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The current release of the PepCyber: P~Pep database V1.2 (May 2010) includes 11,269 records of interactions between 387 PPBD proteins and 1,471 substrate proteins, curated from 4,852 published studies.  This release represents a 60% increase in the number proteins covered over the previous release.

PepCyber: P~Pep is the largest public database of human protein-protein interactions mediated by phosphoprotein binding domains (PPBDs).   The database is hand curated from peer-reviewed literature and is a rich information source emphasizing the reported, experimentally validated data for specific PPBD-PPEP interactions, not a simple deposit of computational entries.  PepCyber: P~Pep is freely accessible at http://www.pepcyber.org/PPEP/.

1. Gong W, Zhou D, Ren Y, Wang Y, Zuo Z, Shen Y, Xiao F, Zhu Q, Hong A, Zhou X, Gao X, Li T. (2008) PepCyber:P~PEP: a database of human protein protein interactions mediated by phosphoprotein-binding domains. Nucleic Acids Res 36(Database issue), D679-83. [article]

InDepth Data Analysis Report Includes:

Map to Reference Sequence

• Includes custom construction of reference database(s) for mapping – miRBase, genome, etc
• Sequence data can be aligned to any publicly available small RNA databases for annotation of known small RNA
• Unknown small RNAs can be aligned with reference genomes

Additional Bioinformatics Analysis

• Classification of all mapped reads
• Length distribution of mapped sequences
• Annotation documentation of mapped sequences
• Alignment of sequence variants such as isomirs
• Genomic and chromosomal location of sequence clusters
• Prediction of new possible miRs
• Detailed explanation of miRNA analysis results and their context

 

Download the PDF of the summary report here.  Please contact us to obtain a complete set of sample data files.

The domestic pig is of enormous agricultural significance and valuable models for many human diseases. Information concerning the pig microRNAome (miRNAome) has been long overdue and elucidation of this information will permit an atlas of microRNA (miRNA) regulation functions and networks to be constructed. Here we performed a comprehensive search for porcine miRNAs on ten small RNA sequencing libraries prepared from a mixture of tissues obtained during the entire pig lifetime, from the fetal period through adulthood. The sequencing results were analyzed using mammalian miRNAs, the precursor hairpins (pre-miRNAs) and the first release of the high-coverage porcine genome assembly (Sscrofa9, April 2009) and the available expressed sequence tag (EST) sequences. Read more

Please nte that the sample submission form for microRNA Microarray Service has been updated due to the update of miRBase to version 15.  If you have a previous version of the form saved locally, please replace with this new form.  Click the link below or visit www.lcsciences.com to download the form.

Thank You

T cell activation requires signaling through the TCR and costimulatory molecules, such as CD28. MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression posttranscriptionally and are also known to be involved in lymphocyte development and function. In this paper, we set out to examine potential roles of miRNAs in T cell activation, using genome-wide expression profiling to identify miRNAs differentially regulated following T cell activation. One of the miRNAs upregulated after T cell activation, miR-214, was predicted to be capable of targeting Pten based on bioinformatics and reports suggesting that it targets Pten in ovarian tumor cells. Upregulation of miR-214 in T cells inversely correlated with levels of phosphatase and tensin homolog deleted on chromosome 10. In vivo, transcripts containing the 3′ untranslated region of Pten, including the miR-214 target sequence, were negatively regulated after T cell activation, and forced expression of miR-214 in T cells led to increased proliferation after stimulation. Blocking CD28 signaling in vivo prevented miR-214 upregulation in alloreactive T cells. Stimulation of T cells through the TCR alone was not sufficient to result in upregulation of miR-214. Thus, costimulation-dependent upregulation of miR-214 promotes T cell activation by targeting the negative regulator Pten. Thus, the requirement for T cell costimulation is, in part, related to its ability to regulate expression of miRNAs that control T cell activation.

Jindra PT, Bagley J, Godwin JG, Iacomini J. (2010) Costimulation-Dependent Expression of MicroRNA-214 Increases the Ability of T Cells To Proliferate by Targeting Pten. J Immunol [Epub ahead of print]. [abstract]

Transcriptomics, or genome-wide expression profiling, aims to catalogue the complete set of RNA transcripts produced by the genome, including mRNAs, non-coding RNAs and small RNAs.  Transcriptomics provides new biological insight and can be used to determine the structure of genes, their splicing patterns and other post transcriptional modifications, to detect rare and novel transcripts, and to quantify the changing expression levels of each transcript during development and under different disease conditions.

LC Sciences now provides a one-stop solution (i.e. from sample to data) for transcriptome sequencing using the latest in RNA-Seq technology.  RNA-Seq is a new method and a powerful tool to identify and quantitatively decode the entire population of RNAs in your sample.  Rather than sequencing RNA directly, the RNA-Seq method makes use of the latest high-throughput sequencing technology to sequence cDNA in order to reveal information about your sample’s RNA content.

The transcriptome profiling and analysis services by LC Sciences are comprehensive and provide the most complete picture of RNA content in your samples.  We can help you set up and conduct a high-quality, well-controlled RNA-Seq experiment based on the latest deep-sequencing technologies. (read more…)

30K Custom Array Design - LC Sciences has completed development of a new microfluidic chip design containing 30K features.  We are currently accepting early access orders on a case-by-case basis for custom arrays built on this design for both microRNA profiling and epitope mapping applications.  All of our array designs are based on the patented µParaflo® custom microarray platform.

Oral Presentations From the
WORLD CONGRESS OF CARDIOLOGY
Scientific Sessions
Beijing, China
16–19 June 2010

MicroRNA-378, a Novel Regulator of Heat Shock Transcription Factor-1, Involves Development of Cardiac Hypertrophy

Jie Yuan¹, Hong Ma¹, Hui Gong¹, Ning Zhou¹, Yanyan Liang¹, Yuhong Niu¹, Yunzeng Zou¹,² 1-Shanghai Institute of Cardivascular Diseases, 2- Zhongshan Hospital and Institutes of Biomedical Sciences, Fudan University (Shanghai, China)

Introduction: HSF1, as a protective factor, plays an important role in the development of pressure overload cardiac hypertrophy. However, the exact mechanisms of its regulation are less known. MicroRNAs, one of key regulators for post-transcriptional gene control, have been suggested to involve in the development of cardiac hypertrophy. Aim of our study was to investigate the potential role of microRNA in regulating HSF1 in the development of cardiac hypertrophy.

Methods and Results: Firstly, to identify some microRNAs that may be related to HSF1 expression under pressure overload, we performed miR microarray analysis (LC Sciences _Paraflo™ microRNA chips) on RNA isolated from the hearts of wild-type (C57B/L6) and HSF1 knockout mice subjected to transverse aortic constriction (TAC) or a sham operation for 14 days. After TAC, twenty miRNAs were up-regulated and thirty-five were down-regulated (p_0.05) in wild-type group, and seven miRNAs were up-regulated and ten were downregulated (p_0.05) in HSF1 knockout group compared to sham operated groups. Of these miRNAs, miR-378 expression decreased (0.69 fold) in heart of wild-type group while no change in HSF1 knockout mice, which was confirmed by Northern blot analysis and Real-time PCR. Northern analysis of adult mouse heart tissues revealed that miR-378 is highly expressed in the heart, as well as specific expression in cardiomyocytes. Secondly, to test the potential role of miR-378 in regulating HSF1, we observed HSF1 was up-regulated in wild-type mice after 14-day TAC, together with down-regulation of miR-378. In vitro, the upregulation of HSF1 is also associated with a downregulation of miR-378 by mechanical stretching cardiomyocytes. It seemed that miR-378 functioned as a suppressor of HSF1 protein. To confirm this, cardiomyocytes were transiently transfected with miR-378 mimics and inhibitors in vitro. Our data showed that over-expression of miR-378 inhibited endogenous HSF1 protein synthesis, and down-regulation of miR-378 made HSF1 expression increased. In addition, the miRBase Target database (http: //microrna.sanger.ac.uk/) suggested that a potential target sequence of miR-378 was found in the 3’ UTR of HSF1 in both mouse and human. To determine targeting by miR-378, we inserted a fragment of the HSF1 3’ UTR containing the target sequence, or the fragment whose target site was mutated, into a luciferase reporter vector. Luciferase activity was significantly repressed in the construct harboring the miR-378 target sequence, compared with the control vector harboring a nonrelated fragment or the mutated sequence. Taken together, the negative relationship between miR-378 level and HSF1 indicates that miR-378 is an essential regulator for HSF1 by targeting HSF1 3’UTR.

Conclusion: MiR-378 is a critical factor regulating HSF1 by targeting the HSF1 3’UTR. It suggests that miR-378 may participate in the development of cardiac hypertrophy by inhibiting HSF1 expression.

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