The Virginia Harris Cockrell Cancer Research Center at Science Park
Our research aims to define the mechanisms that control normal cell proliferation, differentiation, survival and genome maintenance to identify the processes that drive cancer. Research in the department is multidisciplinary and falls under three areas:
- Cellular and Molecular Mechanisms of Carcinogenesis
- DNA Damage, Repair and Mutagenesis
- Cancer Epigenetics
The Bedford lab studies the methylation of arginine amino acids in histones and other chromatin-associated proteins. In a recent study, they showed that TDRD3, a reader of methyl-arginine marks on histone tails, interacts with TOP3B, a topoisomerase that unwinds DNA at regions of active gene expression. The study provides evidence that this partnership can prevent DNA breakage and chromosomal translocations, two of the hallmarks of cancer.
Nestled within the Lost Pines forest of Central Texas near Smithville, the Science Park campus is within driving distance from Austin, "The Live Music Capital of the World."
- ATP-dependent chromatin remodeling complexes regulate non-chromatin targets
- Role of SAGA complex in embryonic stem cells and in reprogramming fibroblasts to a stem cell state
- CARM1 promotes nuclear export of special class of RNAs
- YEATS protein potential therapeutic target for cancer
Hogg Seminar Series: Raif S. Geha, M.D. Department of Pediatrics, Harvard Medical School, Children's Hospital, Boston MA. Imunodeficiency in Mouse and Man. Wednesday, June 24, 2015 11:00 am. Conference Center Auditorium.
Departmental Seminar Series: Will resume in the Fall.
Faculty Spotlight: Kevin McBride, PhD
The McBride lab studies the role of activation induced deaminase (AID) in antibody diversification and cancer development. Normally, DNA damage is considered detrimental to genomic stability. However, activation induced deaminase (AID) induces DNA double-stranded breaks (DSBs) and mutations (hypermutation) that are critical for leading to antibody diversity to help fight infectious disease. Yet, AID can also induce unintended DNA damage, including point mutations in oncogenes and chromosome translocations leading to B-cell leukemias and lymphomas. Understanding how AID chooses its targets is fundamental to understanding how it causes deleterious DSBs.
Learn more about Dr. McBride's research.
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