A5063659854- Blood disorders and treatments
- Malaria Research and Control
- Acute Myeloid Leukemia Research
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Medicinal Plants and Neuroprotection
- Endoplasmic Reticulum Stress and Disease
- Fungal and yeast genetics research
- Trypanosoma species research and implications
- RNA modifications and cancer
- Pesticide Exposure and Toxicity
- Mosquito-borne diseases and control
- HIV Research and Treatment
- Heavy Metal Exposure and Toxicity
- Trace Elements in Health
- Computational Drug Discovery Methods
- Alzheimer's disease research and treatments
- Genetics, Aging, and Longevity in Model Organisms
- Iron Metabolism and Disorders
- Pneumocystis jirovecii pneumonia detection and treatment
- Mitochondrial Function and Pathology
- Peroxisome Proliferator-Activated Receptors
- Cholinesterase and Neurodegenerative Diseases
- GABA and Rice Research
- HIV/AIDS drug development and treatment
- Piperaceae Chemical and Biological Studies
Mahidol University
2014-2022
A major cause of the paucity new starting points for drug discovery is lack interaction between academia and industry. Much global resource in biology present universities, whereas focus medicinal chemistry still largely within Open source discovery, with sharing information, clearly a first step towards overcoming this gap. But interface could especially be bridged through scale-up open physical compounds, which would accelerate finding discovery. The Medicines Malaria Venture Box...
Lysine deacetylases (KDACs) inhibitors may have therapeutic value in anti‐malarial combination therapies with artemisinin. To evaluate connections between KDACs and artemisinin, Saccharomyces cerevisiae deletion mutants KDAC genes were assayed. Deletion of RPD3 , but not other genes, resulted strong sensitivity to which was also observed sit4 Δ impaired endoplasmic reticulum (ER) Golgi protein trafficking. Decreased accumulation the transporters Pdr5p, Fur4p, Tat2p rpd3 cells. The unfolded...
Abstract Mutations in the human SBDS gene is most common cause of Shwachman‐Diamond syndrome (SDS). The protein participates ribosome biogenesis; however, effects beyond reduced translation efficiency are thought to be involved SDS progression. Impaired mitochondrial function has been reported for cells lacking either or Sdo1p, Saccharomyces cerevisiae ortholog. To better understand how loss SBDS/Sdo1p leads mitochondria damage, we utilized S. model SDS. Yeast deleted SDO1 show increased...
Colorectal cancer is a common worldwide and reduced expression of the DNA repair endonuclease XPF (xeroderma pigmentosum complementation group F) associated with colorectal cancer. Bacopa monnieri extracts were previously found to exhibit chemical-genetic synthetic lethal effects in Saccharomyces cerevisiae model lacking Rad1p, structural functional homologue human XPF. However, mechanisms for B. limit proliferation promote an apoptosis-like event RAD1 deleted yeast was not elucidated. Our...
PEX34, encoding a peroxisomal protein implicated in regulating peroxisome numbers, was identified as high copy suppressor, capable of bypassing impaired acetate utilization agc1∆ yeast. However, improved growth yeast on is not mediated through proliferation. Instead, stress to the endoplasmic reticulum and mitochondria from PEX34 overexpression appears contribute enhanced The citrate/2-oxoglutarate carrier Yhm2p required for stimulated medium, suggesting that suppressor effect increased...
Shwachman-Diamond syndrome (SDS) is a congenital disease that affects the bone marrow, skeletal system, and pancreas. The majority of patients with SDS have mutations in SBDS gene, involved ribosome biogenesis as well other processes. A Saccharomyces cerevisiae model SDS, lacking Sdo1p yeast orthologue SBDS, was utilized to better understand molecular pathogenesis development this disease. Deletion SDO1 resulted three-fold over-accumulation intracellular iron. Phenotypes associated impaired...
Artemisinins are widely used to treat Plasmodium infections due their high clinical efficacy; however, the antimalarial mechanism of artemisinin remains unresolved. Mutations in P. falciparum ATPase6 (PfATP6), a sarcoplasmic endoplasmic reticulum Ca2+-transporting ATPase, associated with increased tolerance artemisinin. We utilized Saccharomyces cerevisiae as model examine involvement Pmr1p, functional homolog PfATP6, on toxicity Our analysis demonstrated that cells lacking Pmr1p less...