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Genetic function could help cancer therapies

A team of researchers has discovered a genetic function that helps one of the most important “tumor suppressor” genes to do its job and prevent cancer.

According to scientists from OSU and Oregon Health and Science University, finding ways to maintain or increase the effectiveness of this gene – called Grp1-associated scaffold protein, or Grasp – could offer an important new avenue for human cancer therapies.

The Grasp gene was studied in the skin of mice in this research, but is actually expressed at the highest levels in the brain, heart and lung, studies have shown. It appears to play a fundamental role in the operation of the p53 tumor suppressor gene, which is a focus of much modern cancer research.

The new study has found that the Grasp gene is significantly involved in maintaining the proper function of p53. When “Grasp” is not being adequately expressed, the p53 protein that has entered the cell nucleus to either repair or destroy the cell comes back out of the nucleus before its work is finished.

“It appears that a primary function of Grasp is to form sort of a halo around the nucleus of a damaged skin cell, and act as kind of a plug to keep the p53 cell inside the nucleus until its work is done,” one of the lead authors of this study Mark Leid said.
“A drug that could enhance Grasp function might also help enhance the p53 function, and give us a different way to keep this important tumor suppressor working the way that it is supposed to,” the researcher added.

Autoinflammatory diseases treatment comes closer

Researchers have discovered a new signaling pathway in sterile inflammation that could impact the treatment of diseases such as cancer, multiple sclerosis and rheumatoid arthritis.

Their findings offer insight into the role that activation of interferon-regulatory factor 1 (IRF1), a protein that functions as a transcriptional activator of a variety of target genes, plays in the production of chemokines and the recruitment of mononuclear cells to sites of sterile inflammation.

In this study, investigators Tomasz Kordula, PhD, and Sarah Spiegel, PhD, members of the Cancer Cell Signaling research program at Massey and professors in the Department of Biochemistry and Molecular Biology at the VCU School Medicine, found a new signaling pathway that links IL-1 to IRF1 in sterile inflammation.

IL-1, a key regulator of sterile inflammation, governs immune and inflammatory responses and has an important role in autoinflammatory diseases. IL-1 signaling triggers a process called polyubiquitination. Polyubiquitination is important to a variety of cellular functions.

While one form of polyubiquitination has been called the “kiss of death” because it targets proteins for degradation, another form known as K63-linked polyubiquitination is important to cell signaling.

‘Shy’ tots understand more than their words indicate

Researchers have suggested that the lag in using words does not mean that shy kids are not able to understand what’s being said.

The new study tests four possible explanations for the association: that shy children practice speaking less and so their speech becomes delayed, that children with delayed speech become shy because they have difficulty talking, that shy children understand what’s being said but are simply reticent to speak, and that shy children’s speech is actually normal while outgoing children’s speech is above average.

The research team, from CU-Boulder’s Institute for Behavioral Genetics (IBG) and the Department of Psychology and Neuroscience, found consistent evidence to support only the hypothesis that shy toddlers were delayed in speaking but not in understanding.

For the study, the researchers looked at information collected on 408 sets of twins at 14, 20 and 24 months of age, when children’s language skills are rapidly expanding. The data on inhibition and speech characteristics of the 816 toddlers came from parent reports and researcher observations.

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