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In addition to the three molecules, we identified β-actin, albumin, and PDI ER60 precursor.
Some of the molecules we identified could be used as markers to prevent excess muscle fat accumulation.
By screening > 60 bioactive molecules, we identified two distinct phases during differentiation of hPSCs to the endothelial lineage.
While screening prostate cancers for CXCL12-responsive adhesion molecules, we identified CD164 (MGC-24) as a potential regulator of homing.
In the differentially expressed growth factor pathways (HGF, VEGF, EGF, IGF-1, TGF-β and PDGF), 10 of the 78 molecules we identified are targets of known drugs.
We used a new module in IPA based on literature and public drug target databases to determine how many of the molecules we identified by gene expression profiling in CAN/IFTA are targeted by known drugs (SD6) (Additional file 6).
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In light of these findings, we believe that the putative glial adhesion molecules we identify, including cadherin 22, CD164 and junction adhesion molecule 2 (Jameritmerit further investigation.
Given that the molecules we identify have been identified before as produced on human skin, we conclude that these were likely endogenous skin-bound molecules.
The only compatible fluorogenic molecule we identified was resazurin (Figure 1a, also known as AlamarBlue), which was irreversibly reduced to the fluorescent resorufin (Figure 1b) by electrons liberated from hydrogen gas by CpI.
TP represents the predictions that turn out to be correct, and our analysis yielded 379 (the number of known ncRNA molecules that we "identified") plus the 11 molecules we confirmed experimentally.
After screening 3,000 compounds from a preselected, kinase-based small molecule library, we identified 18 small molecule compounds that can significantly increase chemotherapy drug-induced cell death in human osteosarcoma cell lines U-2OSMR and KHOSR2 (Additional file 1: Table S1).
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