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Pancreatic Adenocarcinoma: An Analysis of Drug Therapy Options through Interaction Maps and Graph Theory

Gupta et al. | Feb 04, 2014

Pancreatic Adenocarcinoma: An Analysis of Drug Therapy Options through Interaction Maps and Graph Theory

Cancer is often caused by improper function of a few proteins, and sometimes it takes only a few proteins to malfunction to cause drastic changes in cells. Here the authors look at the genes that were mutated in patients with a type of pancreatic cancer to identify proteins that are important in causing cancer. They also determined which proteins currently lack effective treatment, and suggest that certain proteins (named KRAS, CDKN2A, and RBBP8) are the most important candidates for developing drugs to treat pancreatic cancer.

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Testing HCN1 channel dysregulation in the prefrontal cortex using a novel piezoelectric silk neuromodulator

Mathew et al. | May 05, 2021

Testing HCN1 channel dysregulation in the prefrontal cortex using a novel piezoelectric silk neuromodulator

Although no comprehensive characterization of schizophrenia exists, there is a general consensus that patients have electrical dysfunction in the prefrontal cortex. The authors designed a novel piezoelectric silk-based implant and optimized electrical output through the addition of conductive materials zinc oxide (ZnO) and aluminum nitride (AlN). With further research and compatibility studies, this implant could rectify electrical misfiring in the infralimbic prefrontal cortex.

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Investigating the Role of the Novel ESCRT-III Recruitment Factor CCDC11 in HIV Budding: A Potential Target for Antiviral Therapy

Takemaru et al. | Feb 24, 2020

Investigating the Role of the Novel ESCRT-III Recruitment Factor CCDC11 in HIV Budding: A Potential Target for Antiviral Therapy

Acquired immunodeficiency syndrome (AIDS) is a life-threatening condition caused by the human immunodeficiency virus (HIV). In this work, Takemaru et al explored the role of Coiled-Coil Domain-Containing 11 (CCDC11) in HIV-1 budding. Their results suggest that CCDC11 is critical for efficient HIV-1 budding, potentially indicating CCDC11 a viable target for antiviral therapeutics without major side effects.

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The role of CYP46A1 and its metabolic product, 24S-hydroxycholesterol, in Neuro 2A cell death

Ni et al. | May 11, 2021

The role of CYP46A1 and its metabolic product, 24S-hydroxycholesterol, in Neuro 2A cell death

Cholesterol is a major component of neuronal cell membrane and myelin sheath. In this study, the authors either transfected Neuro 2A cells with CYP46A1 cDNA or treated the cells with 24SHC. Cells expressing CYP46A1 had significantly less viability compared to the negative control. Up to 55% reduction in cell viability was also observed in 24S-HC-treated cells. This work supports that CYP46A1 and 24S-HC could directly trigger cell death. The direct involvement of 24S-HC in cell death provides further evidence that 24S-HC can be a promising biomarker for diagnosing brain damage severity.

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Expression of Anti-Neurodegeneration Genes in Mutant Caenorhabditis elegans Using CRISPR-Cas9 Improves Behavior Associated With Alzheimer’s Disease

Mishra et al. | Sep 14, 2019

Expression of Anti-Neurodegeneration Genes in Mutant <em>Caenorhabditis elegans</em> Using CRISPR-Cas9 Improves Behavior Associated With Alzheimer’s Disease

Alzheimer's disease is one of the leading causes of death in the United States and is characterized by neurodegeneration. Mishra et al. wanted to understand the role of two transport proteins, LRP1 and AQP4, in the neurodegeneration of Alzheimer's disease. They used a model organism for Alzheimer's disease, the nematode C. elegans, and genetic engineering to look at whether they would see a decrease in neurodegeneration if they increased the amount of these two transport proteins. They found that the best improvements were caused by increased expression of both transport proteins, with smaller improvements when just one of the proteins is overly expressed. Their work has important implications for how we understand neurodegeneration in Alzheimer's disease and what we can do to slow or prevent the progression of the disease.

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