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Subject Areas on Research
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A compensatory base change in human U2 snRNA can suppress a branch site mutation.
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A family of long reiterated DNA sequences, one copy of which is next to the human beta globin gene.
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A human gamma globin gene variant binds SP1.
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A naturally occurring gamma globin gene mutation enhances SP1 binding activity.
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A novel beta-globin mutation, beta Durham-NC [beta 114 Leu-->Pro], produces a dominant thalassemia-like phenotype.
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Altered ligand rebinding kinetics due to distal-side effects in hemoglobin chico (Lysbeta66(E10) --> thr).
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Analysis of globin gene structure in patients with beta thalassemia by restriction endonuclease mapping.
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Analysis of the stimulatory effect of splicing on mRNA production and utilization in mammalian cells.
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Antagonism of catecholamine receptor signaling by expression of cytoplasmic domains of the receptors.
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BP1, a homeodomain-containing isoform of DLX4, represses the beta-globin gene.
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Beta-thalassemia resulting from a single nucleotide substitution in an acceptor splice site.
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Binding of HMG-I(Y) elicits structural changes in a silencer of the human beta-globin gene.
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Characterization of the DNase I hypersensitive site 3' of the human beta globin gene domain.
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Cloning and characterization of DNA sequences surrounding the human gamma-, delta-, and beta-globin genes.
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Differentiation domains of the erythropoietin receptor.
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Distinct functions of two isoforms of a homeobox gene, BP1 and DLX7, in the regulation of the beta-globin gene.
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Divergent regulation of protein synthesis in the cytosol and endoplasmic reticulum compartments of mammalian cells.
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Efficient and specific repair of sickle beta-globin RNA by trans-splicing ribozymes.
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Enhancing RNA repair efficiency by combining trans-splicing ribozymes that recognize different accessible sites on a target RNA.
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Erythroid AP-1/NF-E2 elements vary in their response to NF-E2.
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Erythroid transcription factor NF-E2 coordinates hemoglobin synthesis.
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Erythroid transcription factor NF-E2 is a haematopoietic-specific basic-leucine zipper protein.
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Erythroid-specific expression of human CD59 and transfer to vascular endothelial cells.
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Erythropoietin receptor signals both proliferation and erythroid-specific differentiation.
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Evidence that structural variants within the human delta-globin protein may reflect genetic interactions between the delta- and beta-globin genes.
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Gamma-globin gene promoter elements required for interaction with globin enhancers.
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Globin attenuates the innate immune response to endotoxin.
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Glutathione regulates susceptibility to oxidant-induced mitochondrial DNA damage in human lymphocytes.
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HNF-3 beta as a regulator of floor plate development.
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Hb Catonsville (glutamic acid inserted between Pro-37(C2)alpha and Thr-38(C3)alpha). Nonallelic gene conversion in the globin system?
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Hemoglobin switching in sheep. Cloning and characterization of the beta A and beta-like embryonic globin genes from genomic DNA.
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High affinity of lead for fetal haemoglobin.
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High levels of human gamma-globin gene expression in adult mice carrying a transgene of deletion-type hereditary persistence of fetal hemoglobin.
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Highly specific epigenome editing by CRISPR-Cas9 repressors for silencing of distal regulatory elements.
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Human MafG is a functional partner for p45 NF-E2 in activating globin gene expression.
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Identification of five hemoglobins in B6C3F1 mice by mass spectrometry and sequence analysis.
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In vivo footprinting of the human alpha-globin locus upstream regulatory element by guanine and adenine ligation-mediated polymerase chain reaction.
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In vivo transfer of GPI-linked complement restriction factors from erythrocytes to the endothelium.
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Inhibition of Bmp signaling affects growth and differentiation in the anagen hair follicle.
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Inhibition of G protein-coupled receptor signaling by expression of cytoplasmic domains of the receptor.
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Integration of foreign genes into the mammalian germ line: genetic engineering enters a new era.
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Microcytic anemia in mk/mk mice is not corrected by retroviral-mediated gene transfer of wild-type p45 NF-E2.
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Mitogen-activated protein kinases enhance long-range activation by the beta-globin locus control region.
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Modeling and superposition of multiple protein structures using affine transformations: analysis of the globins.
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Molecular biology. Enhancers, chromosome position effects, and transgenic mice.
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Molecular cloning and sequence analysis of a cDNA coding for the mouse alpha-like embryonic globin chain x.
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Mouse microcytic anaemia caused by a defect in the gene encoding the globin enhancer-binding protein NF-E2.
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Overproduction of alpha chains provides a proton-insensitive component to the bluefish hemoglobin system.
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Processing of nuclear heterogeneous RNA: recent developments.
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Purification of the human NF-E2 complex: cDNA cloning of the hematopoietic cell-specific subunit and evidence for an associated partner.
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Regression analysis of multiple protein structures.
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Retargeting mobile group II introns to repair mutant genes.
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Ribozyme-mediated repair of sickle beta-globin mRNAs in erythrocyte precursors.
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Sickle hemoglobin (HbS) allele and sickle cell disease: a HuGE review.
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Simultaneous Bayesian estimation of alignment and phylogeny under a joint model of protein sequence and structure.
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Site-specific PEGylation of hemoglobin at Cys-93(beta): correlation between the colligative properties of the PEGylated protein and the length of the conjugated PEG chain.
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Spontaneous delta- to beta-globin switching in K562 human leukemia cells.
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Targeted deletion of 5'HS2 of the murine beta-globin LCR reveals that it is not essential for proper regulation of the beta-globin locus.
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The NF-E2 transcription factor.
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The bZIP transcription factor LCR-F1 is essential for mesoderm formation in mouse development.
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The conserved dinucleotide AG of the 3' splice site may be recognized twice during in vitro splicing of mammalian mRNA precursors.
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The ubiquitous subunit of erythroid transcription factor NF-E2 is a small basic-leucine zipper protein related to the v-maf oncogene.
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Two mouse early embryonic beta-globin gene sequences. Evolution of the nonadult beta-globins.
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UACUAAC is the preferred branch site for mammalian mRNA splicing.
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Using 5'-PTMs to repair mutant beta-globin transcripts.
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