Group items tagged

I learned that gene expression is the process by which the information of genes is used to direct the function of cells. Gene expression is regulated in all cells because not all genes are needed all the time or under all circumstances. For example, brain cells need to express certain genes that are not needed in muscle cells, and muscle cells need to express certain genes that are not needed in brain cells. Likewise, bacteria need to express different genes depending on the availability of food and other aspects of their surroundings.

The study is the first to examine all of the gene networks affected by fructose that result in changes to brain function and metabolism-more than 20,000 genes in total. Although the study was conducted using rats, the researchers report that the majority of the sequenced genes are comparable to those in humans, including more than 200 genes in the hippocampus, a brain area crucial to memory, and 700 in the hypothalamus, the seat of the brain's metabolic control center.

Autism is rooted in genetics, including the mutation of certain genes that result in a failure of neurons in the brain to properly connect. Based on earlier genetic research funded by Autism Speaks, such as the Autism Genome Project (AGP), scientists have discovered some of these genes. But much more gene discovery needs to take place. The Autism Genome 10K Project will mark a substantial leap forward on this journey. The Autism Genome 10K Project builds on the successes of Autism Speaks' Autism Genetic Resource Exchange program (AGRE), a high-quality collection of more than 12,000 DNA samples from families affected by autism. The AGRE program has facilitated many high-impact scientific discoveries in recent years, including the risk genes discovered by the AGP and other researchers. With BGI sequencing the full complement of 10,000 samples collected by AGRE and collaborators in China, Autism Genome 10K leverages BGI's cutting-edge expertise and globally unrivaled capacity for high-quality genome sequencing.

When Jordan is diagnosed with brain cancer (glioblastoma multiform), his college plans are unexpectedly put on hold. This scenario is presented in order to teach students about gene regulation, as the efficacy of the drug Jordan receives for post-surgical treatment is dependent upon the activity level of a gene encoding a protein involved in DNA repair. This "flipped" case study requires students to prepare in advance outside of class by watching several short videos that have been selected to teach the basics of how cancer forms as well as the role of epigenetics in gene silencing. Inside of class, the case is delivered using progressive disclosure format in which students gradually receive additional information to answer a series of directed questions. To determine a treatment plan for Jordan, students analyze data from a research study involving patients treated for his specific type of cancer. The case is designed for advanced high school biology classes as well as lower-level undergraduate general biology courses for non-majors and majors.

Panobinostat is a new type of drug that works by blocking an enzyme responsible for modifying DNA at the epigenetic level. Epigenetics refers to chemical marks on DNA itself or on the protein "spools" called histones that package DNA. These marks influence the activity of genes without changing the underlying sequence, essentially acting as volume knobs for genes. Earlier genomic studies showed that about 80 percent of DIPG tumors carry a mutation that alters a histone protein, resulting in changes to the way DNA is packaged and tagged with those chemical marks. This faulty epigenetic regulation results in activation of growth-promoting genes that should have been turned off, and shutdown of others that should have acted as brakes to cell multiplication. Cancer is the result. Panobinostat appears to work by restoring proper functioning of the cells' chemical tagging system.

Your ancestors' lousy childhoods or excellent adventures might change your personality, bequeathing anxiety or resilience by altering the epigenetic expressions of genes in the brain.

Sure, we know insufficient serotonin levels get a bad rap when it comes to depression, but that's like blaming one person in a full-scale riot. Depression isn't caused by only one factor. In fact, study co-author Elyse Aurbach says we're probably not getting to the core of why people are depressed because "the brain is immensely complex." In this study, the research team conducted eight experiments (four on animal brains, four on brains of the deceased human kind) of varying sample sizes - from 20 to 90 brains in each - and found that the brains of deceased humans who'd been depressed had increased levels of hippocampal FGF9 and that live animals with increased FGF9 levels demonstrated depressive, anxious behavior. "This is not just a correlation," study leader Huda Akil of the University of Michigan says. Less really may be more, at least when it comes to FGF9.

Huntington disease is caused by a mutation in the HTT gene. Understanding how the mutation causes neurodegeneration might help researchers develop treatments that protect brain function. This animation describes the genetic defect that underlies Huntington disease. Created by the editors at Nature Reviews Disease Primers.

In the 2013 Holiday Lectures on Science, Charles L. Sawyers of Memorial Sloan-Kettering Cancer Center and Christopher A. Walsh of Boston Children's Hospital will reveal the breathtaking pace of discoveries into the genetic causes of various types of cancers and diseases of the nervous system, and discuss the impact of those discoveries on our understanding of normal human development and disease.