Druggability of Proteins/Enzymes

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Drug Discovery, Development and Delivery".

Deadline for manuscript submissions: closed (15 May 2022) | Viewed by 6823

Special Issue Editors


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Guest Editor
Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, California Northstate University, Elk Grove, CA, USA
Interests: prostate cancer; bladder cancer; natural products research; biomarkers; targeted therapy; miRNA; mechanisms of chemoresistance
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Guest Editor
Department of Pharmaceutical and Biomedical Sciences, College of Pharmacy, California Northstate University, Elk Grove, CA, USA
Interests: cancer research; transcriptomics; metabolomics; proteomics; Pharmacognosy; molecular genetics; cell biology; molecular physiology; drug discovery

Special Issue Information

Dear Colleagues,

This Special Issue will cover all aspects of research works on druggable proteins and enzymes.

The human genome encodes approximately 20,000 proteins, a handful of which are suitable for drug–protein interactions. Within this group, even fewer are effectively targeted by drugs. This subgroup is defined here as the druggable proteins/enzymes with a specific affinity to bind small molecule(s) or antibodies mediating a signal transduction network involved in disease control.

Suitable manuscripts include, but are not limited to, research and review manuscripts that address enzyme and protein activities targeted by drugs converting signal transduction from the site of interaction into specific responses inside the cell resulting, for example, in gene expression, cell division, and/or cell death.

Research works of antibody-based drugs that cannot pass the plasma membrane are also welcome as they are mostly directed against protein targets on the cell surface (receptors) affecting their activities.

Additional druggable proteins that are of interest include, but are not limited to, all works on transporters, G-protein coupled receptors, CD markers, nuclear receptors, voltage-gated ion channels, etc.

Dr. Ruth Vinall
Dr. Simeon Kotchoni
Guest Editors

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Keywords

  • drug
  • antibodies
  • enzymes
  • target
  • druggable proteomics
  • druggable enzymolomics
  • disease
  • signal transduction
  • transporters
  • channel proteins
  • cell division
  • cell death
  • pathway inhibition
  • gene expression
  • computational biology
  • vaccine

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Published Papers (1 paper)

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Review

33 pages, 4421 KiB  
Review
Epigenetic Mechanisms as Emerging Therapeutic Targets and Microfluidic Chips Application in Pulmonary Arterial Hypertension
by Linh Ho, Nazir Hossen, Trieu Nguyen, Au Vo and Fakhrul Ahsan
Biomedicines 2022, 10(1), 170; https://doi.org/10.3390/biomedicines10010170 - 13 Jan 2022
Cited by 12 | Viewed by 6263
Abstract
Pulmonary arterial hypertension (PAH) is a disease that progress over time and is defined as an increase in pulmonary arterial pressure and pulmonary vascular resistance that frequently leads to right-ventricular (RV) failure and death. Epigenetic modifications comprising DNA methylation, histone remodeling, and noncoding [...] Read more.
Pulmonary arterial hypertension (PAH) is a disease that progress over time and is defined as an increase in pulmonary arterial pressure and pulmonary vascular resistance that frequently leads to right-ventricular (RV) failure and death. Epigenetic modifications comprising DNA methylation, histone remodeling, and noncoding RNAs (ncRNAs) have been established to govern chromatin structure and transcriptional responses in various cell types during disease development. However, dysregulation of these epigenetic mechanisms has not yet been explored in detail in the pathology of pulmonary arterial hypertension and its progression with vascular remodeling and right-heart failure (RHF). Targeting epigenetic regulators including histone methylation, acetylation, or miRNAs offers many possible candidates for drug discovery and will no doubt be a tempting area to explore for PAH therapies. This review focuses on studies in epigenetic mechanisms including the writers, the readers, and the erasers of epigenetic marks and targeting epigenetic regulators or modifiers for treatment of PAH and its complications described as RHF. Data analyses from experimental cell models and animal induced PAH models have demonstrated that significant changes in the expression levels of multiple epigenetics modifiers such as HDMs, HDACs, sirtuins (Sirt1 and Sirt3), and BRD4 correlate strongly with proliferation, apoptosis, inflammation, and fibrosis linked to the pathological vascular remodeling during PAH development. The reversible characteristics of protein methylation and acetylation can be applied for exploring small-molecule modulators such as valproic acid (HDAC inhibitor) or resveratrol (Sirt1 activator) in different preclinical models for treatment of diseases including PAH and RHF. This review also presents to the readers the application of microfluidic devices to study sex differences in PAH pathophysiology, as well as for epigenetic analysis. Full article
(This article belongs to the Special Issue Druggability of Proteins/Enzymes)
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