Category Health/Medical

Widespread Tumor Suppression Mechanism Stops Cancer Progression by interfering with cancer cell Metabolism

Novel Parkin ubiquitome in cancer.(A) Bioinformatics analysis of predicted protein networks regulated by Parkin ubiquitination in the absence of mitochondrial uncoupling, including cell death (HK1, MCL1, and HMGB1), glucose metabolism involving glycolysis (HK1 and TPI1) and the PPP (TALDO1 and TKT), protein folding (CCT7 and HSPA1A, also known as HSP72), and mitochondrial dynamics (RHOT1, FIS1, and MFN2). Parkin-directed ubiquitination sites (Lys, K) identified by SILAC proteomics in each target protein are indicated. (B) PC3 cells in the presence or absence of Parkin were immunoprecipitated with an antibody to MFN2, and immune complexes were probed with antibodies to ubiquitin (Ub) or MFN2 by Western blotting. IP, immunoprecipitation; IB, immunoblot. (C) The conditions are as in (B) exce...
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Like venom coursing through the body: Researchers identify Mechanism driving COVID-19 Mortality

Students in white lab coats and safety gear stand around a microscope in Dr. Chilton's lab
In a photo taken prior to the pandemic, Dr. Chilton (second from left) and his lab team examine how genetic and epigenetic variations interact with human diets to drive inflammation and inflammatory disorders, as well as psychiatric and developmental disorders.Chris Richards/University of Arizona

An enzyme with an elusive role in severe inflammation may be a key mechanism driving COVID-19 severity and could provide a new therapeutic target to reduce COVID-19 mortality, according to a study published in the Journal of Clinical Investigation.

Researchers from the University of Arizona, in collaboration with Stony Brook University and Wake Forest University School of Medicine, analyzed blood samples from two COVID-19 patient cohorts and found that circulation of the enzyme – secreted p...

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High Cholesterol Fuels Cancer by Fostering Resistance to a form of Cell Death

The proposed model to explain how cancer cells respond to 27HC treatment. Acute (left) treatment with 27HC disrupts lipid metabolism via interfering with SREBPs and LXR signaling, and this results in the inhibition of cell growth and migration. Cancer cells can adapt to the metabolic stress imposed by chronic treatment by 27HC (right). The cells that survive (27HC resistant cells) increase lipid uptake and accommodate the metabolic stress associated with this activity by upregulating the activity of processes that allow them to withstand lipid oxidative stress (ferroptosis); an activity which confers upon them enhanced tumor growth and metastatic capabilities. Numerical source data are reported in the Source Data File.

Chronically high cholesterol levels are known to be associated with...

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Eyes provide peek at Alzheimer’s Disease Risk

Amyloid deposits tagged by curcumin fluoresce in a retinal scan. Photo credit: NeuroVision

Amyloid plaques are protein deposits that collect between brain cells, hindering function and eventually leading to neuronal death. They are considered a hallmark of Alzheimer’s disease (AD), and the focus of multiple investigations designed to reduce or prevent their formation, including the nationwide A4 study.

But amyloid deposits may also occur in the retina of the eye, often in patients clinically diagnosed with AD, suggesting similar pathologies in both organs...

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