| Field | Specification |
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| Mfr No | |
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| Product Type | |
| Promoter | |
| Reporter | |
| Selection Marker | Blasticidin, N/A, Puromycin |
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Background
Insulin-like growth factor binding protein 2 (IGFBP2) is a secreted protein that binds insulin-like growth factors IGF-1 and IGF-2, modulating their availability and interaction with the IGF-1 receptor. By regulating IGF bioactivity, IGFBP2 influences cell growth, survival, and metabolism. IGFBP2 also exerts IGF-independent functions through cell-surface and matrix interactions that affect cell adhesion, migration, and signaling. IGFBP2 is implicated in metabolic regulation and is frequently overexpressed in cancers, where it has been associated with tumor progression and invasion, making it a target of interest in endocrine, metabolic, and oncology research.
Product Description & Applications
The IGFBP2 ORF cDNA Lentivirus enables stable overexpression of human IGFBP2 in mammalian cells. The ORF cDNA is fused to a C-terminal V5 epitope tag and expressed under a strong constitutive promoter (CMV or EF1-alpha), while a fluorescent reporter (GFP or RFP) and drug selection marker (puromycin or blasticidin) are separated from the ORF by a self-cleaving peptide for independent translation; in some constructs a PGK promoter drives the reporter and marker. Cloning accuracy is confirmed by sequencing and protein expression validated by transient transfection.
The particles are ultra-purified by PEG precipitation and sucrose gradient centrifugation and efficiently transduce difficult-to-transfect cells, including primary and cryopreserved cultures, supporting reliable genome integration and long-term stable cell lines for gain-of-function studies.
About This Product
This ORF cDNA lentivirus enables stable overexpression of IGFBP2 (NCBI Accession: NM_000597) in mammalian cells via a third-generation, VSV-G pseudotyped delivery system. The ORF cDNA is fused to a C-terminal epitope tag (V5, Myc, or HA) and expressed under a strong constitutive promoter (CMV). Reporter and selection marker components (GFP, RFP; Blasticidin, Puromycin) are co-expressed via self-cleaving P2A peptides, enabling independent protein production without fusion-tag artifacts.
Ultra-purification by PEG precipitation and sucrose gradient centrifugation yields high-titer particles suitable for primary cells, suspension cultures, and stem cells. Stable polyclonal cell lines are established within 10–14 days by antibiotic selection or FACS sorting. For in vivo applications, the serum-free formulation and VSV-G envelope support direct administration or further concentration for stereotactic injection.
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.