ABSTRACT
The Mouse Tumor Biology Database (MTB) is designed to provide an electronic data storage, search, and analysis system for information on mouse models of human cancer. The MTB includes data on tumor frequency and latency, strain, germ line, and somatic genetics, pathologic notations, and photomicrographs. The MTB collects data from the primary literature, other public databases, and direct submissions from the scientific community. The MTB is a community resource that provides integrated access to mouse tumor data from different scientific research areas and facilitates integration of molecular, genetic, and pathologic data. Current status of MTB, search capabilities, data types, and future enhancements are described in this article.
Subject(s)
Databases, Factual , Information Storage and Retrieval , Neoplasms, Experimental/pathology , Neoplasms/pathology , Animals , Computational Biology , Disease Models, Animal , Humans , Internet , Mice , Neoplasms/genetics , Neoplasms, Experimental/genetics , User-Computer InterfaceSubject(s)
Coronary Thrombosis/therapy , Stents , Adult , Coronary Angiography , Coronary Thrombosis/diagnostic imaging , Humans , Male , UltrasonographyABSTRACT
The Gene Expression Database (GXD) is a community resource of gene expression information for the laboratory mouse. By combining the different types of expression data, GXD aims to provide increasingly complete information about the expression profiles of genes in different mouse strains and mutants, thus enabling valuable insights into the molecular networks that underlie normal development and disease. GXD is integrated with the Mouse Genome Database (MGD). Extensive interconnections with sequence databases and with databases from other species, and the development and use of shared controlled vocabularies extend GXD's utility for the analysis of gene expression information. GXD is accessible through the Mouse Genome Informatics web site at http://www.informatics.jax.org/ or directly at http://www.informatics.jax.org/menus/expression_menu. shtml.
Subject(s)
Databases, Factual , Gene Expression Profiling , Mice/genetics , Animals , Information Services , InternetABSTRACT
We have previously shown that several protein kinases are present in higher activity levels in multidrug resistant cell lines, such as KB-V1. We have now isolated a gene that codes for a putative protein kinase, PKY, of over 130 kDa that is expressed at higher levels in multidrug-resistant cells. RNA from KB-V1 multidrug-resistant cells was reverse-transcribed and amplified by using primers derived from consensus regions of serine threonine kinases and amplified fragments were used to recover overlapping clones from a KB-V1 cDNA library. An open reading frame of 3648 bp of DNA sequence predicting 1215 aa, has been identified. This cDNA hybridizes to a mRNA of about 7 kb which is expressed at high levels in human heart and muscle tissue and overexpressed in drug-resistant KB-V1 and HL60/ADR cells. Because its closest homolog is the yeast serine/threonine kinase, Yak1, we have called this gene PKY. PKY is also related to the protein kinase family that includes Cdks, Gsk-3, and MAPK proline-directed protein kinases. This protein represents the first of its type known in mammals and may be involved in growth control pathways similar to those described for Yak1, as well as possibly playing a role in multidrug resistance.
Subject(s)
Carrier Proteins , Drug Resistance, Multiple/genetics , Protein Kinases/biosynthesis , Protein Kinases/chemistry , Protein Serine-Threonine Kinases/biosynthesis , Protein Serine-Threonine Kinases/chemistry , Saccharomyces cerevisiae Proteins , Saccharomyces cerevisiae/genetics , Amino Acid Sequence , Animals , Base Sequence , Cloning, Molecular , Consensus Sequence , Drosophila/genetics , Gene Expression , Gene Library , HL-60 Cells , Humans , Intracellular Signaling Peptides and Proteins , KB Cells , Mammals , Molecular Sequence Data , Organ Specificity , Polymerase Chain Reaction , Protein Kinases/genetics , Protein Serine-Threonine Kinases/genetics , RNA, Messenger/biosynthesis , Rats , Saccharomyces cerevisiae/enzymology , Sequence Alignment , Sequence Homology, Amino Acid , Transcription, Genetic , Tumor Cells, CulturedABSTRACT
Exposure of HL-60 promyelocytic leukemia cells to calcitriol results in a decrease in steady-state levels of c-myc mRNA and induces cellular differentiation. We have asked whether calcitriol has a direct effect on the transcription of the c-myc gene. 1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) decreased RNA elongation in a nuclear run-off transcription assay by 4 h after treatment. In the continuous presence of 1,25-(OH)2D3, HL-60 cell transcription of c-myc was decreased by 38% at 4 h and was abolished by 48 h. In contrast, the transcription of beta-actin was not affected by 1,25-(OH)2D3 treatment. The rate of transcription of c-myc and beta-actin was proportional to the number of nuclei and to time. Furthermore, specific hybridization of c-myc and beta-actin RNA was a linear function of RNA input. After a 48-h treatment, the c-myc/beta-actin ratio was decreased by 80-100% at [32P]RNA inputs ranging from 2 to 20 X 10(6) cpm/ml. These data temporally correlate inhibition of c-myc transcription with decreases in the steady-state levels of c-myc mRNA as assessed by Northern blot analysis. We conclude that the effect of 1,25-(OH)2D3 on c-myc expression occurs at the transcriptional level.
