Role of p53 inhibitor in tumor suppression and aging

The p53 tumor suppressor plays a critical role in cancer formation, and many anticancer strategies aim to activate p53 in order to curb tumor formation. Mdm2 is a key inhibitor of p53 and therefore an attractive target to modulate p53 activity in cells. However, conflicting evidence exists regarding whether or not p53-mediated tumor suppression comes at the cost of accelerated aging.

In the January 1 issue of Genes & Development, Dr. Mary Ellen Perry and colleagues validate the p53 inhibitor, Mdm2, as a promising target for cancer therapies.

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Brain Activity Could Affect Alzheimer’s Disease Risk

The activity of connections among brain cells significantly affects levels of the toxic protein beta-amyloid (Aß) that is a major cause of Alzheimer’s disease (AD), researchers have found. Aß is produced by the cleavage of amyloid precursor protein (APP) within brain cells.

Findings suggest that the kind of mental activity people practice or drugs they might take for depression or anxiety could affect their AD risk or the disease progression.
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Modified Atomic Force Microscopy Proves Critical to Uncovering Cell-growth Secret

Researchers using a customized atomic force microscope (AFM) have discovered new evidence for how the fibrous scaffolding within our cells, which is made of the protein actin, responds to obstacles in its environment.

The discovery demonstrates a technique for tracking a cell’s growth history, and if it proves valid outside of the laboratory, researchers may one day look for actin-growth clues while tracking the pathways of spreading cancers, immune cells, and other free-moving cells that crawl throughout the body.
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Study suggests way to re-energize immune response to chronic viral infection

Like boxers wearied by a 15-round bout, the immune system’s CD8 T cells eventually become “exhausted” in their battle against persistent viral infection, and less effective in fighting the disease.

In a study to be published Dec. 28 on the journal Nature’s website, researchers at Dana-Farber Cancer Institute and Emory University have traced the problem to a gene that turns off the infection-fighting drive of CD8 T cells in mice. The discovery raises the possibility that CD8 cell exhaustion can be reversed in human patients, reinvigorating the immune system’s defenses against chronic viral infections ranging from hepatitis to HIV, the virus that causes AIDS.

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Scientists lift malaria’s cloak of invisibility

The world’s deadliest malaria parasite, Plasmodium falciparum, sneaks past the human immune system with the help of a wardrobe of invisibility cloaks. If a person’s immune cells learn to recognize one of the parasite’s many camouflage proteins, the surviving invaders can swap disguises and slip away again to cause more damage. Malaria kills an estimated 2.7 million people annually worldwide, 75 percent of them children in Africa.

Howard Hughes Medical Institute (HHMI) international research scholars in Australia have determined how P. falciparum can turn on one cloaking gene and keep dozens of others silent until each is needed in turn. Their findings, published in the December 28, 2005, issue of Nature, reveal the mechanism of action of the genetic machinery thought to be the key to the parasite’s survival.

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Researchers discover how a high-fat diet causes type 2 diabetes

Howard Hughes Medical Institute researchers have discovered a molecular link between a high-fat, Western-style diet, and the onset of type 2 diabetes. In studies in mice, the scientists showed that a high-fat diet disrupts insulin production, resulting in the classic signs of type 2 diabetes.

In an article published in the December 29, 2005, issue of the journal Cell, the researchers report that knocking out a single gene encoding the enzyme GnT-4a glycosyltransferase (GnT-4a ) disrupts insulin production. Importantly, the scientists showed that a high-fat diet suppresses the activity of GnT-4a and leads to type 2 diabetes due to failure of the pancreatic beta cells.

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Decoding The Genome of a Fungus May Help Combat Disease And Lead To New Drugs

An international consortium of researchers led by the University of Manchester has cracked the gene code behind a key family of fungi, which includes both the leading cause of death in leukaemia and bone marrow transplant patients and an essential ingredient of soy sauce.

The ‘genome sequences’ or genetic maps for the fungi Aspergillus fumigatus, Aspergillus nidulans and Aspergillus oryzae are published on 22 December in Nature magazine. Despite being from the same fungal family, they have been found to be as genetically different as fish and man.

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Cleistothecium – sexual spore container, false coloured from Aspergillus nidulans. (Courtesy of Professor Rheinhard Fischer, Institut für Angewandte Biowissenschaften Abt. für Angewandte Mikrobiologie der Universität Karlsruh, with whom copyright remains)

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