Genomes and Genes
J M Liu
Affiliation: National Institutes of Health
- Engraftment of hematopoietic progenitor cells transduced with the Fanconi anemia group C gene (FANCC)J M Liu
Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892, USA
Hum Gene Ther 10:2337-46. 1999..These experiments highlight both the potential and difficulties in applying gene therapy to FA...
- Retroviral-mediated transduction of the fanconi anemia C complementing (FACC) gene in two murine transplantation modelsJ M Liu
Hematology Branch, NHLBI, NIH, Bethesda, MD 20892, USA
Blood Cells Mol Dis 21:56-63. 1995..Our data suggest that retroviral-mediated transfer of the normal human FACC cDNA to hematopoietic progenitor and stem cells of mice is feasible and not associated with direct harmful effects to the hematopoietic organ...
- Persistent low-level engraftment of rhesus peripheral blood progenitor cells transduced with the fanconi anemia C gene after conditioning with low-dose irradiationE M Kang
Molecular and Clinical Hematology Branch, National Institutes of Health, Bethesda, Maryland 20892, USA
Mol Ther 3:911-9. 2001....
- Upstream sequences within the terminal hairpin positively regulate the P6 promoter of B19 parvovirusJ M Liu
Clinical Hematology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland 20892
Virology 185:39-47. 1991..The hairpin termini of parvoviruses were known to serve as origins of replication and to catalyze virion packaging. We now suggest that, in addition to these functions, they exert cis-acting effects on B19 P6-promoted gene expression...
- Tumor necrosis factor-alpha and CD95 ligation suppress erythropoiesis in Fanconi anemia C gene knockout miceT Otsuki
Hematology Branch, NHLBI, NIH, Bethesda, Maryland 20892, USA
J Cell Physiol 179:79-86. 1999..We conclude that mutation in the Fac protein induces heightened sensitivity to TNF-alpha and Fas receptor ligation, results that may explain the mechanism of anemia in FA-C patients...
- Fanconi anemia protein, FANCG, is a phosphoprotein and is upregulated with FANCA after TNF-alpha treatmentM Futaki
Hematology Branch, NHLBI, National Institutes of Health, Bethesda, Maryland 20892, USA
Biochem Biophys Res Commun 281:347-51. 2001..These results show that FANCG is a phosphoprotein and suggest that the cellular accumulation of FA proteins is subject to regulation by TNF-alpha signaling...
- Indiscriminate activity from the B19 parvovirus p6 promoter in nonpermissive cellsJ M Liu
Clinical Hematology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland
Virology 182:361-4. 1991..A putative second B19 promoter at map unit 44 (P44) was nonfunctional and unable to confer tissue specificity. Thus, tropism is unlikely to be regulated at the level of transcriptional initiation from either the P6 or P44 promoter...
- A block in full-length transcript maturation in cells nonpermissive for B19 parvovirusJ M Liu
Clinical Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892
J Virol 66:4686-92. 1992..These results suggest that the abundance of B19 virus RNAs is determined by active 3' processing and is coupled to DNA template replication...
- Invasive infection with Fusarium chlamydosporum in a patient with aplastic anemiaB H Segal
Laboratory of Host Defenses, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA
J Clin Microbiol 36:1772-6. 1998..chlamydosporum. This case illustrates the ever-increasing spectrum of pathogenic Fusarium spp. in immunocompromised patients and emphasizes the potential pitfalls in histologic diagnosis, which may have important treatment implications...
- Chromosomal breakage syndromes and the BRCA1 genome surveillance complexM Futaki
Hematology Branch, NHLBI, National Institutes of Health, Building 10, Room 7C103, Bethesda, MD 20892, USA
Trends Mol Med 7:560-5. 2001..Although still controversial, this finding suggests similarities in the pathogenesis of the human chromosome breakage syndromes and a complementary role for each protein in DNA structure surveillance or damage repair...
- ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complexJ Wang
Hematology Branch, National Heart, Lung, and Blood Institute, Bethesda MD 20892, USA
Proc Natl Acad Sci U S A 95:10860-5. 1998..This observation provides a mechanism for how the AML1/ETO fusion may inhibit expression of AML1-responsive target genes and disturb normal hematopoiesis...