An Overview of Transgenic Mice as Future Models of Human Diseases, in Drug Development, and for Genotoxicity and Carcinogenesis Studies

1992 ◽  
pp. 133-153
Author(s):  
J. C. Cordaro
Keyword(s):  
Transgenic Mice ◽  
Drug Development ◽  
Human Diseases

Targeting microRNAs involved in human diseases: A novel approach for modification of gene expression and drug development

2011 ◽  
Vol 82 (10) ◽  
pp. 1416-1429 ◽  
Author(s):  
Roberto Gambari ◽  
Enrica Fabbri ◽  
Monica Borgatti ◽  
Ilaria Lampronti ◽  
Alessia Finotti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Drug Development ◽  
Human Diseases ◽  
Novel Approach

scholarly journals Revealing the Therapeutic Uses of Garlic (Allium sativum) and Its Potential for Drug Discovery

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Azene Tesfaye
Keyword(s):  
Drug Development ◽  
Therapeutic Potential ◽  
Biologically Active ◽  
Human Diseases ◽  
Active Components ◽  
Runny Nose ◽  
Medicinal Value ◽  
Therapeutic Uses ◽  
Tract Disease ◽  
Chronic Fever

Background. Garlic is a common bulb vegetable that is used to flavor and flavor food. The plant contains biologically active components that contribute to its pharmacological properties. This paper attempts to examine the therapeutic uses and potential role in the drug development of garlic for various human diseases. Methods. To obtain crucial data and scientific knowledge about the therapeutic uses of garlic, systematic literature searches were conducted using key terms on well-known indexed platforms such as PubMed, Scopus, Web of Science, Medline, Embase, and popular search engines. Results. Garlic, which is utilized as a spice and flavoring ingredient, is found to have fundamental nutritional components. Carbohydrates, protein, fat, minerals, water, and vitamins are all found in abundance in this plant. The plant also has a high medicinal value and is used to cure a variety of human diseases. It has anti-inflammatory, rheumatological, ulcer inhibiting, anticholinergic, analgesic, antimicrobial, antistress, antidiabetes, anticancer, liver protection, anthelmintics, antioxidants, antifungal, and wound healing properties, as well as properties that help with asthma, arthritis, chronic fever, tuberculosis, runny nose, malaria, leprosy, skin discoloration, and itching, indigestion, colic, enlarged spleen, hemorrhoids, fistula, bone fracture, gout, urinary tract disease, diabetes, kidney stones, anemia, jaundice, epilepsy, cataract, and night blindness. Conclusions. The nutritional content of the plant is significant, and it has incredible therapeutic potential. The findings of this study are needed to investigate the therapeutic potential, as it may be a promising option for drug development.

Transgenic mice with cardiomyopathy — An attractive model for drug development?

1999 ◽  
Vol 65 (2) ◽  
pp. 204-204
Author(s):  
B KNOLLMANN ◽  
K TRIVEDI ◽  
N WEISSMAN ◽  
M MORAD
Keyword(s):  
Transgenic Mice ◽  
Drug Development

scholarly journals The nuclear receptor 4A family members: mediators in human disease and autophagy

2020 ◽  
Vol 25 (1) ◽  
Author(s):  
Liqun Chen ◽  
Fengtian Fan ◽  
Lingjuan Wu ◽  
Yiyi Zhao
Keyword(s):  
Drug Development ◽  
Signaling Pathways ◽  
Nuclear Receptor ◽  
Human Disease ◽  
Family Members ◽  
Current Understanding ◽  
Human Diseases ◽  
Disease Therapy ◽  
Development Processes

Abstract The Nuclear receptor 4A (NR4A) subfamily, which belongs to the nuclear receptor (NR) superfamily, has three members: NR4A1 (Nur77), NR4A2 (Nurr1) and NR4A3 (Nor1). They are gene regulators with broad involvement in various signaling pathways and human disease responses, including autophagy. Here, we provide a concise overview of the current understanding of the role of the NR4A subfamily members in human diseases and review the research into their regulation of cell autophagy. A deeper understanding of these mechanisms has potential to improve drug development processes and disease therapy.

HLA class II transgenic mice as models of human diseases

1999 ◽  
Vol 169 (1) ◽  
pp. 67-79 ◽  
Author(s):  
Veena Taneja ◽  
Chella S. David
Keyword(s):  
Transgenic Mice ◽  
Class Ii ◽  
Hla Class Ii ◽  
Human Diseases

Increased Mitochondrial Gene Deletions and ROS Production in Transgenic Mice Overexpressing a Human 8-Oxoguanine DNA-Glycosylase Gene: A Causal Association with the Development of Hematopoietic Neoplasms

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 866-866
Author(s):  
Qin Huang ◽  
Haihong Zhang ◽  
Wei Chen ◽  
Serhan Alkan ◽  
Chunyang Fan
Keyword(s):  
Mitochondrial Dna ◽  
Transgenic Mice ◽  
Mitochondrial Gene ◽  
Myeloproliferative Disorder ◽  
Human Diseases ◽  
Wild Type ◽  
Gene Deletions ◽  
Mitochondrial Dna Damage ◽  
Hogg1 Gene ◽  
Wild Type Control

Abstract Alterations of nuclear genes in human diseases including neoplasms have been well investigated in past several decades and unequivocally established their predominant role in the pathogenesis. However, the relationship of mitochondrial genome alteration with human diseases remains largely unknown. Mitochondria are dynamic organelles involved in oxidative phosphorylation and production of reactive oxygen species (ROS). Accumulated evidence supports that mitochondrial DNA damage and dysfunction play vital roles in the development of a wide array of mitochondria-related human diseases, such as obesity, diabetes, infertility, neurodegenerative disorders and malignant tumors. We previously described the development of a transgenic (TG) mouse model for mitochondrial DNA damage by overexpressing human mitochondrial isoform of 8-oxoguanine DNA Glycosylase 1 (hOGG1) gene. Over-expression of this gene produced a wide range of adverse biological phenotypes, manifesting early-onset obesity, metabolic disturbance, female infertility, high frequency of B-cell lymphoma and human essential thrombocythemia like myeloproliferative disorder, involving the lymph node, bone marrow, spleen, liver and other extranodal sites. Development of these hematopoietic neoplasms appeared to be age-dependent. In the current study, we focused on the pathogenesis of the hematopoietic neoplasms by characterization of the neoplasms via pathologic, biochemical and molecular approaches. While expression of mOGG1 was very similar in parallel organs from transgenic and wild-type control mice, the hOGG1 TG mice expressed very high levels of human OGG1 transgene mRNA, being 6.8- and 112-fold as high as the endogenous mouse OGG, in the spleen and bone marrow. By contrast, hOGG1 transgene mRNA were not detected at all in the above two organs from control mice, indicating that the transgene is highly expressed in the hematopoietic organs in TG mice. We then measured mitochondrial NADH dehydrogenase 1 (ND1) gene expression as an indirect measure of mitochondrial respiratory function. ND1 mRNA levels in the spleen (4) and lymphoma (4) of TG mice were 83% and 58% higher, respectively, than those in the spleen (4) of wild-type control mice (P < 0.01), indicative of increased mitochondrial respiration in the lymphoma and spleen of hOGG1 TG mice. We next measured the levels of intracellular H2O2 production in the lymphoma and spleen of hOGG1 transgenic (4) and the spleen from wild-type control (4) mice. The amount of H2O2 produced in the lymphoma and the spleen of hOGG1 transgenic mice was ~166% and ~66% higher, respectively, than that in the spleen from wild-type control mice (P < 0.001). The amount of H2O2 produced in the lymphoma was ~60% higher than that in the spleen from hOGG1 transgenic mice (P < 0.05). Finally, we examined mitochondrial DNA alterations in TG mice. Mitochondrial DNA samples were extracted from various organs and lymphoma tissues from hOGG1 TG and age-matched non-TG control animals and subjected to PCR analysis using specific primer sets franking the breakpoints of 7 major mitochondrial DNA deletions. Six deletions (3.7, 3.82, 3.86, 4.2, 4.9 and 5.2 kilobase in length) have been previously reported in the literatures. One novel deletion of 15.kilobase was identified in hOGG1 TG mouse in our laboratory. Among 7 major mitochondrial DNA deletion analyzed, Five (3.7, 3.86, 4.2, 5.2 and 15 kilobase in length) deletions were detected in higher frequency in various organs of hOGG1 TG but not in non-TG control mice, suggesting that those deletions might be resulted from overexpression of the transgene hOGG1. Notably, 3 deletions (del3729, del3868, and del15139) were present in significantly higher frequencies in spleen with myeloproliferative disorders or lymphoma from TG mice in comparison to the spleen of the age-matched wild type animals (P<0.01). While the precise mechanisms leading to the development of hematopoietic neoplasms remain elusive, we hypothesized that major mitochondrial gene deletions and increased mitochondrial respiration, as a result of overexpressed hOGG1 gene in the mitochondria, may contribute significantly to the increased intracellular ROS in hematopoietic progenitor cell populations, which, in turn, causes further genetic mutation and the development of lymphoma and myeloproliferative disorder seen in these TG mice. Disclosures No relevant conflicts of interest to declare.

AGC protein kinases: From structural mechanism of regulation to allosteric drug development for the treatment of human diseases

2013 ◽  
Vol 1834 (7) ◽  
pp. 1302-1321 ◽  
Author(s):  
José M. Arencibia ◽  
Daniel Pastor-Flores ◽  
Angelika F. Bauer ◽  
Jörg O. Schulze ◽  
Ricardo M. Biondi
Keyword(s):  
Drug Development ◽  
Protein Kinases ◽  
Human Diseases ◽  
Structural Mechanism
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