This menu provides the list of EV mRNAs identified by high-throughput analyses.

Search:
Superdomain: All Prokaryote Eukaryote
Filter datasets:
  - "Sample type" indicates the source from which EVs originated (e.g. B cell, serum).
  - "Sample status" indicates the condition of the source from which EVs originated (e.g. Normal, miR-146a-treated, Patients of hernia).
Maximum false positive rate (FPR): Maximum true positive rate (TPR):
  - FPR is the probability that an absent mRNA accidently have higher intensity than that mRNA.
  - TPR is the percentile of mRNA among the present mRNAs.
    Please see user manual in the contact us/help menu for detail.
Number of molecules in one page:

The downloaded CSV file is not exactly the same as the displayed table. Opening CSV file with Excel can impair its content.

Since there are multiple primers in the microarray, the same mRNA can have several FPR and TPR values.

mRNA name UniProt accession FPR TPR Publication Orthologous group Identification count
All / Prokaryote / Eukaryote
(FPR<0.05,TPR<0.5)
Sulfotransferase 1A3 (ST1A3) (EC 2.8.2.1) (Aryl sulfotransferase 1A3/1A4) (Catecholamine-sulfating phenol sulfotransferase) (HAST3) (M-PST) (Monoamine-sulfating phenol sulfotransferase) (Placental estrogen sulfotransferase) (Sulfotransferase 1A3/1A4) (Sulfotransferase, monoamine-preferring) (Thermolabile phenol sulfotransferase) (TL-PST)P0DMM9 0.0e+0 4.7e-1Exosomes reflect the hypoxic status of glioma cells and mediate hypoxia-dependent activation of vascular cells during tumor development.
Proc Natl Acad Sci U S A. 2013 Apr 30;110(18):7312-7. doi: 10.1073/pnas.1220998110. Epub 2013 Apr 15.		ENOG4111H5614 / 0 / 14
Sulfotransferase 1A3 (ST1A3) (EC 2.8.2.1) (Aryl sulfotransferase 1A3/1A4) (Catecholamine-sulfating phenol sulfotransferase) (HAST3) (M-PST) (Monoamine-sulfating phenol sulfotransferase) (Placental estrogen sulfotransferase) (Sulfotransferase 1A3/1A4) (Sulfotransferase, monoamine-preferring) (Thermolabile phenol sulfotransferase) (TL-PST)P0DMM9 0.0e+0 4.5e-1Exosomes reflect the hypoxic status of glioma cells and mediate hypoxia-dependent activation of vascular cells during tumor development.
Proc Natl Acad Sci U S A. 2013 Apr 30;110(18):7312-7. doi: 10.1073/pnas.1220998110. Epub 2013 Apr 15.		ENOG4111H5614 / 0 / 14
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