Nirjal Mainali

ORCID: 0000-0001-9679-1174
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Endoplasmic Reticulum Stress and Disease
  • Reproductive Biology and Fertility
  • Computational Drug Discovery Methods
  • Cholinesterase and Neurodegenerative Diseases
  • 14-3-3 protein interactions
  • Bioinformatics and Genomic Networks
  • Mitochondrial Function and Pathology
  • Autophagy in Disease and Therapy
  • Advanced Glycation End Products research
  • Tryptophan and brain disorders
  • Microtubule and mitosis dynamics
  • Wnt/β-catenin signaling in development and cancer
  • Ubiquitin and proteasome pathways
  • Protein Degradation and Inhibitors
  • Enzyme Catalysis and Immobilization
  • Genetics, Aging, and Longevity in Model Organisms
  • Protein Structure and Dynamics
  • Neuroscience and Neuropharmacology Research
  • Biotin and Related Studies
  • Cardiomyopathy and Myosin Studies

University of Arkansas for Medical Sciences
2020-2025

University of Arkansas at Little Rock
2020-2025

Institute on Aging
2023-2024

Abstract Glycogen synthase kinase-3β (GSK3β) controls many physiological pathways, and is implicated in diseases including Alzheimer’s several cancers. GSK3β-mediated phosphorylation of target residues microtubule-associated protein tau (MAPTAU) contributes to MAPTAU hyperphosphorylation subsequent formation neurofibrillary tangles. Inhibitors GSK3β protect against disease are therapeutic for A thiadiazolidinone drug, TDZD-8, a non-ATP-competitive inhibitor targeting with demonstrated...

10.1038/s41598-020-75020-w article EN cc-by Scientific Reports 2020-10-27

Abstract Cardiovascular diseases, including myocardial infarction (MI), constitute the leading cause of morbidity and mortality worldwide. Protein-aggregate deposition is a hallmark aging neurodegeneration. Our previous study reported that aggregation strikingly elevated in hearts hypertensive aged mice; however, no prior has addressed MI effects on heart or brain. Here, we present novel data brain mice following experimental MI, induced by left coronary artery (LCA) ligation. Infarcted...

10.1007/s11010-023-04856-3 article EN cc-by Molecular and Cellular Biochemistry 2023-11-03

Many age-progressive diseases are accompanied by (and likely caused by) the presence of protein aggregation in affected tissues. Protein aggregates conjoined complex protein-protein interactions, which remain poorly understood. Knowledge proteins that comprise aggregates, and their adherent interfaces, can be useful to identify therapeutic targets treat or prevent pathology, discover small molecules for disease interventions. We present web-based software evaluate rank influential...

10.6026/973206300200004 article EN cc-by Bioinformation 2024-01-31

Cryoprotectant toxicity is a limiting factor for the cryopreservation of many living systems. We were moved to address this problem by potential organ vitrification relieve severe shortage viable donor organs available human transplantation. The M22 solution presently only that has enabled and subsequent transplantation with survival large mammalian organs, but its remains an obstacle stockpiling therefore undertook series exploratory studies identify pretreatment interventions might reduce...

10.1016/j.cryobiol.2024.104881 article EN cc-by Cryobiology 2024-03-02

Protein homeostasis, the balance between protein synthesis and degradation, requires clearance of misfolded aggregated proteins is therefore considered to be an essential aspect establishing a physiologically effective proteome. Aging alters this balance, termed "proteostasis", resulting in progressive accumulation proteins. Defective proteostasis leads functional deterioration diverse regulatory processes during aging implicated etiology multiple pathological conditions underlying variety...

10.20517/jca.2023.4 article EN The Journal of Cardiovascular Aging 2023-01-01

The mammalian 14-3-3 family comprises seven intrinsically unstructured, evolutionarily conserved proteins that bind >200 protein targets, thereby modulating cell-signaling pathways. presence of in cerebrospinal fluid provides a sensitive and specific biomarker neuronal damage associated with Alzheimer’s disease (AD), Creutzfeldt−Jakob (CJD), spongiform encephalitis, brain cancers, stroke. We observed significant enrichment paralogs G, S, Z human aggregates diagnostic AD. used intra-aggregate...

10.3390/ijms232415457 article EN International Journal of Molecular Sciences 2022-12-07

Chronic, low-grade inflammation has been implicated in aging and age-dependent conditions, including Alzheimer’s disease, cardiomyopathy, cancer. One of the age-associated processes underlying chronic is protein aggregation, which neuroinflammation a broad spectrum neurodegenerative diseases such as Alzheimer’s, Huntington’s, Parkinson’s diseases. We screened panel bioactive thiadiazolidinones (TDZDs) from our in-house library for rescue aggregation human-cell C. elegans models...

10.3390/ph16101498 article EN cc-by Pharmaceuticals 2023-10-20

Alzheimer's disease (AD) is characterized by peri-neuronal amyloid plaque and intra-neuronal neurofibrillary tangles. These aggregates are identified the immunodetection of "seed" proteins (Aβ

10.1016/j.isci.2023.108745 article EN cc-by-nc-nd iScience 2023-12-19
Coming Soon ...