| Field | Specification |
|---|---|
| Product Type | |
| Promoter | |
| Reporter | |
| Selection Marker | Puromycin, Blasticidin |
| Shipping | |
| Species |
Background
Myocyte enhancer factor 2 (MEF2) is a family of MADS-box transcription factors with at least four members in vertebrates (MEF2A, MEF2B, MEF2C, and MEF2D) expressed in distinct but overlapping patterns from embryogenesis through adulthood. MEF2 factors are critical regulators of embryonic development and of cardiac and skeletal muscle differentiation, controlling myocyte gene expression. In adult tissues, MEF2 proteins mediate stress-responsive transcription, including in neurons and the heart. Through these roles, MEF2 is widely studied in developmental biology, cardiovascular, and myogenic research.
Product Description & Applications
The MEF2 Reporter Lentivirus is a transcription factor reporter system built with tandem repeats of consensus MEF2 DNA-binding elements upstream of a minimal promoter and a reporter gene, giving a sensitive fluorescent or luminescent readout of the transcriptional activity of MEF2 family factors, including MEF2A, MEF2B, MEF2C, and MEF2D. Reporter options include EGFP, GFP, mCherry, RFP, d2GFP, and firefly luciferase, with optional blasticidin or puromycin selection for stable polyclonal cell line generation. Particles are purified by PEG precipitation and sucrose gradient centrifugation and efficiently transduce difficult-to-transfect cells, including primary and thawed cells.
It supports stable reporter cell line generation for studying muscle differentiation, cardiac development, and stress-responsive transcription.
About This Product
This reporter lentivirus places a d2GFP, EGFP, Firefly Luc, mCherry, GFP, RFP reporter gene under the control of tandem consensus response elements specific for the MEF2 Transcription Factors transcription factor, coupled to a minimal TATA-box promoter and a proprietary upstream enhancer that maximizes signal-to-noise. The constitutively expressed selection marker (Puromycin, Blasticidin) and/or secondary reporter enables stable polyclonal cell line generation and flexible readout by fluorescence microscopy, flow cytometry, or luminometry.
Stable integration via the lentiviral backbone ensures consistent, clonally representative reporter expression in dividing and post-mitotic target cells — including primary T cells, macrophages, organoids, and cryopreserved material — eliminating the variability inherent to transient transfection. The self-inactivating LTR design and third-generation packaging minimize insertional mutagenesis risk and ensure biosafety classification at BSL-2.
Can't find the lentiviral construct you need, or want to adjust key design elements? Contact us to discuss custom LV design and optional add-ons.
Common customization requests
- Insert / payload: replace the gene/sequence, swap to a different isoform, add mutations, or optimize cloning features.
- Expression design: change promoter (e.g., CMV/EF1α/PGK), add enhancers, or adjust regulatory elements.
- Reporters: add/swap GFP/RFP/mCherry/luciferase (single or dual reporters where applicable).
- Selection markers: add/swap puromycin/blasticidin/neomycin or fluorescent selection options.
- Vector format: switch between OE, shRNA, CRISPR (sgRNA/Cas systems), or control vectors (where supported).
Add-ons you can request
- Control viruses: empty vector, non-targeting shRNA, reporter-only controls, or matched backbone controls.
- Packaging / format: concentration options, aliquoting, or custom fill volume for screening workflows.
- Documentation: construct map/sequence confirmation package (as available) and batch documentation.
What to include in your request
- Target cell type/model (cell line or primary cells) and intended readout (reporter, knockdown, OE, etc.)
- Insert sequence (FASTA) or reference ID, plus any required tags/mutations
- Promoter, reporter, and selection marker preferences
- Desired scale and preferred format (aliquots / concentration requests)
Email us at support@biohippo.com or use the Talk to a Scientist request form.
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