Viromer® YELLOW

mRNA / DNA transfection

Selected for specific cells such as primary cardiomyocytes and hepatocytes. Highly efficient and safe.

Standard and other challenging cells might prefer RED.

 

Sufficient for the average number of * transfections in a 24-well format.

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Powerful mRNA and DNA transfection reagent

Viromer® YELLOW is designed for the DNA transfection into very challenging cells. This reagent differs from the versatile Viromer® RED in its structural chemistry but follows the same workflow: an Active Endosome Escape to deliver properly nucleic acids of interest into cells with no off-target effects. It allows the mRNA or DNA transfection (plasmids) of cells known as “non-transfectable” so far or only accessible by electroporation. Among others, very high efficacy was reported for human primary chondrocytes, rat primary cardiomyocytes, FAO hepatocytes, as for CHO and HeLa standard cell lines. Viromer® YELLOW is a ready-to-use product for DNA transfection coming with an easy and straightforward protocol, and it is compatible with any culture medium and antibiotics.


Convincing results in plasmid transfection in hard-to-transfect cells

fibroblast-transfection-viromer-yellowcardiomyocyte-transfection-viromer-yellowFAO-hepatocytes-transfection-viromer-yellow

 


Applications

  • protein expression / overexpression
  • RNA interference with plasmids encoding for shRNA
  • reporter gene assays
  • cancer research
  • stem cell research
  • cell signaling

Features and Benefits

  • High transfection efficiency due to an active escape of Viromer® complexes from the endosome.
  • Great safety because Viromer complexes are non-charged, gentle on cells and compatible with serum and antibiotics.
  • Easy and fast transfection with consistent results ascribed to straightforward protocol including initial optimization.

Notes

  • Buffer YELLOW, pH 6.0 is supplied with the kit
  • for research use only
  • store dry at 2-8°C

Publications for mRNA / DNA transfection with Viromer® YELLOW

METHYL CAP BINDING PROTEIN 2 IN SYSTEMIC SCLEROSIS

O’Reilly – 2017

The endothelial transcription factor ERG mediates Angiopoietin-1-dependent control of Notch signalling and vascular stability.

Shah et. al., Nat Commun., 2017

FGF23 is synthesised locally by renal tubules and activates injury-primed fibroblasts.

Smith et. al., Sci Rep., 2017

Point mutations in murine Nkx2-5 phenocopy human congenital heart disease and induce pathogenic Wnt signaling.

Furtado et. al., JCI Insight., 2017

EPHB4 kinase-inactivating mutations cause autosomal dominant lymphatic-related hydrops fetalis.

Martin-Almedina et. al., J Clin Invest. 2016

HIV-Infected Dendritic Cells Present Endogenous MHC Class II-Restricted Antigens to HIV-Specific CD4+ T Cells.

Coulon et. al., J Immunol., 2016

p53 coordinates base excision repair to prevent genomic instability

Poletto et.al., Nucleic Acids Res, 2016

Hypoxia Differentially Modulates the Genomic Stability of Clinical-Grade ADSCs and BM-MSCs in Long-Term Culture.

Bigot et.al., Stem Cells, 2015

Vernakalant activates human cardiac K(2P)17.1 background K(+) channels.

Seyler et. al., Biochem Bophys Res Commun., 2014