In a recent Cell paper, a team led by Hao Wu, PhD, used electronic microscopy to reveal how RAG1 and 2 interact at a structural level, both with each other and with DNA.
Researchers in Dr. Fred Alt's laboratory used a novel in vivo mouse model system to resolve longstanding questions regarding the influence of DNA sequences on AID targeting and mutational outcomes during antibody diversification.
In a new paper in Cell Stem Cell, Dr. Yi Zhang's team report that they’ve extended their work to improve the efficiency of SCNT in human cells.
A study, reported in Cell, of where and how an enzyme cuts DNA may have inadvertently revealed a basic principle of gene regulation. This study suggests that the cell can lock or "sandbox" genes and enzymes that act on them within loops of DNA and protein, confining their activity to minimize the risk of genetic disaster.
A team in Frederick Alt's laboratory, led by Junchao Dong, Rohit A. Panchakshari, and Tingting Zhang, have made important strides towards resolving a long-standing question about how different classes of antibodies are made.
Delayed wound healing in people with type 1 or 2 diabetes can be caused by complications such as reduced blood flow, neuropathy and impaired signaling between cells. According to research by Denisa Wagner, PhD, a poorly understood feature of our immune system’s neutrophils may be one more ingredient in the storm.
An 880-pound digital media sculpture, "Absorption", by artist Rudolfo Quintas, is the result of discussions had with Dr. Tomas Kirchhausen, Principal Investigator in the Program in Cellular and Molecular Medicine at Boston Children’s Hospital and Professor Cell Biology at Harvard Medical School, regarding the essential cellular process of endocytosis.
Millions of people worldwide suffer from co-infection with tuberculosis (TB) and HIV. While prompt antibiotic and antiretroviral treatment can be a recipe for survival, over the years, physicians have noticed something: two or three weeks after starting antiretrovirals, about 30 percent of co-infected patients get worse.
Not all cancer cells are created equal. To call a cancer a cancer, in the singular, is something of a misnomer. A patient could be said to have cancers, as every tumor is actually a mixture of cells with different mutations and capabilities. One of those capabilities is the ability to escape the main tumor and spread, or metastasize, to other sites in the body.
Life teems with interactions. Proteins bind. Bonds form between atoms, and break. Enzymes cut. Drugs attach to cell receptors. DNA hybridizes. Those interactions make the processes of life work, and capturing them has led to many medical advances.
Labs the world over are jumping on the gene editing bandwagon. But one question keeps coming up: How precise are these systems? After all, a method that selectively mutates, deletes or swaps specific gene sequences is only as good as its accuracy.
Researchers in the laboratory of Frederick Alt have identified a relationship between sites of convergent gene transcription, the presence of intragenic super-enhancers, and the mis-targeting of the mutagenic activity of activation-induced cytidine deaminase (AID).
Harvard researchers genetically ‘edit’ human blood stem cells
To help find barriers associated with a cloning technique called somatic cell nuclear transfer (SCNT), Drs. Yi Zhang and Shogo Matoba generated mouse embryos through either SCNT or IVF and compared their gene expression profiles at the very early stages of development.
Researchers in the laboratory of Frederick Alt at the Howard Hughes Medical Institute and Program in Cellular and Molecular Medicine (PCMM) at Children's Hospital Boston, led by Leng-Siew Yeap and Joyce K. Hwang, have fundamentally changed our understanding of how the crucial mutagenic activity of activation-induced cytidine deaminase (AID) is targeted during antibody maturation.
In an article published online in Cell on November 19, 2015, they demonstrate that the DNA sequence encoding the antigen-binding variable (V) region of B-cell antibodies lies in a genomic location privileged for mutational diversification by AID. Their study further reveals that no specialized mechanism beyond sufficient exposure to AID is required to generate antibodies whose neutralizing function depends on high levels of variable-region mutations and… Read More »
Dr. Ba, a postdoctoral fellow in Frederick Alt's lab, will investigate the mechanisms that mediate the intra-locus and inter-locus regulation… Read More »
Minchul Kim will investigate molecular mechanisms of totipotency, a transient developmental state which possesses the ability to differentiate into both placental… Read More »