Dr. Roger Brent, President and Director of Research at the Molecular Sciences Institute ("MSI"), announced today the release of a new approach to simulation of intracellular biochemical networks in the January 2005 edition of Nature Biotechnology. The research article, entitled "Automatic generation of cellular reaction networks with Moleculizer 1.0" (pdf) describes MSI's discrete stochastic event simulator, which keeps track of the thousands of complex species formed from pathway proteins as it simulates reactions between them by a standard Monte Carlo method. A distinguishing aspect of Moleculizer is its ability to generate protein complexes and reactions as they are needed, as opposed to generating all potential complexes and reactions all at once, a task that requires tremendous computer resources beyond the scope of most research labs.

A team led by Johns Hopkins scientists has found the first clear evidence that the process behind the human immune system's remarkable ability to recognize and respond to a million different proteins might have originated from a family of genes whose only apparent function is to jump around in genetic material. "Jumping genes" essentially cut themselves out of the genetic material, and scientists have suspected that this ability might have been borrowed by cells needing to build many different proteins from a specific, single set of instructions -- the key to recognizing a million immune-stimulating proteins. But until now, no jumping gene was known to behave just right.

Biologists at the University of California, San Diego have found a fundamental mechanism used by embryonic stem cells to assure that genetically damaged stem cells do not divide and pass along the damage to daughter stem cells. Their discovery, detailed in an advance online publication of the journal Nature Cell Biology, solves the longstanding mystery of how embryonic stem cells, which have the potential to divide an unlimited number of times and differentiate to make all of the cell types in the body, are able to avoid duplicating cells that have sustained genetic damage.