miR-AT

miR-AT identifies transcripts targeted by a specified list of microRNAs and quantifies the combinatorial impact of multiple miRNAs on target gene repression to elucidate regulatory mechanisms and disease-relevant pathways.


Key Features:

  • Combinatorial Analysis: Assesses collective binding of multiple miRNAs to single transcripts to evaluate combined repression effects.
  • Disease Relevance: Links concurrent dysregulation of multiple miRNAs to diseases such as metastatic cancer by highlighting affected genes and pathways.
  • Enrichment Analysis: Performs enrichment analysis on transcripts with multiple target sites to identify pathways including cell cycle regulation, cytoskeleton organization, and cell adhesion.
  • Network Analysis: Constructs network analyses to identify target genes upstream of regulatory nodes such as cyclin D1 and c-Myc.
  • Identification of Key Targets: Predicts combinatorial targets implicated in cancer metastasis, including TGFB1, ARPC3, and RANKL.

Scientific Applications:

  • Cancer Research: Elucidates how loss or dysregulation of multiple miRNAs alters gene expression networks involved in metastatic processes, aiding biomarker and therapeutic target discovery.
  • Gene Regulation Studies: Enables analysis of combinatorial miRNA effects to investigate multilayer gene regulation mechanisms.

Methodology:

Integrates miRNA binding site data, assesses the collective impact of specified miRNA lists on transcripts, and applies enrichment and network analysis to identify significant pathways and upstream regulators.

Topics

Details

Tool Type:
web application
Operating Systems:
Linux, Windows, Mac
Programming Languages:
Java
Added:
8/3/2017
Last Updated:
11/25/2024

Operations

Data Inputs & Outputs

Gene expression profiling

Publications

Dombkowski AA, Sultana Z, Craig DB, Jamil H. In silico Analysis of Combinatorial microRNA Activity Reveals Target Genes and Pathways Associated with Breast Cancer Metastasis. Cancer Informatics. 2011;10:CIN.S6631. doi:10.4137/cin.s6631. PMID:21552493. PMCID:PMC3085424.

Documentation

Links