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Applies R statistical methods to determine gene, exon, promoter, and splice variation from RNA-seq data.
Assigns probabilities to alternative splicing events including exon skipping, intron retention, and alternative promoter usage.
Compares transcription start sites (TSS) and transcription termination sites (TTS) across multiple tissues or conditions, and identifies preferred termination sites.
Assigns new transcript annotations from RNA-seq data, and visualizes the abundance of alternative splicing isoforms.
Analyzes alternative splicing events detected in RNA-seq data using junction files.
Compares two aligned sequences for small indels.
Compares alignment of multiple samples.
Converts the output of AltAnalyze into a simple text format.
During the time of the study, I have successfully used AltAnalyze to successfully identify gene and exon variations in human astrocytoma and prostate cancer, identify imprinting events in human placenta, identify microRNA-target sites, and identify transcription start sites.
The following examples are all of those that I was able to accomplish using AltAnalyze, in either human or mouse, although there are plenty of other variations that it has successfully handled with no problem.
A gene variant table:
This table is output from AltAnalyze. It shows the genes with a gene variant at the exon level.
The source for this table is junction file. And this is one of the typical examples that AltAnalyze was able to identify gene variant using junction files.
Imprinting events:
In this example, we can see the expression of maternally expressed genes (MEGs) in human placenta.
To be MEGs, genes should have a preferential expression of maternally inherited allele in human placenta.
Because of that, in this example, we are able to see that this gene did not have expression of the maternal allele in human placenta.
In this table, you can see two different transcripts of mST8S9. All of the transcripts are spliced between exon 4 and exon 10.
However, some of them start from exon 5, and others start from exon 10.
This is the result of TSS. And exon 4 and exon 5 are excluded as TSS.
It is highly likely that these are two splice variants of mST8S9 in human placenta