Biomedical subjects

H Lehvaslaiho

Publications and source records attributed to H Lehvaslaiho.

5 recordsLinked to original sources

PubMed2004

Ensembl 2004.

The Ensembl (http://www.ensembl.org/) database project provides a bioinformatics framework to organize biology around the sequences of large genomes. It is a comprehensive and integrated source of annotation of large genome sequences, available via interactive website, web services or flat files. As well as being one of the leading sources of genome annotation, Ensembl is an open source software engineering project to develop a portable system able to handle very large genomes and associated requirements. The facilities of the system range from sequence analysis to data storage and visualization and installations exist around the world both in companies and at academic sites. With a total of nine genome sequences available from Ensembl and more genomes to follow, recent developments have focused mainly on closer integration between genomes and external data.

Animals↗

PubMed2003

Ensembl 2002: accommodating comparative genomics.

The Ensembl (http://www.ensembl.org/) database project provides a bioinformatics framework to organise biology around the sequences of large genomes. It is a comprehensive source of stable automatic annotation of human, mouse and other genome sequences, available as either an interactive web site or as flat files. Ensembl also integrates manually annotated gene structures from external sources where available. As well as being one of the leading sources of genome annotation, Ensembl is an open source software engineering project to develop a portable system able to handle very large genomes and associated requirements. These range from sequence analysis to data storage and visualisation and installations exist around the world in both companies and at academic sites. With both human and mouse genome sequences available and more vertebrate sequences to follow, many of the recent developments in Ensembl have focusing on developing automatic comparative genome analysis and visualisation.

Animals↗

PubMed2002

The Ensembl genome database project.

The Ensembl (http://www.ensembl.org/) database project provides a bioinformatics framework to organise biology around the sequences of large genomes. It is a comprehensive source of stable automatic annotation of the human genome sequence, with confirmed gene predictions that have been integrated with external data sources, and is available as either an interactive web site or as flat files. It is also an open source software engineering project to develop a portable system able to handle very large genomes and associated requirements from sequence analysis to data storage and visualisation. The Ensembl site is one of the leading sources of human genome sequence annotation and provided much of the analysis for publication by the international human genome project of the draft genome. The Ensembl system is being installed around the world in both companies and academic sites on machines ranging from supercomputers to laptops.

Computational Biology↗

PubMed1998

The Androgen Receptor Gene Mutations Database.

The current version of the androgen receptor (AR) gene mutations database is described. The total number of reported mutations has risen from 272 to 309 in the past year. We have expanded the database: (i) by giving each entry an accession number; (ii) by adding information on the length of polymorphic polyglutamine (polyGln) and polyglycine (polyGly) tracts in exon 1; (iii) by adding information on large gene deletions; (iv) by providing a direct link with a completely searchable database (courtesy EMBL-European Bioinformatics Institute). The addition of the exon 1 polymorphisms is discussed in light of their possible relevance as markers for predisposition to prostate or breast cancer. The database is also available on the internet (http://www.mcgill. ca/androgendb/ ), from EMBL-European Bioinformatics Institute (ftp. ebi.ac.uk/pub/databases/androgen ), or as a Macintosh FilemakerPro or Word file (MC33@musica.mcgill.ca).

Computer Communication Networks↗

PubMed1989

Activation of an EGFR/neu chimeric receptor: early intracellular signals and cell proliferation responses.

Two clones of NIH3T3 fibroblasts, NEN37 and NEN7, overexpressing chimeric EGF/neu receptors (3 x 10(5) and 1 x 10(6) receptors/cell, respectively), were treated with EGF in order to identify the array of intracellular signals generated after activation of the neu proto-oncogene product. The results thus obtained were correlated with the effects of EGF on cell growth, investigated by both [3H]thymidine incorporation and long term (5 days) proliferation studies. In addition to the stimulation of the neu tyrosine kinase, previously reported by Lehvaslaiho et al. (EMBO J., 8, 159-166, 1989), EGF (10(-9)-10(-8) M) was found to induce marked increases of both [Ca2+]i and plasma membrane potential (investigated by the fura-2 and bis-oxonol techniques) which, in their initial phase, were only marginally dependent on the presence of Ca2+ in the incubation medium. These responses were inhibited, but only in part (40-50%) by phorbol ester activators of protein kinase C. Moreover, inositolphosphate analysis (by anion exchange chromatography) revealed hydrolysis of membrane polyphosphoinositides. All these effects of EGF were more prompt and much larger in NEN7 than NEN37 cells. The EGF concentration-dependence curves (measured by both [3H]thymidine incorporation and long-term proliferation assay) were quite different in the two cell clones. In the cells expressing the lower number of receptors measurable growth stimulation was observed at 10(-10), and maximal effect at 10(-9) M EGF. In NEN7 cells the curve was much more shallow, with measurable stimulation already at 10(-12) and maximal effect at 10(-8) M EGF. The maximal growth effect was approximately the same for the two cell clones. It is concluded that the intracellular signals identified here may play a limited role in the neu-induced cell proliferation, but are possibly involved in the acquisition of the tumoral phenotype typically expressed by the EGF-treated NEN7 cells.

Animals↗