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http://rstats.immgen.org/Skyline/skyline.html

Browser for general overview of expression profiles for RNA-seq data. Presents expression profiles of selected gene in chosen group of cell types, in either microarray or ULI RNA-seq data.

Proper citation: Gene Skyline (RRID:SCR_019014) Copy   

•   Source: SciCrunch Registry

https://www.ucl.ac.uk/ncl-disease/mutation-and-patient-database

Collection of published mutations and sequence variations in genes that cause Neuronal Ceroid Lipofuscinoses together with unpublished data included with permission. There are two tables for each human NCL disease gene - Patient Datasheets list all published or reported patients and families, and Mutation Datasheets list all published or reported mutations, cross-referenced to patient table. Datasheets are available to view or download as excel files for off-site use to aid local needs or interests. Database follows mutation nomenclature recommendations of Human Genome Variation Society.

Proper citation: Mutation and Patient Database (RRID:SCR_018806) Copy   

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https://www.sanger.ac.uk/collaboration/sequencing-idd-regions-nod-mouse-genome/

Genetic variations associated with type 1 diabetes identified by sequencing regions of the non-obese diabetic (NOD) mouse genome and comparing them with the same areas of a diabetes-resistant C57BL/6J reference mouse allowing identification of single nucleotide polymorphisms (SNPs) or other genomic variations putatively associated with diabetes in mice. Finished clones from the targeted insulin-dependent diabetes (Idd) candidate regions are displayed in the NOD clone sequence section of the website, where they can be downloaded either as individual clone sequences or larger contigs that make up the accession golden path (AGP). All sequences are publicly available via the International Nucleotide Sequence Database Collaboration. Two NOD mouse BAC libraries were constructed and the BAC ends sequenced. Clones from the DIL NOD BAC library constructed by RIKEN Genomic Sciences Centre (Japan) in conjunction with the Diabetes and Inflammation Laboratory (DIL) (University of Cambridge) from the NOD/MrkTac mouse strain are designated DIL. Clones from the CHORI-29 NOD BAC library constructed by Pieter de Jong (Children's Hospital, Oakland, California, USA) from the NOD/ShiLtJ mouse strain are designated CHORI-29. All NOD mouse BAC end-sequences have been submitted to the International Nucleotide Sequence Database Consortium (INSDC), deposited in the NCBI trace archive. They have generated a clone map from these two libraries by mapping the BAC end-sequences to the latest assembly of the C57BL/6J mouse reference genome sequence. These BAC end-sequence alignments can then be visualized in the Ensembl mouse genome browser where the alignments of both NOD BAC libraries can be accessed through the Distributed Annotation System (DAS). The Mouse Genomes Project has used the Illumina platform to sequence the entire NOD/ShiLtJ genome and this should help to position unaligned BAC end-sequences to novel non-reference regions of the NOD genome. Further information about the BAC end-sequences, such as their alignment, variation data and Ensembl gene coverage, can be obtained from the NOD mouse ftp site.

Proper citation: Sequencing of Idd regions in the NOD mouse genome (RRID:SCR_001483) Copy   

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http://metscape.ncibi.org

A software program that allows users to visualize and interpret human metabolim and expression profiling data by providing users with a bioinformatics framework. Its features include bulding and analyzing networks of genes and compounds, identifying enriched pathways from expression profiling data, and visualizing changes in metabolite data.

Proper citation: Metscape (RRID:SCR_014687) Copy   

•   Source: SciCrunch Registry

http://soap.genomics.org.cn/

Software package that provides full solution to next generation sequencing data analysis consisting of an alignment tool (SOAPaligner/soap2), a re-sequencing consensus sequence builder (SOAPsnp), an indel finder ( SOAPindel ), a structural variation scanner ( SOAPsv ), a de novo short reads assembler ( SOAPdenovo ), and a GPU-accelerated alignment tool for aligning short reads with a reference sequence. (SOAP3/GPU)., THIS RESOURCE IS NO LONGER IN SERVICE. Documented on September 16,2025.

Proper citation: SOAP (RRID:SCR_000689) Copy   

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http://www.cs.cmu.edu/~jernst/stem/

The Short Time-series Expression Miner (STEM) is a Java program for clustering, comparing, and visualizing short time series gene expression data from microarray experiments (~8 time points or fewer). STEM allows researchers to identify significant temporal expression profiles and the genes associated with these profiles and to compare the behavior of these genes across multiple conditions. STEM is fully integrated with the Gene Ontology (GO) database supporting GO category gene enrichment analyses for sets of genes having the same temporal expression pattern. STEM also supports the ability to easily determine and visualize the behavior of genes belonging to a given GO category or user defined gene set, identifying which temporal expression profiles were enriched for these genes. (Note: While STEM is designed primarily to analyze data from short time course experiments it can be used to analyze data from any small set of experiments which can naturally be ordered sequentially including dose response experiments.) Platform: Windows compatible, Mac OS X compatible, Linux compatible, Unix compatible

Proper citation: Short Time-series Expression Miner (STEM) (RRID:SCR_005016) Copy   

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http://www.bumc.bu.edu/cardiovascularproteomics/cpctools/strap/

Software program that automatically annotates a protein list with information that helps in the meaningful interpretation of data from mass spectrometry and other techniques. It takes protein lists as input, in the form of plain text files, protXML files (usually from the TPP), or Dat files from MASCOT search results. From this, it generates protein annotation tables, and a variety of GO charts to aid individual and differential analysis of proteomics data. It downloads information from mainly the Uniprot and EBI QuickGO databases. STRAP requires Windows XP or higher with at least version 3.5 of the Microsoft .NET Framework installed. Platform: Windows compatible

Proper citation: STRAP (RRID:SCR_005675) Copy   

•   Source: SciCrunch Registry

http://www.ebi.ac.uk/Tools/blast2/index.html

It is used to compare a novel sequence with those contained in nucleotide and protein databases by aligning the novel sequence with previously characterized genes.

Proper citation: Washington University Basic Local Alignment Search Tool (RRID:SCR_008285) Copy   

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http://www.gepas.org/

THIS RESOURCE IS NO LONGER IN SERVICE. Documented on May 12,2023. An integrated packages of tools for microarray data analysis. GEPAS provides a web-based interface that offers diverse analysis options from the early step of preprocessing (normalization of Affymetrix and two-color microarray experiments and other preprocessing options), to the final step of the functional profiling of the experiment (using Gene Ontology, pathways, PubMed abstracts etc.), which include different possibilities for clustering, gene selection, class prediction and array-comparative genomic hybridization management.

Proper citation: Gene Expression Profile Analysis Suite (RRID:SCR_008341) Copy   

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https://cran.r-project.org/web/packages/LDheatmap/index.html

Software application that plots measures of pairwise linkage disequilibria for SNPs (entry from Genetic Analysis Software)

Proper citation: LDHEATMAP (RRID:SCR_006312) Copy   

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https://www.braintest.org/brain_test/BrainTest

A portal of online studies that encourage community participation to tackle the most challenging problems in neuropsychiatry, including attention-deficit / hyperactivity disorder, schizophrenia, and bipolar disorder. Our approach is to engage the community and try to recruit tens of thousands of people to spend an hour of their time on our site. You folks will provide data in both brain tests and questionnaires, as well as DNA, and in return, we will provide some information about your brain and behavior. You will also be entered to win amazon.com gift cards. While large collaborative efforts were made in genetics in order to discover the secrets of the human genome, there are still many mysteries about the behaviors that are seen in complex neuropsychiatric syndromes and the underlying biology that gives rise to these behaviors. We know that it will require studying tens of thousands of people to begin to answer these questions. Having you, the public, as a research partner is the only way to achieve that kind of investment. This site will try to reach that goal, by combining high-throughput behavioral assessment using questionnaires and game-like cognitive tests. You provide the data and then we will provide information and feedback about why you should help us achieve our goals and how it benefits everyone in the world. We believe that through this online study, we can better understand memory and attention behaviors in the general population and their genetic basis, which will in turn allow us to better characterize how these behaviors go awry in people who suffer from mental illness. In the end, we hope this will provide better, more personalized treatment options, and ultimately prevention of these widespread and extremely debilitating brain diseases. We will use the data we collect to try to identify the genetic basis for memory and impulse control, for example. If we can achieve this goal, maybe we can then do more targeted research to understand how the biology goes awry in people who have problems with cognition, including memory and impulse control, like those diagnosed with ADHD, Schizophrenia, Bipolar Disorder, and Autism Spectrum Disorders. By participating in our research, you can learn about mental illness and health and help researchers tackle these complex problems. We can''t do it without your help.

Proper citation: Brain Test (RRID:SCR_006212) Copy   

•   Source: SciCrunch Registry

http://www.gwascentral.org/

Publicly available database of summary level findings from genetic association studies in humans, including genome wide association studies (GWAS). Previously named HGBASE, HGVbase and HGVbaseG2P.

Proper citation: GWAS Central (RRID:SCR_006170) Copy   

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http://intramural.nimh.nih.gov/gcap/index.htm

Schizophrenia related portal that aims to solve the mystery of genetic predisposition to psychosis, develop new methods for early diagnosis and prevention, and discover new treatments that will cure people suffering from it. Our objectives are to fully characterize: # neurobiological mechanisms related to susceptibility genes for schizophrenia and related clinical disorders; # genetic variation in aspects of cognition and emotionality associated with schizophrenia; and # small molecular targets for novel therapies. A unique feature of this Program is that its diverse scientific resources will be focused on a highly specific scientific agenda, that is to acquire the critical biological information about the susceptibility genes associated with schizophrenia and related illnesses. Our mission and goal, to understand the basic mechanisms of serious mental illness, has again guided us into new areas of research and to new insights. We have found evidence of new genes implicated in the cause of schizophrenia and involved in brain functions related to cognition and emotion and we have begun to explore how genes interact with each other and with the environment to individualize risk for these conditions. We are working now with over 20 genes related to schizophrenia. One of the key developments in our research over the past year has been the emergence of some targets for the development of novel therapeutics. We have discovered a new schizophrenia susceptibility gene, KCNH2, which represents the first clear target for the development of novel treatments. Just in this past year, for example, we published the first extensive statistical analysis of how schizophrenia genes may vary in their risk effects based on different genetic background (Nicodemus et al Hum Gen 2006), the first studies of schizophrenia genes interacting in effecting gene expression in brain (Lipska et al Hum Mol Genetics 2006a, Lipska et al Hum Mol Gen 2006 b); the first evidence that the mechanism of genetic association of NRG1 with schizophrenia involves a novel isoform of the gene in human brain (Law et al PNAS 2006), and the first evidence that MAOA may be linked to mood and impulse control because it effects critical mood regulatory neural networks (Meyer-Lindenberg et al PNAS 2006).

Proper citation: Genes Cognition and Psychosis Program (RRID:SCR_006292) Copy   

•   Source: SciCrunch Registry

http://www.umd.be/BRCA1/

The UMD-BRCA1/BRCA2 databases have been set up in a joined national effort through the network of 16 diagnostic laboratories to provide up-to-date information about mutations of the BRCA1 and BRCA2 genes identified in patients with breast and/or ovarian cancer. These databases currently contain published and unpublished information about the BRCA1/BRCA2 mutations reported in French diagnostic laboratories. This database includes 28 references and 5530 mutations (1440 different mutations and 786 protein variants) The databases of BRCA1 and BRCA2 mutations were built using the Universal Mutation Database tool. For each mutation, information is provided at several levels: * at the gene level: exon and codon number, wild type and mutant codon, mutation event, mutation name and, * at the protein level: wild type and mutant amino acid, binding domain, affected domain. If you want to submit a mutation, please contact R. Lidereau., S. Caputo. or E. Rouleau.

Proper citation: UMD-BRCA1/ BRCA2 databases (RRID:SCR_006128) Copy   

•   Source: SciCrunch Registry

http://isaac.bioapps.biozentrum.uni-wuerzburg.de/isaac/modules/genome/species.xhtml

Web based tool to enable the analysis of sets of genes, transcripts and proteins under different biological viewpoints and to interactively modify these sets at any point of the analysis. Detailed history and snapshot information allows tracing each action. One can switch back to previous states and perform new analyses. Sets can be viewed in the context of genomes, protein functions, protein interactions, pathways, regulation, diseases and drugs. Additionally, users can switch between species with an automatic, orthology based translation of existing gene sets. Sets as well as results of analyses can be exchanged between members of groups.

Proper citation: InterSpecies Analysing Application using Containers (RRID:SCR_006243) Copy   

•   Source: SciCrunch Registry

http://ogeedb.embl.de/#summary

Online GEne Essentiality database containing genes that were tested experimentally for essentiality and their features; it also provides a set of tools to systematically explore and analyze these data. The main purpose of this project is to better understand gene essentiality by facilitating the comparisons of the differences and similarities between essential and non-essential genes. This is achieved by collecting not only experimentally tested essential and non-essential genes, but also associated gene features such as expression profiles, duplication status, conservation across species, evolutionary origins and involvement in embryonic development. We focus on large-scale experiments and complement our data with text-mining results. Genes are organized into data sets according to their sources. Genes with variable essentiality status across data sets are tagged as conditionally essential, highlighting the complex interplay between gene functions and environments. Linked tools allow the user to compare gene essentiality among different gene groups, or compare features of essential genes to non-essential genes, and visualize the results. Why is it different from existing databases? * we included both essential and non-essential genes so that we could better understand the gene essentiality by comparing the similarities and differences between the two gene sets; * we compiled a list of features for each gene, including whether they are duplicates or involved in development, the number of other homologous genes in the same genome, as well as their earliest expression stages during development. These features are keys to understand the essentiality of genes; * we also provide a set of tools to explore our data and visualize the results. For example, users can simply divide genes into two groups according to whether they are duplicates, calculate the proportion of essential genes (PE%) in each group and then visualize the results in a bar plot; or they can classify genes into multiple groups according to their earliest expression stages during evolution, compare the essentiality of genes that were expressed earlier with those were latter, and plot the results in a line chart.

Proper citation: OGEE - Online GEne Essentiality database (RRID:SCR_006080) Copy   

•   Source: SciCrunch Registry

http://crezoo.org/

The CreZOO database is the European virtual repository of Cre and other targeted conditional driver strains. CreZOO is being developed in the context of the CREATE consortium, a core of major European and international mouse database holders and research groups involved in conditional mutagenesis. Its aim is to capture and disseminate extant and new information on Cre driver strains. CreZOO also aims to contribute data to the CREATE portal for worldwide access of related information. All transgenic strains carry detailed information on the promoter, specificity (using Adult Mouse Anatomy terms and Theiler Stages) and expressed gene(s) including IDs and direct links where available. Allele details are also presented, in addition to strain, background and availability (in the form of live mice, cryopreserved embryos or sperm etc) information (including EMMA, MGI, MMRRC etc hyperlinks where available). Handling and genotyping details (in the form of documents or hyperlinks) together with all relevant publications are clearly presented with PMID(s) and direct PubMed links.

Proper citation: CreZOO (RRID:SCR_006132) Copy   

•   Source: SciCrunch Registry

http://www.creline.org/

The CREATE consortium represents a core of major European and international mouse database holders and research groups involved in conditional mutagenesis, primarily to develop a strategy for the integration and dissemination of Cre driver strains for modelling aspects of complex human diseases in the mouse. Collectively the participants have amassed a significant number of these strains in their respective databases. Therefore one of the goals of CREATE is to provide a unified portal for worldwide access to these critical resources. The portal can either be searched through an advanced BioMart interface, by driver name, or by anatomical site of expression using Embryonic Mouse Anatomy Project (EMAP) and Mouse Anatomy (MA) ontology terms. Search results link back to the original source of the data for more detailed information and to IMSR to order mice if available. The ontology browser is particularly useful as it enables the CREATE consortium to identify cell and tissues that are not currently covered by existing lines. CREATE also aims to coordinate the production of suitable lines by the Cre generation projects described above. Through the CREATE portal, the CREATE consortium aims to develop a strategy for the production, integration and dissemination of new Cre driver strains for modelling aspects of complex human diseases in the mouse. CREATE is also developing a roadmap for harnessing emerging technologies and methods for improving Cre-mediated recombination in vivo through targeted, intensive workshops and discussion forums on the portal. This will entail review of construct design options for classical transgenic constructs (promoter/enhancer used, small size <2025 Kb) vs large transgenic constructs (BAC, P1, YAC etc.); methods used for Cre transgenic lines including random vs targeted integration, position independent expression loci, or replacement of endogenous coding sequences with Cre recombinase under the control of the endogenous locus. CREATE provides a platform for discussion of additional issues specific to inducible Cre strategies including background activity before induction, inducibility (kinetics), efficiency, and protocols used for induction of Cre recombinase activity. Additional components of the technology roadmap will be the cataloguing of other existing methodologies (rtTA, FLP, Dre) of mouse genome modification, sharing information on validated Cre mutant lines as well as identification and assessment of new methods of mutagenesis such as RNAi and other emerging technologies. Other discussion topics addressed through surveys on the CREATE portal include the characterization of Cre lines (specificity of expression/deletion; efficiency of expression/ deletion; reproducibility of deletion from animal to animal for the same floxed allele; reproducibility with different floxed alleles; timing of expression/deletion, etc.), the extent to which Cre expression changes upon backcrossing to specific genetic backgrounds through variegation and silencing; potential phenotypes caused by either integration- mediated mutagenesis or Cre ''toxicity''; and other factors affecting the specificity of Cre-mediated expression/deletion. CREATE regularly integrates common fields from the Cre-X, CreZOO and the MGI recombinase portal resources described below. The data in common consists of: * Transgene or Knock-in name. * MGI ID of allele. * Driver. * Anatomical site of expression. * Pubmed ID. * IMSR strain name and link. * Inducibility (YES/NO).

Proper citation: CREATE (RRID:SCR_006133) Copy   

•   Source: SciCrunch Registry

http://phenomebrowser.net/

PhenomeNet is a cross-species phenotype similarity network. It contains the experimentally observed phenotypes of multiple species as well as the phenotypes of human diseases. PhenomeNet provides a measure of phenotypic similarity between the phenotypes it contains. The latest release (from 22 June 2012) contains 124,730 complex phenotype nodes taken from the yeast, fish, worm, fly, rat, slime mold and mouse model organism databases as well as human disease phenotypes from OMIM and OrphaNet. The network is a complete graph in which edge weights represent the degree of phenotypic similarity. Phenotypic similarity can be used to identify and prioritize candidate disease genes, find genes participating in the same pathway and orthologous genes between species. To compute phenotypic similarity between two sets of phenotypes, we use a weighted Jaccard index. First, phenotype ontologies are used to infer all the implications of a phenotype observation using several phenotype ontologies. As a second step, the information content of each phenotype is computed and used as a weight in the Jaccard index. Phenotypic similarity is useful in several ways. Phenotypic similarity between a phenotype resulting from a genetic mutation and a disease can be used to suggest candidate genes for a disease. Phenotypic similarity can also identify genes in a same pathway or orthologous genes. PhenomeNet uses the axioms in multiple species-dependent phenotype ontologies to infer equivalent and related phenotypes across species. For this purpose, phenotype ontologies and phenotype annotations are integrated in a single ontology, and automated reasoning is used to infer equivalences. Specifically, for every phenotype, PhenomeNet infers the related mammalian phenotype and uses the Mammalian Phenotype Ontology for computing phenotypic similarity. Tools: * PhenomeBLAST - A tool for cross-species alignments of phenotypes * PhenomeDrug - method for drug-repurposing

Proper citation: phenomeNET (RRID:SCR_006165) Copy   

•   Source: SciCrunch Registry

http://compbio.charite.de/phenexplorer/

The PhenExplorer allows you to browse the Human Phenotype Ontology (HPO) in different ways, using the tabs ''''by features'''', ''''by disease'''', ''''by ontology'''' or ''''by genes''''. Clicking on a particular phenotypic feature (HPO-term) you can get a list of disease entries that are linked to it (i.e. diseases that are annotated with this HPO-term). You can also visualize this term in the context of the ontological structure. Finally, a lists of genes can be displayed, that are known to cause (when mutated) the linked diseases mentioned above. For each disease you can get the list of linked HPO-terms and genes. You can also search for specific genes and explore to which HPO-terms and diseases they are linked.

Proper citation: Phenexplorer (RRID:SCR_006156) Copy   

•   Source: SciCrunch Registry