News

Whitehead Institute scientists have used a yeast cell-based drug screen to identify a class of molecules that target the amyloid-β (Aβ) peptide involved in Alzheimer’s disease (AD).  

Whitehead Institute researchers have determined that poly(A) tails on messenger RNAs (mRNAs) shift their role in the regulation of protein production during early embryogenesis. This finding about the regulation of mRNA translation also provides insight into how microRNAs control protein production. 

Whitehead Institute researchers have determined that the lipid storage disorder Niemann-Pick type C1 (NPC1) disease is caused not only by defects in cholesterol processing but also in autophagy—a key cellular degradation pathway that malfunctions in many neurodegenerative diseases.

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.

Since the completion of the Human Genome Project, which identified nearly 20,000 protein-coding genes, scientists have been trying to decipher the roles of those genes. A new approach developed at MIT, the Broad Institute, and the Whitehead Institute should speed up the process by allowing researchers to study the entire genome at once.

A team of researchers from Whitehead Institute and Sanford-Burnham Research Institute has brought new clarity to the picture of how gene-environmental interactions can kill nerve cells that make dopamine. The study uses patient-derived stem cells to show that a mutation in the α-synuclein gene causes increased vulnerability to pesticides, leading to Parkinson’s disease.

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.   

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.

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.

Revealing influenza’s truly insidious nature, Whitehead Institute scientists have discovered that the virus is able to infect its host by first killing off the cells of the immune system that are actually best equipped to neutralize the virus.