Nucleoside Deaminases

• 

  Subject Areas on Research

  • A high proportion of ADA point mutations associated with a specific alanine-to-valine substitution. 
  • A role for adenosine deaminase in human monocyte maturation. 
  • A single amino acid difference in the host APOBEC3G protein controls the primate species specificity of HIV type 1 virion infectivity factor. 
  • ADA deficiency treatment. 
  • Abnormalities in S-adenosylhomocysteine hydrolysis, ATP catabolism, and lymphoid differentiation in adenosine deaminase deficiency. 
  • Adenosine deaminase (ADA) deficiency due to deletion of the ADA gene promoter and first exon by homologous recombination between two Alu elements. 
  • Adenosine deaminase and purine nucleoside phosphorylase deficiencies: evaluation of therapeutic interventions in eight patients. 
  • Adenosine deaminase deficiency with late onset of recurrent infections: response to treatment with polyethylene glycol-modified adenosine deaminase. 
  • Altered regulation of S-adenosylmethionine dependent methylation in adenosine deaminase deficiency. 
  • Biochemical consequences of adenosine deaminase inhibition in vivo. Differential effects in acute and chronic T cell leukemia. 
  • Comparison of red cell transfusion and polyethylene glycol-modified adenosine deaminase therapy in an adenosine deaminase-deficient child: measurement of erythrocyte deoxyadenosine triphosphate as a useful tool. 
  • Conversion of a stem cell leukemia from a T-lymphoid to a myeloid phenotype induced by the adenosine deaminase inhibitor 2'-deoxycoformycin. 
  • Elucidation of aberrant purine metabolism: application to hypoxanthine-guanine phosphoribosylstransferase- and adenosine kinase-deficient mutants, and IMP dehydrogenase- and adenosine deaminase-inhibited human lymphoblasts. 
  • Foamy virus Bet proteins function as novel inhibitors of the APOBEC3 family of innate antiretroviral defense factors. 
  • Further investigation of simian immunodeficiency virus Vif function in human cells. 
  • HIV-1 Vif: counteracting innate antiretroviral defenses. 
  • Identification of a deletion in the adenosine deaminase gene in a child with severe combined immunodeficiency. 
  • Improved gene expression upon transfer of the adenosine deaminase minigene outside the transcriptional unit of a retroviral vector. 
  • In vivo inactivation of erythrocyte S-adenosylhomocysteine hydrolase by 2'-deoxyadenosine in adenosine deaminase-deficient patients. 
  • Inhibition of a yeast LTR retrotransposon by human APOBEC3 cytidine deaminases. 
  • Mechanism of deoxyadenosine-induced catabolism of adenine ribonucleotides in adenosine deaminase-inhibited human T lymphoblastoid cells. 
  • Paradoxical expression of adenosine deaminase in T cells cultured from a patient with adenosine deaminase deficiency and combine immunodeficiency. 
  • Role and mechanism of action of the APOBEC3 family of antiretroviral resistance factors. 
  • S-Adenosylhomocysteine metabolism in adenosine deaminase deficient cells. 
  • S-adenosylhomocysteine hydrolase is an adenosine-binding protein: a target for adenosine toxicity. 
  • Selective inhibition of Alu retrotransposition by APOBEC3G. 
  • Specific packaging of APOBEC3G into HIV-1 virions is mediated by the nucleocapsid domain of the gag polyprotein precursor. 
  • The human genes for S-adenosylhomocysteine hydrolase and adenosine deaminase are syntenic on chromosome 20. 
  • The intrinsic antiretroviral factor APOBEC3B contains two enzymatically active cytidine deaminase domains. 
  • Treatment of adenosine deaminase deficiency with polyethylene glycol-modified adenosine deaminase. 
• 

  Keywords of People

  • Buckley, Rebecca Hatcher, James Buren Sidbury Professor of Pediatrics, in the School of Medicine, Immunology