽

Caizhi Wu ◽

Henry Markram

Keyword(s):

Gene Expression ◽

Calcium Binding ◽

Protein Gene ◽

Binding Protein ◽

Expression Profiles ◽

Gene Expression Profiles ◽

Calcium Binding Protein ◽

Binding Protein Gene

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Creb-binding protein (CBP) is a transcriptional coactivator for hepatocyte nuclear factor-4 HNF-4) and enhances apolipoprotein gene expression

Atherosclerosis ◽

10.1016/s0021-9150(99)80037-9 ◽

1999 ◽

Vol 144 ◽

pp. 11

Author(s):

M. Hadzopoulou-Cladaras ◽

H. Dell

Keyword(s):

Gene Expression ◽

Binding Protein ◽

Nuclear Factor ◽

Creb Binding Protein ◽

Hepatocyte Nuclear Factor ◽

Transcriptional Coactivator ◽

Hepatocyte Nuclear Factor 4

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Carbohydrate-response-element-binding protein (ChREBP) and not the liver X receptor α (LXRα) mediates elevated hepatic lipogenic gene expression in a mouse model of glycogen storage disease type 1

Biochemical Journal ◽

10.1042/bj20101225 ◽

2010 ◽

Vol 432 (2) ◽

pp. 249-254 ◽

Cited By ~ 26

Author(s):

Aldo Grefhorst ◽

Marijke Schreurs ◽

Maaike H. Oosterveer ◽

Victor A. Cortés ◽

Rick Havinga ◽

...

Keyword(s):

Gene Expression ◽

Binding Protein ◽

Glycogen Storage Disease Type ◽

Glycogen Storage ◽

Hepatic Glycogen ◽

Lipogenic Gene ◽

Lipogenic Gene Expression ◽

Liver X Receptor Α ◽

Element Binding Protein

GSD-1 (glycogen storage disease type 1) is caused by an inherited defect in glucose-6-phosphatase activity, resulting in a massive accumulation of hepatic glycogen content and an induction of de novo lipogenesis. The chlorogenic acid derivative S4048 is a pharmacological inhibitor of the glucose 6-phosphate transporter, which is part of glucose-6-phosphatase, and allows for mechanistic studies concerning metabolic defects in GSD-1. Treatment of mice with S4048 resulted in an ~60% reduction in blood glucose, increased hepatic glycogen and triacylglycerol (triglyceride) content, and a markedly enhanced hepatic lipogenic gene expression. In mammals, hepatic expression of lipogenic genes is regulated by the co-ordinated action of the transcription factors SREBP (sterol-regulatory-element-binding protein)-1c, LXRα (liver X receptor α) and ChREBP (carbohydrate-response-element-binding protein). Treatment of Lxra−/− mice and Chrebp−/− mice with S4048 demonstrated that ChREBP, but not LXRα, mediates the induction of hepatic lipogenic gene expression in this murine model of GSD-1. Thus ChREBP is an attractive target to alleviate derangements in lipid metabolism observed in patients with GSD-1.

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