Tag: Protein Function

Schematic of how interrupting ATPIF1 rescues cells with mitochondrial dysfunction

Scientists find potential target for treating mitochondrial disorders

March 27, 2014

Mitochondria, long known as “cellular power plants” for their generation of the key energy source adenosine triphosphate (ATP), are essential for proper cellular functions. Mitochondrial defects are often observed in a variety of diseases, including cancer, Alzheimer’s disease, and Parkinson’s disease, and are the hallmarks of a number of untreatable genetic mitochondrial disorders whose manifestations range from muscle weakness to organ failure. Whitehead Institute scientists have identified a protein whose inhibition could hold the key to alleviating suffering caused by such disorders.

Image comparing a surface form and cave form of the fish Astyanax mexicanus

Rapid evolution of novel forms: Environmental change triggers inborn capacity for adaptation

December 12, 2013

A team of researchers from Harvard Medical School and Whitehead Institute report that, at least in the case of one variety of cavefish, one agent of evolutionary change is the heat shock protein known as HSP90.

Image showing how cells with and without normal FLCN gene react to nutrients

Gene responsible for hereditary cancer syndrome found to disrupt critical growth-regulating pathway

November 7, 2013

Whitehead Institute scientists report that the gene mutated in the rare hereditary disorder known as Birt-Hogg-Dubé cancer syndrome prevents activation of mTORC1, a critical nutrient-sensing and growth-regulating cellular pathway.   

Microscope image of filamentation in Candida albicans with and without amphotericin B resistance

Understanding the evolution of drug resistance points to novel strategy for developing better antimicrobials

October 29, 2013

The most common fungal pathogen in humans, Candida albicans, rarely develops resistance to the antifungal drug amphotericin B (AmB).  This has been puzzling as the drug has been in clinical use for over 50 years. Whitehead Institute scientists have now discovered why.  The genetic mutations that enable certain strains of C. albicans to resist AmB simultaneously render it highly susceptible to environmental stressors and disarm its virulence factors.

Schematic showing nerve cells and person with Parkinson's disease within a yeast cell

Yeast, human stem cells drive discovery of new Parkinson’s disease drug targets

October 24, 2013

Using a discovery platform whose components range from yeast cells to human stem cells, Whitehead Institute scientists have identified a novel Parkinson’s disease drug target and a compound capable of repairing neurons derived from Parkinson’s patients.

Slides of mouse brain tissue from CJD mice that are infected with prions compared to tissue from FFI mice.

New models advance the study of deadly human prion diseases

August 19, 2013

By directly altering the gene coding for the prion protein (PrP), Whitehead Institute researchers have created mouse models of two neurodegenerative prion diseases, each of which manifests in different regions of the brain.  These new models for fatal familial insomnia (FFI) and Creutzfeldt-Jakob disease (CJD) accurately reflect the distinct patterns of destruction caused by the these diseases in humans.  Remarkably, as different as each disease is, they both spontaneously generate infectious prions.

Thwarting protein production slows cancer cells’ malignant march

July 18, 2013

Protein production or translation is tightly coupled to a highly conserved stress response—the heat shock response and its primary regulator, heat shock factor 1 (HSF1)—that cancer cells rely on for survival and proliferation, according to Whitehead Institute researchers. In mouse models of cancer, therapeutic inhibition of translation interrupts HSF1’s activity, dramatically slowing tumor growth and potentially rendering drug-resistant tumors responsive to other therapies.

Image showing how a cell with a misaligned spindle corrects the problem

Bearing witness to the phenomenon of symmetric cell division

July 18, 2013

For more than 125 years, scientists have been peering through microscopes, carefully watching cells divide. Until now, however, none has actually seen how cells manage to divide precisely into two equally-sized daughter cells during mitosis. Such perfect division depends on the position of the mitotic spindle (chromosomes, microtubules, and spindle poles) within the cell, and it’s now clear that human cells employ two specific mechanisms during the portion of division known as anaphase to correct mitotic spindle positioning.

Image: Glucocorticoids stimulates the production of ZFP36l2, which promotes the self-renewal of BFU-Es.

Scientists identify potential drug target for treatment-resistant anemias

June 9, 2013

Researchers at Whitehead Institute have identified a key target protein of glucocorticoids, the drugs that are used to increase red blood cell production in patients with certain types of anemia, including those resulting from trauma, sepsis, malaria, kidney dialysis, and chemotherapy.

Image of GATOR1's location in cells where it is functional and nonfunctional

Protein complex in key cell-growth pathway could help predict response to cancer therapy

May 30, 2013

Whitehead Institute researchers have identified a protein complex that, when mutated, sends the master growth regulatory pathway known as mTORC1 into overdrive. Researchers believe that mutations in this complex could serve as biomarkers to predict response to rapamycin treatment in cancer patients.

Diagram comparing enhancers and super-enhancers of two cell types

Genetic master controls expose cancers’ Achilles’ heel

April 11, 2013

In a surprising finding that helps explain fundamental behaviors of normal and diseased cells, Whitehead Institute scientists have discovered a set of powerful gene regulators dubbed “super-enhancers” that control cell state and identity.

Model for a function for Mot3 prion switching in teh repiro-fermentative cycle of wine yeasts

Protective prion keeps yeast cells from going it alone

March 28, 2013

A team of scientists from Whitehead Institute and the University of Texas Southwestern Medical Center has added markedly to the job description of prions as agents of change, identifying a prion capable of triggering a transition in yeast from its conventional single-celled form to a cooperative, multicellular structure. This change, which appears to improve yeast’s chances for survival in the face of hostile environmental conditions, is an epigenetic phenomenon—a heritable alteration brought about without any change to the organism’s underlying genome.

Pages

© Whitehead Institute for Biomedical Research         Nine Cambridge Center    Cambridge, MA 02142