scholarly journals Targeting protein–protein interactions within the cyclic AMP signaling system as a therapeutic strategy for cardiovascular disease

2013 ◽  
Vol 5 (4) ◽  
pp. 451-464 ◽  
Author(s):  
Louisa CY Lee ◽  
Donald H Maurice ◽  
George S Baillie
Keyword(s):  
Cardiovascular Disease ◽  
Cyclic Amp ◽  
Protein Interactions ◽  
Therapeutic Strategy ◽  
Signaling System ◽  
Protein Protein Interactions ◽  
Cyclic Amp Signaling

Inhibition of bromodomain-mediated protein–protein interactions as a novel therapeutic strategy

MedChemComm ◽  
2012 ◽  
Vol 3 (2) ◽  
pp. 123-134 ◽  
Author(s):  
Silviya D. Furdas ◽  
Luca Carlino ◽  
Wolfgang Sippl ◽  
Manfred Jung
Keyword(s):  
Small Molecule ◽  
Protein Interactions ◽  
Therapeutic Strategy ◽  
Small Molecule Inhibitors ◽  
Protein Protein Interactions ◽  
Therapeutic Approaches ◽  
Novel Therapeutic

Small molecule inhibitors of acetyl lysine–bromodomain interactions emerge as novel epigenetic tools with potential for therapeutic approaches.

scholarly journals The disruption of protein-protein interactions as a therapeutic strategy for prostate cancer

2020 ◽  
Vol 161 ◽  
pp. 105145
Author(s):  
Bárbara Matos ◽  
John Howl ◽  
Carmen Jerónimo ◽  
Margarida Fardilha
Keyword(s):  
Prostate Cancer ◽  
Protein Interactions ◽  
Therapeutic Strategy ◽  
Protein Protein Interactions

scholarly journals Integrated Analysis of the Association Between Alzheimer`s Disease (AD) and Cardiovascular Disease (CVD)

2021 ◽  
Author(s):  
Katherine Liu Wei
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Cause Of Death ◽  
Protein Interactions ◽  
Brain Regions ◽  
Gene Expression Omnibus ◽  
Integrated Analysis ◽  
Biological Processes ◽  
Protein Protein Interactions ◽  
The Us

Alzheimer`s Disease (AD), the sixth leading cause of death in the US, and cardiovascular disease (CVD), the first leading cause of death in the US, are frequently associated. Past studies hypothesize that amyloid deposits damage organs, causing this association. Examining how vascular factors can influence AD pathogenesis can help in understanding the link between the blood to the brain, which can provide alternative paths of exploration for disease treatment. This study analyzes gene expression and shared biological processes between AD and CVD, specifically myocardial infarction and heart failure, via bioinformatic approaches and published datasets from the Gene Expression Omnibus (GEO). First, 73 differentially expressed genes (DEGs) were identified among four datasets using blood samples from AD and CVD patients. Panther`s Gene Ontology Analysis validated several biological processes such as xylulose biosynthetic process and toll-like receptor TLR1:TLR2 signaling pathway along with molecular functions, cellular components, and pathways to be significantly enriched in the list of 73 DEGs. Analysis of protein-protein interactions and the associated gene network indicated that from the list of 73 DEGs, only six (MAPK14, TLR2, HCK, GRB2, PRKCD, PTPN6) had eight or more degrees. Next, those six genes were identified in a normalized dataset containing different brain regions of AD and non-AD patients. Two-sample t-tests for differences in mean showed statistically significant differences in GRB2 and PRKCD, supporting a blood-brain relationship in the association between AD and CVD. This study can help in developing new medications to target AD and CVD susceptible genes.

scholarly journals Gain-of-Function Mutant p53: All the Roads Lead to Tumorigenesis

2019 ◽  
Vol 20 (24) ◽  
pp. 6197 ◽  
Author(s):  
Yan Stein ◽  
Varda Rotter ◽  
Ronit Aloni-Grinstein
Keyword(s):  
Protein Interactions ◽  
Therapeutic Strategy ◽  
P53 Protein ◽  
Mutant P53 ◽  
Wild Type ◽  
Protein Protein Interactions ◽  
Gain Of Function ◽  
Central Node ◽  
Type Form ◽  
Wild Type Form

The p53 protein is mutated in about 50% of human cancers. Aside from losing the tumor-suppressive functions of the wild-type form, mutant p53 proteins often acquire inherent, novel oncogenic functions, a phenomenon termed mutant p53 gain-of-function (GOF). A growing body of evidence suggests that these pro-oncogenic functions of mutant p53 proteins are mediated by affecting the transcription of various genes, as well as by protein–protein interactions with transcription factors and other effectors. In the current review, we discuss the various GOF effects of mutant p53, and how it may serve as a central node in a network of genes and proteins, which, altogether, promote the tumorigenic process. Finally, we discuss mechanisms by which “Mother Nature” tries to abrogate the pro-oncogenic functions of mutant p53. Thus, we suggest that targeting mutant p53, via its reactivation to the wild-type form, may serve as a promising therapeutic strategy for many cancers that harbor mutant p53. Not only will this strategy abrogate mutant p53 GOF, but it will also restore WT p53 tumor-suppressive functions.

scholarly journals Identification of Disease-Related Genes That Are Common between Alzheimer’s and Cardiovascular Disease Using Blood Genome-Wide Transcriptome Analysis

Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1525
Author(s):  
Taesic Lee ◽  
Hyunju Lee ◽  
Keyword(s):  
Cardiovascular Disease ◽  
Protein Interactions ◽  
Regulatory Networks ◽  
Nucleotide Polymorphisms ◽  
Protein Protein Interactions ◽  
Gene Expressions ◽  
Genome Wide ◽  
Cell Gene Expression ◽  
Cell Gene ◽  
Disease Related Gene

Accumulating evidence has suggested a shared pathophysiology between Alzheimer’s disease (AD) and cardiovascular disease (CVD). Based on genome-wide transcriptomes, specifically those of blood samples, we identify the shared disease-related signatures between AD and CVD. In addition to gene expressions in blood, the following prior knowledge were utilized to identify several candidate disease-related gene (DRG) sets: protein–protein interactions, transcription factors, disease–gene relationship databases, and single nucleotide polymorphisms. We selected the respective DRG sets for AD and CVD that show a high accuracy for disease prediction in bulk and single-cell gene expression datasets. Then, gene regulatory networks (GRNs) were constructed from each of the AD and CVD DRG sets to identify the upstream regulating genes. Using the GRNs, we identified two common upstream genes (GPBP1 and SETDB2) between the AD and CVD GRNs. In summary, this study has identified the potential AD- and CVD-related genes and common hub genes between these sets, which may help to elucidate the shared mechanisms between these two diseases.

scholarly journals The Functions of BET Proteins in Gene Transcription of Biology and Diseases

2021 ◽  
Vol 8 ◽  
Author(s):  
Ka Lung Cheung ◽  
Claudia Kim ◽  
Ming-Ming Zhou
Keyword(s):  
Transcription Factors ◽  
Rna Polymerase Ii ◽  
Gene Transcription ◽  
Protein Interactions ◽  
Therapeutic Strategy ◽  
Regulation Of Gene Expression ◽  
Transcriptional Elongation ◽  
Protein Protein Interactions ◽  
Inflammatory Disorders ◽  
Damage Repair

The BET (bromodomain and extra-terminal domain) family proteins, consisting of BRD2, BRD3, BRD4, and testis-specific BRDT, are widely acknowledged as major transcriptional regulators in biology. They are characterized by two tandem bromodomains (BDs) that bind to lysine-acetylated histones and transcription factors, recruit transcription factors and coactivators to target gene sites, and activate RNA polymerase II machinery for transcriptional elongation. Pharmacological inhibition of BET proteins with BD inhibitors has been shown as a promising therapeutic strategy for the treatment of many human diseases including cancer and inflammatory disorders. The recent advances in bromodomain protein biology have further uncovered the complex and versatile functions of BET proteins in the regulation of gene expression in chromatin. In this review article, we highlight our current understanding of BET proteins’ functions in mediating protein–protein interactions required for chromatin-templated gene transcription and splicing, chromatin remodeling, DNA replication, and DNA damage repair. We further discuss context-dependent activator vs. repressor functions of individual BET proteins, isoforms, and bromodomains that may be harnessed for future development of BET bromodomain inhibitors as emerging epigenetic therapies for cancer and inflammatory disorders.

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