A once-a-month electronic newsletter of basic, preclinical and translational
research news from the Johns Hopkins School of Medicine. Please forward
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RESEARCH HIGHLIGHTS:
End Time
Master Myc
Where Did I Put Those Keys?
Tiling TIP Chips
From the Annals of Drug Design…
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RESEARCH HIGHLIGHTS:
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End Time
To prevent loss of genetic information or chromosome damage each time a cell divides, chromosome ends—telomeres—must be lengthened during each cell division. Carol Greider and colleagues have shown that an enzyme critical for regulating the process of cell division, called CDK1, also is responsible for controlling when telomeres are elongated. Blocking CDK1 activity in yeast prevents lengthening of a de novo telomere generated by a break near the end of chromosome VII. Now they’re looking to see if the same occurs in mammalian cells.
Read the paper here.
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Master Myc
Myc, a gene implicated in many human cancers, normally acts to turn on other genes. To better understand how myc contributes to disease progression, Chi Dang and colleagues have identified nearly every gene activated by myc in a human lymphoid tumor. They find 668 targets, of which 48 are genes that also turn on other genes, suggesting that myc acts in a domino-like fashion to induce tumorigenesis.
Read the paper here.
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Where Did I Put Those Keys?
Long-term memory storage depends on the strength of the connections between neurons in the brain. Now, Paul Worley and colleagues have figured out how these cells strengthen their connections. A protein called Arc has long been implicated in memory storage, yet until now, how it works has remained a mystery. The research team discovered that Arc controls the strength of neuron connections by controlling how often the molecules joining two cells are recycled, ultimately controlling how many of these molecules are at the surface of the cell.
Read the news release here.
Read the paper on Arc function here.
Read the paper on Arc controlling receptor number here.
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Tiling TIP Chips
High-throughput biology remains costly and selective because DNA microarrays are expensive they often contain only limited bits of genetic information—often only sequences of genes and not intervening DNA. Jef Boeke and colleagues in the High Throughput Biology (HiT) Center now have invented genomic tiling DNA chips containing evenly spaced DNA sequences from the genome, w/o any preselection as to whether the sequence is inside or outside a gene. And they have piled on a second layer of tiling so that each spot contains 2 bits of info; one layer reading in spots from left to right, and the second layer reading in spots top to bottom. The new high-density chips cram twice the amount of info in to one standard chip, effectively halving the price of one experiment. One thing they’ve done with their new chip is to identify all the transposon insertion points in different strains of yeast. They hope this can be translated to humans in the future to identify disease-causing mutations caused by these pesky jumping genes.
Read the news release here.
Read the PNAS paper here.
Read the Nature Methods paper here.
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From the Annals of Drug Design…
Cancer arises when cells divide uncontrollably and protein manufacture is critical for all cell division and survival. In studying two closely related enzymes important for cells in making proteins, Jun Liu and colleagues have identified a class of chemicals that selectively inhibit one of the enzymes. Since human cells missing the enzyme cannot divide, they reason that the inhibitory chemical may pave the road to new anti-cancer drugs. In fact, applying the chemical to human cancer cells not only causes the cells to stop dividing, it also causes the cells to die.
Read the paper here.
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-- JHM --
