AAV Serotype Testing Panel
Adeno-associated viruses (AAVs) have emerged as the most effective viral vectors for gene therapy due to their ability to transduce a wide variety of mammalian cell types and their low immunogenicity in host organisms. VectorBuilder offers the AAV serotype testing panel to enable users to select the optimal AAV serotype for specific applications by systematic comparison of a variety of serotypes in cells or in animals.
Highlights
- Our AAV serotype testing panel is the only commercially available AAV serotype testing kit that offers you the flexibility to customize your AAV panel with 3 or more AAV units from our wide collection of 18 serotypes, based on your project needs.
- Furthermore, when ordering your AAV panel you have the option to select between either CAG or CMV promoter for driving AAV-mediated EGFP reporter expression, which allows you to monitor and compare the performance of different serotypes on the panel
Ordering Information Price Match
| Product Name | Catalog No. | Titer & Volume | Unit Price (USD) | Availability |
|---|---|---|---|---|
| In vitro grade AAV serotype testing panel (CMV-EGFP) | PANEL-AAVS01 | 1012 GC/ml, 25 ul | $79 per aliquot | In stock |
| In vitro grade AAV serotype testing panel (CAG-EGFP) | PANEL-AAVS02 | |||
| In vivo grade AAV serotype testing panel (CMV-EGFP) | PANEL-AAVSP01 | 1013 GC/ml, 25 ul | $159 per aliquot | |
| In vivo grade AAV serotype testing panel (CAG-EGFP) | PANEL-AAVSP02 |
Notes:
a. Our standard AAV serotype collection includes AAVs 1, 2, 3, 4, 5, 6, 6.2, 7, 8, 9, rh10, DJ, DJ/8, PHP.eB, PHP.S, AAV2-retro, AAV2-QuadYF and AAV2.7m8.
b. The AAVs packaged in this offering are ssAAVs. If you need scAAVs (self-complementary AAVs), please send a design request to us.
c. A minimum of three units with the same or different serotypes is required for each panel. To customize and order your panel, please send a design request to us.
Shipping and storage
Our non-ultra-purified AAV is stored in a Tris-based buffer and our ultra-purified AAV is stored in a PBS-based buffer. Upon receiving, they should be stored at -80°C for long term (stable for at least 1 year), or -20°C for short term, e.g. 2-3 weeks. Thawed AAV can be stored at 4 °C for 1-2 weeks.
Technical Information
AAV vector
The AAV serotype testing panel contains premade AAVs expressing EGFP using our highly optimized AAV vector system. Users have the option to select between either CAG or CMV promoter for driving EGFP expression. Our AAV vector system is optimized for high copy number replication in E. coli, high-titer packaging of live virus, efficient transduction of host cells, and high-level transgene expression. Our AAV vectors can be packaged into virus using all known capsid serotypes, is capable of very high transduction efficiency, and presents a low safety risk.
Figure 1. Maps of EGFP-expressing AAV vectors with (A) CMV promoter or (B) CAG promoter.
Tissue tropism of AAV serotypes
Many strains of AAV have been identified in nature. They are divided into different serotypes based on different antigenicity of the capsid protein on the viral surface. Different serotypes can render the virus with different tissue tropism (i.e. tissue specificity of infection). When our AAV vectors are packaged into the virus, different serotypes can be conferred to the virus by using different capsid proteins for the packaging. The AAV serotype testing panel is designed for a systematic comparison of the tissue specificity of multiple AAV serotypes to help you select the optimal serotype for your experiment. The tables below list the tissue specificity conferred by different AAV serotypes.
List by Serotype
List by Tissue Type
| Serotype | Tissue Tropism |
|---|---|
| AAV1 | Smooth muscle, skeletal muscle, CNS, brain, lung, retina, inner ear, pancreas, heart, liver |
| AAV2 | Smooth muscle, CNS, brain, liver, pancreas, kidney, retina, inner ear, testes |
| AAV3 | Smooth muscle, liver, lung |
| AAV4 | CNS, retina, lung, kidney, heart |
| AAV5 | Smooth muscle, CNS, brain, lung, retina, heart |
| AAV6 | Smooth muscle, heart, lung, pancreas, adipose, liver |
| AAV6.2 | Lung, liver, inner ear |
| AAV7 | Smooth muscle, retina, CNS, brain, liver |
| AAV8 | Smooth muscle, CNS, brain, retina, inner ear, liver, pancreas, heart, kidney, adipose |
| AAV9 | Smooth muscle, skeletal muscle, lung, liver, heart, pancreas, CNS, retina, inner ear, testes, kidney, adipose |
| AAV-rh10 | Smooth muscle, lung, liver, heart, pancreas, CNS, retina, kidney |
| AAV-DJ | Liver, heart, kidney, spleen |
| AAV-DJ/8 | Liver, brain, spleen, kidney |
| AAV-PHP.eB | CNS |
| AAV-PHP.S | PNS |
| AAV2-retro | Spinal nerves |
| AAV2-QuadYF | Endothelial cell, retina |
| AAV2.7m8 | Retina, inner ear |
| Tissue Type | Recommended AAV Serotypes |
|---|---|
| Smooth muscle | AAV1, AAV2, AAV3, AAV5, AAV6, AAV7, AAV8, AAV9, AAV-rh10 |
| Skeletal muscle | AAV1, AAV9 |
| CNS | AAV1, AAV2, AAV4, AAV5, AAV7, AAV8, AAV9, AAV-rh10, AAV-PHP.eB |
| PNS | AAV-PHP.S |
| Brain | AAV1, AAV2, AAV5, AAV7, AAV8, AAV-DJ/8 |
| Retina | AAV1, AAV2, AAV4, AAV5, AAV7, AAV8, AAV9, AAV-rh10, AAV2-QuadYF, AAV2.7m8 |
| Inner ear | AAV1, AAV2, AAV6.2, AAV8, AAV9, AAV2.7m8 |
| Lung | AAV1, AAV3, AAV4, AAV5, AAV6, AAV6.2, AAV9, AAV-rh10 |
| Liver | AAV1, AAV2, AAV3, AAV6, AAV6.2, AAV7, AAV8, AAV9, AAV-rh10, AAV-DJ, AAV-DJ/8 |
| Pancreas | AAV1, AAV2, AAV6, AAV8, AAV9, AAV-rh10 |
| Heart | AAV1,AAV4, AAV5, AAV6, AAV8, AAV9, AAV-rh10, AAV-DJ |
| Kidney | AAV2, AAV4, AAV8, AAV9, AAV-rh10, AAV-DJ, AAV-DJ/8 |
| Adipose | AAV6, AAV8, AAV9 |
| Testes | AAV2, AAV9 |
| Spleen | AAV-DJ, AAV-DJ/8 |
| Spinal nerves | AAV2-retro |
| Endothelial cells | AAV2-QuadYF |
Experimental validation
We have developed a number of proprietary techniques to optimize our triple transfection-based AAV packaging protocol and our virus has been validated to exhibit high transduction efficiency in mammalian cells.
Figure 2. HEK293T cells were transduced with 18 serotypes of recombinant AAV packaged from the same CMV>EGFP vector (VB010000-9394npt). Representative EGFP expression at 48 h post transduction in different serotypes is shown as indicated. Scale bars: 100 μm.
Figure 3. HeLa cells were transduced with 18 serotypes of recombinant AAV packaged from the same CMV>EGFP vector (VB010000-9394npt). EGFP (A) Mean Fluorescence Intensity (MFI) and (B) positivity were quantified using flow cytometry 48 h post transduction. (C) Representative EGFP expression in different serotypes is shown as indicated. Scale bars: 100 μm.
Figure 4. Huh-7 cells were transduced with 18 serotypes of recombinant AAV packaged from the same CMV>EGFP vector (VB010000-9394npt). EGFP (A) Mean Fluorescence Intensity (MFI) and (B) positivity were quantified using flow cytometry 48 h post transduction. (C) Representative EGFP expression in different serotypes is shown as indicated. Scale bars: 100 μm.
Resources
Documents
User Instructions Certificate of Analysis (COA) Brochures & FlyersFeatured Citations
Trb3 Controls Mesenchymal Stem Cell Lineage Fate and Enhances Bone Regeneration by Scaffold-Mediated Local Gene Delivery
Jiabing Fan, et al.
Biomaterials, 2020, doi: 10.1016/j.biomaterials.2020.120445
Products used:
- Adeno-Associated Virus (AAV) Packaging (AAV1, 2, 5, 6, 8 & 9)
- Lentivirus Packaging
- Vector Cloning
Abstract: Aberrant lineage commitment of mesenchymal stem cells (MSCs) in marrow contributes to abnormal bone formation due to reduced osteogenic and increased adipogenic potency. While several major transcriptional factors associated with lineage differentiation have been found during the last few decades, the molecular switch for MSC fate determination and its role in skeletal regeneration remains largely unknown, limiting creation of effective therapeutic approaches. Tribbles homolog 3 (Trb3), a member of tribbles family pseudokinases, is known to exert diverse roles in cellular differentiation. Here, we investigated the reciprocal role of Trb3 in the regulation of osteogenic and adipogenic differentiation of MSCs in the context of bone formation, and examined the mechanisms by which Trb3 controls the adipo-osteogenic balance. Trb3 promoted osteoblastic commitment of MSCs at the expense of adipocyte differentiation. Mechanistically, Trb3 regulated cell-fate choice of MSCs through BMP/Smad and Wnt/β-catenin signals. Importantly, in vivo local delivery of Trb3 using a novel gelatin-conjugated caffeic acid-coated apatite/PLGA (GelCA-PLGA) scaffold stimulated robust bone regeneration and inhibited fat-filled cyst formation in rodent non-healing mandibular defect models. These findings demonstrate Trb3-based therapeutic strategies that favor osteoblastogenesis over adipogenesis for improved skeletal regeneration and future treatment of bone-loss disease. The distinctive approach implementing a scaffold-mediated local gene transfer may further broaden the translational use of targeting specific therapeutic gene related to lineage commitment for clinical bone treatment.
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Fructose-1, 6-bisphosphatase is a nonenzymatic safety valve that curtails AKT activation to prevent insulin hyperresponsiveness
Li Gu, et al.
Cell Metabolism, 2023, doi: 10.1016/j.cmet.2023.03.021
Products used:
- Adeno-Associated Virus (AAV) Packaging (AAV8)
- Vector Cloning
Abstract: Insulin inhibits gluconeogenesis and stimulates glucose conversion to glycogen and lipids. How these activities are coordinated to prevent hypoglycemia and hepatosteatosis is unclear. Fructose-1,6-bisphosphatase (FBP1) is rate controlling for gluconeogenesis. However, inborn human FBP1 deficiency does not cause hypoglycemia unless accompanied by fasting or starvation, which also trigger paradoxical hepatomegaly, hepatosteatosis, and hyperlipidemia. Hepatocyte FBP1-ablated mice exhibit identical fasting-conditional pathologies along with AKT hyperactivation, whose inhibition reversed hepatomegaly, hepatosteatosis, and hyperlipidemia but not hypoglycemia. Surprisingly, fasting-mediated AKT hyperactivation is insulin dependent. Independently of its catalytic activity, FBP1 prevents insulin hyperresponsiveness by forming a stable complex with AKT, PP2A-C, and aldolase B (ALDOB), which specifically accelerates AKT dephosphorylation. Enhanced by fasting and weakened by elevated insulin, FBP1:PP2A-C:ALDOB:AKT complex formation, which is disrupted by human FBP1 deficiency mutations or a C-terminal FBP1 truncation, prevents insulin-triggered liver pathologies and maintains lipid and glucose homeostasis. Conversely, an FBP1-derived complex disrupting peptide reverses diet-induced insulin resistance.
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SERCA2 phosphorylation at serine 663 is a key regulator of Ca2+ homeostasis in heart diseases
Fabrice Gonnot, et al.
Nature Communications, 2023, doi: 10.1038/s41467-023-39027-x
Products used:
- Adeno-Associated Virus (AAV) Packaging (AAV9)
- Vector Cloning
Abstract: Despite advances in cardioprotection, new therapeutic strategies capable of preventing ischemia-reperfusion injury of patients are still needed. Here, we discover that sarcoplasmic/endoplasmic reticulum Ca2+ ATPase (SERCA2) phosphorylation at serine 663 is a clinical and pathophysiological event of cardiac function. Indeed, the phosphorylation level of SERCA2 at serine 663 is increased in ischemic hearts of patients and mouse. Analyses on different human cell lines indicate that preventing serine 663 phosphorylation significantly increases SERCA2 activity and protects against cell death, by counteracting cytosolic and mitochondrial Ca2+ overload. By identifying the phosphorylation level of SERCA2 at serine 663 as an essential regulator of SERCA2 activity, Ca2+ homeostasis and infarct size, these data contribute to a more comprehensive understanding of the excitation/contraction coupling of cardiomyocytes and establish the pathophysiological role and the therapeutic potential of SERCA2 modulation in acute myocardial infarction, based on the hotspot phosphorylation level of SERCA2 at serine 663 residue.
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