January 31, 2006
In 1991, a team of scientists isolated a gene whose protein regulates the copying of genes, called a transcription factor. They named their find acute myeloid leukemia 1, or AML1, highlighting the fact that the gene is one of the most common chromosomal breakpoints in people with acute myeloid leukemia. As often happens with initial gene names, however, the AML1 moniker has proved to be biologically shortsighted. AML1, now also known as Runx1, has over the last 15 years been linked to the differentiation of red blood cells, bone cells, and certain immune cells. Now, in the February 2 issue of the journal Neuron, NIDCR grantees and colleagues show in mouse studies that AML1/Runx1 seems to play a major role in coordinating the differentiation of a broad subset of nociceptive cells, the front line sensory nerve cells that initiate the sensation that we recognize as pain. By adulthood, the scientists determined the Runx1 protein is restricted to nociceptive cells that express the surface-bound receptor for neurotrophin, an important family of growth factors. The scientists then showed that within these cells the Runx1 protein helps to turn on and off many ion channels, the pore-forming proteins that allow the cell to cell transfer of nociceptive information. In fact, the scientists reported that adult mice lacking Runx1 showed specific defects in their perception of thermal and neuropathic pain. They noted the identification of Runx1 as “a core transcriptional control program for many ion channels and receptors known transduce noxious stimuli has intriguing implications for the design of more effective pain therapies.”
- Read more about this paper by Chen, Ma, et. al.