all Lewis Cantley stories

Dinosaur protein preserved over time

50443248 — Fri, 01 May 2009 20:08:29 -0400

Ancient protein dating back 80 million years to the Cretaceous geologic period has been preserved in bone fragments and soft tissues of a type of duck-billed dinosaur, according to a study in the May 1 issue of Science.

Led by scientists at Beth Israel Deaconess Medical Center (BIDMC) and North Carolina State University (NCSU), the new findings support earlier results from analyses suggesting that collagen protein survived in the bones of a well-preserved Tyrannosaurus rex, and offer robust new evidence supporting previous conclusions that birds and dinosaurs are evolutionarily related.

Molecular analysis confirms T. Rex's evolutionary link to birds

yvette — Mon, 21 Apr 2008 16:25:39 -0400

Putting more meat on the theory that dinosaurs' closest living relatives are modern-day birds, molecular analysis of a shred of 68-million-year-old Tyrannosaurus rex protein -- along with that of 21 modern species -- confirms that dinosaurs share common ancestry with chickens, ostriches, and to a lesser extent, alligators.

Functional protein changes caught and quantified

70652986 — Mon, 26 Mar 2007 06:17:58 -0400

Just knowing that a protein is expressed in a cell does not reveal what it is up to; increasingly, the chemical modifications it undergoes are the key to understanding its function at any given time. A study from the laboratory of Steven Gygi, Harvard Medical School assistant professor of cell biology, uses one of the most powerful tools of proteomics, mass spectrometry, to pinpoint the dynamics of a common alteration in cells: protein phosphorylation, or the addition of phosphate groups. In order to track the changes, Gygi's team bathed cells in a brew that contained two amino acids made from the stable isotope carbon-13 instead of standard carbon-12. Proteins in these cells were slightly heavier, so they could be distinguished from normal proteins in a mass spectrometer.

Faulty gene signaling could lead to development of Crohn's disease

70652986 — Mon, 26 Mar 2007 07:10:00 -0400

Crohn's disease is an inflammatory bowel disease that afflicts up to 1 million Americans, with approximately 30,000 new cases diagnosed each year.

According to the study's lead author, BWH's Derek W. Abbott, MD, PhD, "The discovery of this faulty signaling process is a first step in helping us understand and ultimately address the underlying mechanism that causes Crohn's disease to develop. We hope that this first step will ultimately lead to the development of novel strategies to treat or prevent the disease from occurring."

While working with the Crohn's disease gene NOD2, researchers discovered that the mutant forms of NOD2 fail to trigger a key signaling process. The activation of NOD2 impacts the regulation of the body's inflammatory responses. It is thought that Crohn's disease flare-ups are caused by the interruption of these inflammatory responses. Understanding how the disease develops will ultimately help researchers identify treatments for this frequently debilitating disease.

According to senior author Lewis C. Cantley PhD, of BIDMC, "Understanding the mechanisms underlying Crohn's disease could ultimately lead to new drug therapies. Our next steps are to further elucidate this signaling pathway to determine optimal targets for therapeutic intervention."

Study yields insights into precancerous condition

70652986 — Mon, 26 Mar 2007 07:10:18 -0400

Caused by a mutation that inactivates the tumor suppressor gene LKB1, PJS causes gastrointestinal polyps that have a 30 to 50 percent chance of becoming cancerous, says senior author Lewis Cantley, PhD, chief of the Division of Signal Transduction at Beth Israel Deaconess Medical Center (BIDMC) and a member of the Department of Systems Biology at Harvard Medical School.

Research conducted by Cantley's laboratory on two other genetic conditions with symptoms similar to PJS had found that the diseases involved defects in the regulation of a protein called mTOR, so the researchers decided to look for a link between LKB1 and mTOR.

As predicted, they found that mouse cells lacking LKB1 and cells from PJS mouse polyps showed the activation of molecules known to be downstream of the mTOR protein.

"We knew that the drug rapamycin [commonly used to prevent newly transplanted organs from being rejected] could block mTOR," says Cantley. "These new results suggest that the use of mTOR inhibitors, including rapamycin analogs currently being tested in clinical trials for the treatment of cancers and tuberous sclerosis, may be useful for the treatment of polyps arising in PJS patients, and possibly in other tumors that result from the sporadic loss of LKB1."

New study identifies inhibitor of anthrax toxin

70652986 — Mon, 26 Mar 2007 05:33:57 -0400

Findings by a research team could eventually lead to the development of a protease inhibitor drug, which in combination with antibiotics could be used to treat anthrax cases later in the disease, at a point when antibiotics alone are no longer effective. “Unlike most types of bacteria, bacillus anthracis has the ability to produce large amounts of a toxin that can kill the patient even after antibiotics have destroyed the bacteria,” explains the study's senior author, Lewis Cantley, chief of the Division of Signal Transduction at Beth Israel Deaconess Medical Center (BIDMC) and professor of systems biology at Harvard Medical School. “This toxin is released within days of the initial infection, and is impervious to antibiotics.” Using a “mixture-based peptide library” technique developed by BIDMC scientist Benjamin Turk, the researchers analyzed trillions of peptides to determine an optimal peptide substrate for lethal factor, the active agent in the anthrax toxin. Funding for this study came from the National Institutes of Health, the U.S. National Science Foundation and the U.S. Army. The discovery was described in the January 2004 issue of Nature Structural & Molecular Biology.