Humans normally have 46 chromosomes in each cell, divided into 23 pairs. Two copies of chromosome 11, one copy inherited from each parent, form one of the pairs. Chromosome 11 spans about 134 million DNA building blocks (base pairs) and represents between 4 percent and 4.5 percent of the total DNA in cells.
Identifying genes on each chromosome is an active area of genetic research. Because researchers use different approaches to predict the number of genes on each chromosome, the estimated number of genes varies. Chromosome 11 likely contains about 1,500 genes. More than 150 of these genes provide instructions for making olfactory receptors, which are proteins that are used to detect different smells.
Genes on chromosome 11 are among the estimated 20,000 to 25,000 total genes in the human genome.
Ten genetic variants associated with type 2 diabetes, a disease which impacts more than 170 million people worldwide, have been identified or confirmed by a U.S.-Finnish team led by scientists at the University of Michigan School of Public Health.
In the most comprehensive look at genetic risk factors for type 2 diabetes to date, a U.S.-Finnish team, working in close collaboration with two other groups, has identified at least four new genetic variants associated with increased risk of diabetes and confirmed existence of another six.
Yale School of Medicine autism experts Fred Volkmar, M.D. and Ami Klin are part of a global research consortium from 19 countries to identify a gene and a region of a chromosome that may lead to autism in children.
The genomes of the largest collection of families with multiple cases of autism ever assembled have been scanned and the preliminary results published in Nature Genetics. They provide new insights into the genetic basis of autism.
An international team of scientists have discovered two new genetic links that may predispose children to develop autism.
Preliminary findings from the largest genome scan ever completed in the history of autism research are being published in Nature Genetics. University of Pittsburgh researchers with a consortium of scientists from across the world contributed to this landmark research endeavor through the Autism Genome Project.
Using molecular and cell-based models, researchers at Georgetown University Medical Center have refined the picture of how a cancer-promoting protein associated with Ewing's sarcoma functions.
Virginia Commonwealth University Massey Cancer Center researchers have identified the role of a protein in hemoglobin gene silencing that may one day be a potential target for the treatment of genetic blood disorders like sickle-cell anemia and beta-thalassemia on the molecular level.
A new study reports that a loss of genes on chromosome 1 or chromosome 11 raises the risk of death from the children's cancer neuroblastoma, even when other indicators seem to point to a lower-risk form of the disease.
Johns Hopkins Kimmel Cancer Center researchers have linked alterations in a gene, called Rsf-1, to the most deadly ovarian cancers. The scientists say the discovery is the first to establish a role for the gene in ovarian cancer and may lead to a test that can predict, early on, which patients will develop aggressive disease.
Rather than covering the entire genome, the microarray focuses on suspect regions of chromosomes for signs of deleted genetic material known to play a role in the cancer.
Genetics researchers have developed a customized gene chip to rapidly scan tumor samples for specific DNA changes that offer clues to prognosis in cases of neuroblastoma, a common form of children's cancer.
When genes are deleted on a particular section of chromosome 11, the result is an aggressive form of the childhood cancer neuroblastoma. A new study suggests that detecting this genetic deletion during the initial evaluation of children with neuroblastoma may indicate to physicians that they should recommend a more aggressive regimen of chemotherapy to fight the cancer.
Scientists at the University of North Carolina at Chapel Hill have identified an enzyme that helps trigger the development of leukemia, a cancer of blood cells.
UCLA scientists have devised a novel way to repair one of the genetic mutations that causes ataxia-telangiectasia, (A-T), a life-shortening disorder that devastates the neurological and immune systems of one in 40,000 young children.
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