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This Week in Cell: Mar 9, 2016

Protein isoforms generated through alternative splicing don't always interact with the same targets, as researchers from the Dana-Farber Cancer Institute report in Cell. Marc Vidal and his colleagues cloned full-length open reading frames of alternatively spliced transcripts for nearly 1,500 human genes. Then, using protein-protein interaction profiling, they compared the pairs to find that they only shared about half their targets. This, the researchers note, suggests that protein isoforms act more like distinct proteins rather than as variations of the same protein.

Harvard Medical School researchers have characterized recurrent double-strand breaks in primary neural stem/progenitor cells to find that they may influence neurodevelopment and neural functions. The team used a high-throughput, genome-wide, translocation sequencing approach to map genome-wide double-strand breaks. From this, they found 27 recurrent break clusters, all of which fall within gene bodies. Most of those clusters, the team adds, are in long, transcribed, and late-replicating genes, and 90 percent of the genes are involved in synapse function or neural cell adhesion.

Researchers from the University of California, Los Angeles, and Northwestern University analyzed lipid A-induced transcription using a combination of nascent transcript RNA-seq, ChIP-seq, and binding motif datasets. This, they say, enabled them to examine the molecular mechanisms that regulate genes that make up the inflammatory cascade. In particular, they report that NF-κB and IRF3 act through different mechanisms to activate inflammatory genes.