Frederick Alt, Ph.D.
Charles A. Janeway Professor of Pediatrics, Boston Children's Hospital
Professor of Genetics, Boston Children's Hospital
Charles A. Janeway Professor of Pediatrics and Genetics, Harvard Medical School
The Alt laboratory studies mechanisms that maintain genomic stability in mammalian cells. The programmed recombination and hypermutation events in lymphocytes and the general DNA repair mechanisms involved in these processes are a focus. The laboratory also studies mechanisms that promote and prevent oncogenic translocations. Approaches range from molecular genetics and biochemistry to animal models.
Replication protein A interacts with AID to promote deamination of somatic hypermutation targets.
The role of the non-homologous end-joining pathway in lymphocyte development.
Class-switch recombination: interplay of transcription, DNA deamination and DNA repair.
p63 and p73 are not required for the development and p53-dependent apoptosis of T cells.
Collaboration of homologous recombination and nonhomologous end-joining factors for the survival and integrity of mice and cells.
Authors: Authors: Couëdel C, Mills KD, Barchi M, Shen L, Olshen A, Johnson RD, Nussenzweig A, Essers J, Kanaar R, Li GC, Alt FW, Jasin M.
Genes Dev
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Genes Dev
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Mechanisms of Vdelta1 gammadelta T cell activation by microbial components.
Receptor revision in T cells: an open question?
Rad54 and DNA Ligase IV cooperate to maintain mammalian chromatid stability.
Authors: Authors: Mills KD, Ferguson DO, Essers J, Eckersdorff M, Kanaar R, Alt FW.
Genes Dev
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Genes Dev
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V(D)J recombinational accessibility-heading in the opposite direction?
53BP1 links DNA damage-response pathways to immunoglobulin heavy chain class-switch recombination.
Authors: Authors: Manis JP, Morales JC, Xia Z, Kutok JL, Alt FW, Carpenter PB.
Nat Immunol
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Nat Immunol
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