In a study to be published this week, a research team is challenging a prevailing belief about the behavior of a human protein linked to the formation of cancer, possibly breathing new life into the search for therapies that will inhibit that protein from "turning on" genes involved in abnormal cell proliferation.
"The body is made up of cells that communicate with each other and with external cues via receptors at their surfaces. To generate cellular responses, signaling pathways are activated that initiate movement of proteins to specific locations inside the cells, notably the nucleus, where DNA is situated," said Diane Lidke, assistant professor at the University of New Mexico School of Medicine's department of pathology and lead author on the paper to be published Jan. 29 in the Journal of Biological Chemistry.
One particular pathway, the extracellular signal-regulated kinase (ERK) pathway, is altered in about 30 percent of all human cancers, said Lidke, who worked on the project during a postdoctoral stint in the lab of Thomas Jovin at the Max Planck Institute for Biophysical Chemistry. "It has been suspected for a long time that alterations of the ERK pathway could be the founding mutation behind cancers, and this was shown recently for melanoma."
ERKs act as messenger molecules by relaying signals that are received from outside the cell to the administrative core, the nucleus. To do so, ERK must move from its home in the intracellular fluid to the nucleus of the cell, turn on several genes while turning off others, which in turn finally tells the cell to divide or differentiate.
ERK's entry in the nucleus is unconventional, because the protein lacks the ability to bind to the known nuclear import proteins, Lidke said.
For more than a decade, scientists in this intense field of research thought that two molecules of ERK had to pair with each other after being activated in order to enter in the nu
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