In Nature this week, a team led by investigators at the Institute for Molecular Systems Biology in Zurich show that microRNAs 103 and 107 directly regulate insulin sensitivity in vivo. "Expression of miR-103/107 is upregulated in obese mice," the authors write, adding that "silencing of miR-103/107 leads to improved glucose homeostasis and insulin sensitivity" while "gain of miR-103/107 function in either liver or fat is sufficient to induce impaired glucose homeostasis" in these animals.
Researchers at Rockefeller University, along with their colleagues, report in this week's Nature their generation of a "genetically humanized mouse model for hepatitis C virus infection." The team achieved murine humanization by expressing two human genes and found that was "sufficient to allow HCV infection of fully immunocompetent inbred mice." The Rockefeller-led team says its humanized mouse model for HCV is "an effective platform for testing HCV entry inhibitors in vivo."
An international team led by a slew of researchers in Boston shows that "like RAD51, cyclin D1 is recruited to DNA damage sites in a BRCA2-dependent fashion." The researchers observe that, in human cancer cells, "reduction of cyclin D1 levels … impaired recruitment of RAD51 to damaged DNA, impeded the homologous recombination-mediated DNA repair, and increased sensitivity of cells to radiation in vitro and in vivo." Thus, the team suggests that it has identified an "unexpected function of a core cell cycle protein in DNA repair."
A team led by investigators at Spain's Universidad de Oviedo reports its whole-genome sequencing of four chronic lymphocytic leukemia patients, through which it "identified 46 somatic mutations that potentially affect gene function." By interrogating these mutations in an addition 363 patients, the team found four genes that were recurrently mutated: NOTCH1, XPO1, MYD88, and KLHL6. "Mutations in MYD88 and KLHL6 are predominant in cases of CLL with mutated immunoglobulin genes, whereas NOTCH1 and XPO1 mutations are mainly detected in patients with unmutated immunoglobulins," the authors write, adding that, to their knowledge "this is the first comprehensive analysis of CLL combining whole-genome sequencing with clinical characteristics and clinical outcomes."