scholarly journals Promising Role of Engineered Gene Circuits in Gene Therapy

10.5772/17400 ◽  
2011 ◽  
Author(s):  
Wei-Dong Wang ◽  
Jinyi Lang
Keyword(s):  
Gene Therapy ◽  
Gene Circuits

The Therapeutic Potential and Role of miRNA, lncRNA, and circRNA in Osteoarthritis

2019 ◽  
Vol 19 (4) ◽  
pp. 255-263 ◽  
Author(s):  
Yuangang Wu ◽  
Xiaoxi Lu ◽  
Bin Shen ◽  
Yi Zeng
Keyword(s):  
Gene Expression ◽  
Gene Therapy ◽  
Extracellular Matrix ◽  
Inflammatory Reaction ◽  
Noncoding Rna ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Protein Translation ◽  
Cochrane Library

Background: Osteoarthritis (OA) is a disease characterized by progressive degeneration, joint hyperplasia, narrowing of joint spaces, and extracellular matrix metabolism. Recent studies have shown that the pathogenesis of OA may be related to non-coding RNA, and its pathological mechanism may be an effective way to reduce OA. Objective: The purpose of this review was to investigate the recent progress of miRNA, long noncoding RNA (lncRNA) and circular RNA (circRNA) in gene therapy of OA, discussing the effects of this RNA on gene expression, inflammatory reaction, apoptosis and extracellular matrix in OA. Methods: The following electronic databases were searched, including PubMed, EMBASE, Web of Science, and the Cochrane Library, for published studies involving the miRNA, lncRNA, and circRNA in OA. The outcomes included the gene expression, inflammatory reaction, apoptosis, and extracellular matrix. Results and Discussion: With the development of technology, miRNA, lncRNA, and circRNA have been found in many diseases. More importantly, recent studies have found that RNA interacts with RNA-binding proteins to regulate gene transcription and protein translation, and is involved in various pathological processes of OA, thus becoming a potential therapy for OA. Conclusion: In this paper, we briefly introduced the role of miRNA, lncRNA, and circRNA in the occurrence and development of OA and as a new target for gene therapy.

Artificial RNA Editing with ADAR for Gene Therapy

2020 ◽  
Vol 20 (1) ◽  
pp. 44-54 ◽  
Author(s):  
Sonali Bhakta ◽  
Toshifumi Tsukahara
Keyword(s):  
Gene Therapy ◽  
Genetic Code ◽  
Molecular Mechanism ◽  
Rna Editing ◽  
Comparative Studies ◽  
Genetic Diseases ◽  
Adenosine Deaminases ◽  
Family Protein ◽  
Hydrolytic Deamination

Editing mutated genes is a potential way for the treatment of genetic diseases. G-to-A mutations are common in mammals and can be treated by adenosine-to-inosine (A-to-I) editing, a type of substitutional RNA editing. The molecular mechanism of A-to-I editing involves the hydrolytic deamination of adenosine to an inosine base; this reaction is mediated by RNA-specific deaminases, adenosine deaminases acting on RNA (ADARs), family protein. Here, we review recent findings regarding the application of ADARs to restoring the genetic code along with different approaches involved in the process of artificial RNA editing by ADAR. We have also addressed comparative studies of various isoforms of ADARs. Therefore, we will try to provide a detailed overview of the artificial RNA editing and the role of ADAR with a focus on the enzymatic site directed A-to-I editing.

scholarly journals Gene therapy directed at the neuroimmune component of chronic pain with particular attention to the role of TNFα

2008 ◽  
Vol 437 (3) ◽  
pp. 209-213 ◽  
Author(s):  
Marina Mata ◽  
Shuanglin Hao ◽  
David J. Fink
Keyword(s):  
Gene Therapy ◽  
Chronic Pain

scholarly journals Monitoring HSVtk suicide gene therapy: the role of [18F]FHPG membrane transport

2004 ◽  
Vol 91 (12) ◽  
pp. 2079-2085 ◽  
Author(s):  
A R Buursma ◽  
I J van Dillen ◽  
A van Waarde ◽  
W Vaalburg ◽  
G A P Hospers ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Membrane Transport ◽  
Suicide Gene ◽  
Suicide Gene Therapy

Role of animal models in gene therapy

Gene Therapy ◽  
2020 ◽  
pp. 155-167
Author(s):  
Julia R. Dorin ◽  
David J. Porteous
Keyword(s):  
Gene Therapy ◽  
Animal Models

scholarly journals Role of Oxidative Stress in Heart Failure: Insights from Gene Transfer Studies

Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1645
Author(s):  
Bart De Geest ◽  
Mudit Mishra
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Gene Therapy ◽  
Steady State ◽  
Gene Transfer ◽  
Oxidative Modification ◽  
Heme Oxygenase 1 ◽  
Therapy Studies ◽  
Pathological Remodeling

Under physiological circumstances, there is an exquisite balance between reactive oxygen species (ROS) production and ROS degradation, resulting in low steady-state ROS levels. ROS participate in normal cellular function and in cellular homeostasis. Oxidative stress is the state of a transient or a persistent increase of steady-state ROS levels leading to disturbed signaling pathways and oxidative modification of cellular constituents. It is a key pathophysiological player in pathological hypertrophy, pathological remodeling, and the development and progression of heart failure. The heart is the metabolically most active organ and is characterized by the highest content of mitochondria of any tissue. Mitochondria are the main source of ROS in the myocardium. The causal role of oxidative stress in heart failure is highlighted by gene transfer studies of three primary antioxidant enzymes, thioredoxin, and heme oxygenase-1, and is further supported by gene therapy studies directed at correcting oxidative stress linked to metabolic risk factors. Moreover, gene transfer studies have demonstrated that redox-sensitive microRNAs constitute potential therapeutic targets for the treatment of heart failure. In conclusion, gene therapy studies have provided strong corroborative evidence for a key role of oxidative stress in pathological remodeling and in the development of heart failure.

Prostate cancer gene therapy and the role of radiation

2002 ◽  
Vol 28 (1) ◽  
pp. 49-64 ◽  
Author(s):  
J.M. Kaminski ◽  
K. Nguyen ◽  
M. Buyyounouski ◽  
A. Pollack
Keyword(s):  
Prostate Cancer ◽  
Gene Therapy ◽  
Cancer Gene Therapy ◽  
Cancer Gene
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