IRVINE UC Irvine neurobiologists have found a novel molecular mechanism that helps trigger the formation of long-term memory. The researchers believe the discovery of this mechanism adds another piece to the puzzle in the ongoing effort to uncover the mysteries of memory and, potentially, certain intellectual disabilities. In a study led by Marcelo Wood of UC Irvine's Center for the Neurobiology of Learning & Memory, the team investigated the role of this mechanism a gene designated Baf53b in long-term memory formation. Baf53b is one of several proteins making up a molecular complex called nBAF. Mutations in the proteins of the nBAF complex have been linked to several intellectual disorders, including Coffin-Siris syndrome, Nicolaides-Baraitser syndrome and sporadic autism. One of the key questions the researchers addressed is how mutations in components of the nBAF complex lead to cognitive impairments. In their study, Wood and his colleagues used mice bred with mutations in Baf53b. While this genetic modification did not affect the mice's ability to learn, it did notably inhibit long-term memories from forming and severely impaired synaptic function. "These findings present a whole new way to look at how long-term memories form," said Wood, associate professor of neurobiology & behavior. "They … Continue reading →

Public release date: 24-Mar-2013 [ | E-mail | Share ] Contact: Les Lang llang@med.unc.edu 919-966-9366 University of North Carolina Health Care CHAPEL HILL, N.C. Every time a cell divides it makes a carbon copy of crucial ingredients, including the histone proteins that are responsible for spooling yards of DNA into tight little coils. When these spool-like proteins aren't made correctly, it can result in the genomic instability characteristic of most birth defects and cancers. Seven years ago, Dr. Joe Gall of the Carnegie Institute in Baltimore, Md. and coworkers noticed an aggregation of molecules along a a block of genome that codes for the critical histones, but they had no idea how this aggregate or "histone locus body" was formed. Now, research conducted in fruit flies at the University of North Carolina School of Medicine has pinpointed a specific DNA sequence that both triggers the formation of this "histone locus body" and turns on all the histone genes in the entire block. The finding, published March 25, 2013 in the journal Developmental Cell, provides a model for the coordinated synthesis of histones needed for assembly into chromatin, a process critical to keeping chromosomes intact and passing genetic information from generation … Continue reading →

Mar. 24, 2013 Research conducted in fruit flies at the University of North Carolina School of Medicine has pinpointed a specific DNA sequence that both triggers the formation of the "histone locus body" and turns on all the histone genes in the entire block. Every time a cell divides it makes a carbon copy of crucial ingredients, including the histone proteins that are responsible for spooling yards of DNA into tight little coils. When these spool-like proteins aren't made correctly, it can result in the genomic instability characteristic of most birth defects and cancers. Seven years ago, Dr. Joe Gall of the Carnegie Institute in Baltimore, Md. and coworkers noticed an aggregation of molecules along a a block of genome that codes for the critical histones, but they had no idea how this aggregate or "histone locus body" was formed. Now, research conducted in fruit flies at the University of North Carolina School of Medicine has pinpointed a specific DNA sequence that both triggers the formation of this "histone locus body" and turns on all the histone genes in the entire block. The finding, published March 25, 2013 in the journal Developmental Cell, provides a model for the coordinated synthesis … Continue reading →

Public release date: 25-Mar-2013 [ | E-mail | Share ] Contact: Amy Molnar sciencenewsroom@wiley.com Wiley A new analysis has found that genetic alterations in a particular cellular pathway are linked with bladder cancer risk, recurrence, disease progression, and patient survival. Published early online in CANCER, a peer- reviewed journal of the American Cancer Society, the findings could help improve bladder cancer screening and treatment. Alterations in the regulators of G-protein signaling (RGS) pathway, which is important for various cellular processes, have been implicated in several cancers. Eugene Lee, MD, of the MD Anderson Cancer Center in Houston, and his colleagues sought to determine the role of RGS alterations in bladder cancer risk, recurrence, disease progression, and patient survival. Dr. Lee is currently a fellow of Dr. Ashish M. Kamat. The researchers worked together with Dr. Xifeng Wu's Epidemiology Lab. They studied 803 patients with non-muscle invasive or muscle invasive bladder cancer and 803 healthy individuals. After evaluating 95 single nucleotide alterations or variants in 17 RGS genes, the investigators identified several that were linked with overall risk of bladder cancer. The strongest association was seen with the rs10759 variant on the RGS4 gene: it was linked with a 0.77-fold reduced … Continue reading →

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Panama Panama the pit bull completes the obedience commands that he learned while attending Nora's Dog Training Company. By: NorasDogTrainingCo … Continue reading →