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Blocking a specific protein complex (mTORC2) prevents prostate tumor formation in mice with a deleted PTEN gene. Inhibition of this complex in normal prostate cells, however, appears to have no effect, suggesting that the protein complex may be a future target for drug development.

Scientists at the Whitehead Institute for Biomedical Research have found that a single gene, known as PARK9, protects cells from manganese toxicity and rescues neurons from over-expression of the protein alpha-synuclein. Misfolded alpha-synuclein is the hallmark of Parkinson’s disease.

Whitehead Institute researchers have reliably produced mice and mouse cell lines with identical configurations of the specific factors needed to reprogram adult cells to an embryonic-stem-cell-like state. These cell lines may be used to screen for potential drug substitutions for the virally-inserted reprogramming genes and as a tool to enhance understanding of how reprogramming works.

Jaenisch has been named a recipient of the 2008 Meira and Shaul G. Massry Prize in recognition of his work in creating so-called induced pluripotent stem cells, or IPS cells.

Adult cells, from both humans and mice, can be converted into embryonic stem cell-like cells (induced pluripotent stem cells, or iPS cells) using a single virus to insert four reprogramming genes into the cells’ genomes.

The MLL-AF4 fusion protein, which causes the blood cancer called mixed-lineage leukemia (MLL), binds to several genes responsible for early blood cell development. MLL-AF4 also alters the chromatin proteins associated with these genes, a state that is associated with cancer and leukemia progression.

Expression of the Dazl gene in embryonic germ cells primes these cells for stimulation by an external signal that initiates meiosis (the process of halving the cell’s chromosomes).

Scientists have long struggled for details on how the immune system responds to complex pathogens such as the parasite Toxoplasma gondii and herpes viruses. Adapting an existing technology, researchers have pinpointed precise molecular targets that these pathogens present to signal T cells.

A new quantitative model accurately predicts the three-dimensional forces involved in creating and maintaining certain biological membranes.

In yeast, a protein-misfolding mechanism can reveal hidden genetic variations and thus generate new phenotypes that may increase cell survival. Researchers now have demonstrated that when yeast cells are stressed, this mechanism is triggered much more often.