| Field | Specification |
|---|---|
| Mfr No | |
| Accession Number | |
| Product Type | |
| Promoter | |
| Reporter | |
| Selection Marker | Blasticidin, Puromycin |
| Shipping | |
| Species |
Background
Hypoxia-inducible factor 1 alpha (HIF-1α), encoded by HIF1A, is an oxygen-sensitive transcription factor that orchestrates the cellular response to low oxygen. Under normoxia, HIF-1α is hydroxylated and rapidly degraded; under hypoxia it is stabilized, dimerizes with HIF-1β, and binds hypoxia-response elements (HRE) to activate genes controlling glycolysis, angiogenesis, and erythropoiesis. HIF-1α drives metabolic adaptation in hypoxic tissues and tumors, where it promotes survival, vascularization, and aggressive behavior. HIF-1α is a major focus of oncology, angiogenesis, and hypoxia research, and is mechanistically distinct from the related factor HIF-2α.
Product Description & Applications
The HIF1a Reporter Lentivirus is a transcription factor reporter system that places a reporter gene under the control of tandem hypoxia-response elements coupled to a minimal promoter, giving a sensitive fluorescent or luminescent readout of HIF-1α activity. The construct is preferentially activated by HIF-1α rather than HIF-2α, supporting discrimination between the two factors. Reporter options include GFP, RFP, firefly luciferase, and Renilla 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.
Applications include monitoring hypoxia pathway activation and screening HIF-1α modulators in oncology and angiogenesis research.
About This Product
This reporter lentivirus places a Firefly Luc, GFP, Luc, Renilla Luc, RFP reporter gene under the control of tandem consensus response elements specific for the Hypoxia/HIF pathway (HIF-1a) transcription factor, coupled to a minimal TATA-box promoter and a proprietary upstream enhancer that maximizes signal-to-noise. The constitutively expressed selection marker (Blasticidin, Puromycin) 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.
Restricting metabolic plasticity enhances stress adaptation through the modulation of PDH and HIF1A in TRAP1-depleted colon cancer.
Tsai HY, Chen MH, Yun J, Lai LA, et al.
Cancer Letters, 2025. DOI: 10.1016/j.canlet.2025.217977
Product(s) used: LTV-0006
Usage: HRE Luciferase Reporter Lentivirus (LipExoGen, HIF1α-responsive) transduced into colon cancer cells with 8 μg/mL polybrene, blasticidin selection; luciferase assay quantified HIF1α pathway activity under TRAP1 depletion and metabolic stress conditions.
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