Cohesin is the protein responsible for binding the sister chromatids during mitosis after S phase. At metaphase, most cohesin is removed, except for some at the centromere. At Anaphase, securin, an inhibitory subunit of separase, is hydrolyzed.
The Damon Runyon Cancer Research Foundation, a non-profit organization focused on supporting innovative early career researchers, named 15 new Damon Runyon Fellows at its fall Fellowship Award Committee review. The recipients of this prestigious, four-year award are outstanding postdoctoral scientists conducting basic and translational cancer research in the laboratories of leading senior investigators across the country.
During cell division, chromosomes acquire a characteristic X-shape with the two DNA molecules (sister chromatids) linked at a central "connection region" that contains highly compacted DNA.
Massive sequencing of cancer genomes brings to light new genes every day that could be involved in the process of tumour formation.
Cohesins are protein complexes that join the two copies of each chromosome-called sister chromatids-to ensure that they are shared fairly between the daughter cells during cell division. In this way, each daughter cell receives exactly the same genetic information from the parent cell.
The DNA in human cells is translated into a multitude of proteins required for a cell to function. When, where and how proteins are expressed is determined by regulatory DNA sequences and a group of proteins, known as transcription factors, that bind to these DNA sequences.
nvestigators for The Cancer Genome Atlas Research Network have detailed and broadly classified the genomic alterations that frequently underlie the development of acute myeloid leukemia, a deadly cancer of the blood and bone marrow.
Two studies from The Cancer Genome Atlas program reveal details about the genomic landscapes of acute myeloid leukemia and endometrial cancer.
Scientists have discovered that mutations in the histone deacetylase 8 gene can cause the rare genetic disorder known as Cornelia de Lange syndrome, which is characterized by intellectual disability, limb deformity, and other disabilities resulting from problems in early development.
Genetics researchers have identified a key gene that, when mutated, causes the rare multisystem disorder Cornelia deLange syndrome (CdLS). By revealing how mutations in the HDAC8 gene disrupt the biology of proteins that control both gene expression and cell division, the research sheds light on this disease, which causes intellectual disability, limb deformations and other disabilities resulting from impairments in early development.
Genetics researchers have identified a key gene that, when mutated, causes the rare multisystem disorder Cornelia deLange syndrome (CdLS). By revealing how mutations in the HDAC8 gene disrupt the biology of proteins that control both gene expression and cell division, the research sheds light on this disease, which causes intellectual disability, limb deformations and other disabilities resulting from impairments in early development.
The Damon Runyon Cancer Research Foundation, a non-profit organization focused on supporting innovative early career researchers, named 21 new Damon Runyon Fellows at its spring Fellowship Award Committee review.
Researchers studying rare genetic disorders have uncovered insights into those diseases in biological structures that regulate chromosomes when cells divide. Focusing on the cohesin complex, a group of proteins forming a bracelet that encircles chromosome pairs, scientists have discovered mutations that disrupt cohesin, causing a recently recognized class of diseases called cohesinopathies.
Cohesin is a ring-shaped protein complex involved in the spatial organization of the genome and in mitotic chromosome structure. Vertebrate somatic cells have two versions of cohesin that contain either SA1 or SA2, but their functional specificity has been largely ignored. Researchers of the Spanish National Cancer Research Centre (CNIO) under the direction of Ana Losada have identified new functions of cohesin SA1 that are relevant for two human diseases, cancer and Cornelia de Lange Syndrome.
University of Pennsylvania biologists studying human reproduction have identified what is likely the major contributing factor to the maternal age-associated increase in aneuploidy, the term for an abnormal number of chromosomes during reproductive cell division.
Scientists now are closer to understanding why older women become less fertile, suffer a miscarriage or have a baby with Down's syndrome. This could be ground breaking in infertility treatment in the older women in their late 30s and early 40s.
The genes that are responsible for maintaining each cell type form DNA loops that link control elements for these genes. This surprising genome structure is generated and reinforced by two essential protein complexes that bridge the loops and contribute to proper gene regulation.
An international team of scientists studying a rare genetic disease discovered that a bundle of proteins with the long-established function of keeping chromosomes together also plays an important role in regulating genes in humans.
When a strand of DNA breaks in the body's cells, it normally does not take long until it has been repaired.
Studying mutations that give rise to a rare genetic disease, genetics researchers have identified a novel biological pathway that may have a broader role during human development, potentially in cases of mental retardation and autism.
Researchers have a new understanding of the process cells use to ensure that sperm and eggs begin life with exactly one copy of each chromosome - a process that must be exquisitely regulated to prevent problems such as miscarriages and mental retardation.
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