News Archive

 

Graphic of gene expression machinery and the protein complexes Mediator and Cohesin forming a DNA loop

Surprise in genome structure linked to developmental diseases

August 18, 2010

The genes that are responsible for maintaining each cell type form DNA loops that link control elements for these genes. This surprising genome structure is generated and reinforced by two essential protein complexes that bridge the loops and contribute to proper gene regulation.

RNA snippets control protein production by disabling mRNAs

August 16, 2010

Short pieces of RNA, called microRNAs, control protein production by causing the proteins’ RNA templates (known as messenger RNA or mRNA) to be disabled by the cell, according to Whitehead Institute scientists.

New Whitehead Member Piyush Gupta takes aim at normal and cancer stem cells

August 11, 2010

Cancer biologist Piyush Gupta joins the Whitehead Institute faculty in September on a mission to shed new light on the mechanisms that determine why some cells in our bodies behave appropriately while others venture down destructive, malignant paths.

Human embryonic stem cells and reprogrammed cells virtually identical

August 5, 2010

Human embryonic stem (ES) cells and adult cells reprogrammed to an embryonic stem cell-like state—so-called induced pluripotent stem or iPS cells—exhibit very few differences in their gene expression signatures and are nearly indistinguishable in their chromatin state, according to Whitehead Institute researchers.

Protein that predicts prognosis of leukemia patients may also be a therapeutic target

July 8, 2010

Researchers at Whitehead Institute and Children’s Hospital Boston have identified a protein, called Musashi 2, that is predictive of prognosis in acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) patients. High levels of Musashi 2 protein is associated with increased cell proliferation, decreased cell maturation, and multiple cancer-related cellular pathways in human leukemias.

Image of purple intestinal epithelial cells extracted from a teratoma seeded by reprogrammed blood cells.

Reprogrammed human blood cells show promise for disease research

July 1, 2010

Cells from frozen human blood samples can be reprogrammed to an embryonic stem-cell-like state, according to Whitehead Institute researchers. These cells can be multiplied and used to study the genetic and molecular mechanisms of blood disorders and other diseases.

Gerald Fink awarded 2010 Gruber Genetics Prize

June 30, 2010

Whitehead Institute Founding Member Gerald Fink has been awarded the 2010 Genetics Prize of The Peter and Patricia Gruber Foundation for his groundbreaking research in yeast genetics.

Low oxygen levels prevent X chromosome inactivation in human embryonic stem cells

May 13, 2010

Oxygen levels in the lab can permanently alter human embryonic stem (ES) cells, specifically inducing X chromosome inactivation in female cells, according to Whitehead Institute researchers.

How microtubules let go of their attachments during cell division

May 13, 2010

Whitehead Institute researchers have determined a key part of how cells regulate the chromosome/microtubule interface, which is central to proper chromosomal distribution during cell division.

Scientists create human embryonic stem cells with enhanced pluripotency

May 3, 2010

Whitehead Institute researchers have converted established human induced pluripotent stem (iPS) cells and human embryonic stem (ES) cells to a base state of greater pluripotency. 

Embryonic stem cells reveal oncogene’s secret growth formula

April 29, 2010

Whitehead Institute researchers have identified the mechanism that the protein c-Myc uses to regulate gene transcription, which affects one-third of the expressed genes in the genome. The work also reveals a general role for this mechanism in gene control, which is called transcriptional pause release.

Microscope image of the transitional phase of yeast prions

A different tune: cellular IPOD plays role in prion biology

April 26, 2010

According to Whitehead Institute researchers, cells take advantage of a biologically ancient compartment to sequester prions, an action that can initially prevent the prions’ phenotypic expression. While in this compartment, less stably heritable prion plaques also mature to a more transmissible state.

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