Optogenetics Adeno Associated Virus (AAV) Production Service
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Introduction to Optogenetics Adeno Associated Virus (AAV) Production Service
Optogenetics Adeno Associated Virus (AAV) premade products list
Optogenetics
Optogenetics has been a powerful scientific tool to further the fundamental scientific understanding of how specific cell types contribute to the function of biological tissues, such as neural circuits in vivo and lead to new insights into Parkinson’s disease and other neurological and psychiatric disorders in clinic [1]. By delivering optical signals to precisely control biological processes in living tissues, optogenetics opens up new landscapes for the study of biology, both in health and disease. Optogenetics is now typically used in neuroscience to control electrical potentials in neurons in vivo.
Adeno associated virus (AAV)
Adeno associated virus (AAV) is one kind of human parvovirus. Recombinant AAV vectors can efficiently transfect various cell types, including dividing and quiescent cells, and induce persistent gene expression in vivo without integrating into host genome and causing any disease. These features make AAV an attractive candidate in the application of gene delivery for gene therapy and human disease model establishment. To date, AAV has been proved as the most excellent gene therapy vector. Over 204 clinical trials have been carried out using AAV vectors for gene delivery, and promising gene therapy outcomes have been achieved from clinical trials for a great number of diseases.
Genemedi optogenetics AAV
Genemedi possesses a complete library of optogenetics components into AAV plasmid. These optogenetics AAV can help researchers control and monitor the activities of individual neurons in living tissue, and precisely measure the manipulation effects in real-time.
Properties
| Genemedi Optogenetics AAV | |
|---|---|
| Quantity/Unit | Vials |
| Form | Frozen form |
| Suitable Types of Infection | In vivo infection in animals |
| Sipping and Storage Guidelines | Shipped by dry ice, stored at -80 ℃, effective for 1 year. Avoid repeatedly freezing and thawing. |
| Titer | > 1*10^12v.g/ml |
Advantages
1. Millisecond-scale temporal precision, which allows the researchers to keep pace with fast biological information processing.
2. Fast readouts in optogenetics that can keep pace with the optical control by electrical recordings (“optrodes”) or reporter proteins.
3. Safety. The wild type Adeno Associated Virus (AAV) has not currently been known to cause disease, and further security of recombinant AAV is ensured after removal of most AAV genome elements.
4. Low immunogenicity. AAV causes a very mild immune response, lending further support to its apparent lack of pathogenicity.
5. Broad range of host and specificity targeting. AAV has the ability to infect both dividing and quiescent cells, allowing genetic material to be delivered to a highly diverse range of cell types. More than 12 AAV serotypes and a variety of capsid engineered AAV vectors can be selected according to their tissue tropisms.
6. Long-term stable expression. Long term and stable expression of genes in vivo can be mediated by AAV.
7. Stable physical properties. AAV is still alive at 60℃ and resistant to chloroform.
Applications and Figures
Quality control description
AAV capsid contains VR1 82kDa, VR2 72kDa and VR3 62kDa, which can be detected using the method of polyacrylamide gel electrophoresis (PAGE) followed by silver staining or Coomassie blue staining. Pure AAV should display only three major protein bands, which is shown in Figure 3.
Technical Documents
Lentivirus User Manual.
1. For detailed protocol about how to package and purify Adv, please see the Adenovirus User Manual on the Genemedi website.
1. For further information about AAV administration and transduction results, please see AAV(adeno associated virus) User Manual. Reference
1.Deisseroth K, G Feng, AK Majewska, G Miesenbock, A Ting and MJ Schnitzer. (2006). Next-generation optical technologies for illuminating genetically targeted brain circuits. J Neurosci 26:10380-6.
2.Li C, W Sun, C Gu, Z Yang, N Quan, J Yang, Z Shi, L Yu and H Ma. (2018). Targeting ALDH2 for Therapeutic Interventions in Chronic Pain-Related Myocardial Ischemic Susceptibility. Theranostics 8:1027-1041.
3.Yuan Y, Y Zheng, X Zhang, Y Chen, X Wu, J Wu, Z Shen, L Jiang, L Wang, W Yang, J Luo, Z Qin, W Hu and Z Chen. (2017). BNIP3L/NIX-mediated mitophagy protects against ischemic brain injury independent of PARK2. Autophagy 13:1754-1766.
4.Li S, X Dou, H Ning, Q Song, W Wei, X Zhang, C Shen, J Li, C Sun and Z Song. (2017). Sirtuin 3 acts as a negative regulator of autophagy dictating hepatocyte susceptibility to lipotoxicity. Hepatology 66:936-952.
5.Li L, B Li, M Li, C Niu, G Wang, T Li, E Krol, W Jin and JR Speakman. (2017). Brown adipocytes can display a mammary basal myoepithelial cell phenotype in vivo. Mol Metab 6:1198-1211.
6.Feng D, B Wang, L Wang, N Abraham, K Tao, L Huang, W Shi, Y Dong and Y Qu. (2017). Pre-ischemia melatonin treatment alleviated acute neuronal injury after ischemic stroke by inhibiting endoplasmic reticulum stress-dependent autophagy via PERK and IRE1 signalings. J Pineal Res 62.
7.Du X, H Hao, Y Yang, S Huang, C Wang, S Gigout, R Ramli, X Li, E Jaworska, I Edwards, J Deuchars, Y Yanagawa, J Qi, B Guan, DB Jaffe, H Zhang and N Gamper. (2017). Local GABAergic signaling within sensory ganglia controls peripheral nociceptive transmission. J Clin Invest 127:1741-1756.
8.Yang H, J Yang, W Xi, S Hao, B Luo, X He, L Zhu, H Lou, YQ Yu, F Xu, S Duan and H Wang. (2016). Laterodorsal tegmentum interneuron subtypes oppositely regulate olfactory cue-induced innate fear. Nat Neurosci 19:283-9.
9.Wu X, X Wu, Y Ma, F Shao, Y Tan, T Tan, L Gu, Y Zhou, B Sun, Y Sun, X Wu and Q Xu. (2016). CUG-binding protein 1 regulates HSC activation and liver fibrogenesis. Nat Commun 7:13498.
10.Wei Y, Y Chen, Y Qiu, H Zhao, G Liu, Y Zhang, Q Meng, G Wu, Y Chen, X Cai, H Wang, H Ying, B Zhou, M Liu, D Li and Q Ding. (2016). Prevention of Muscle Wasting by CRISPR/Cas9-mediated Disruption of Myostatin In vivo. Mol Ther 24:1889-1891.
11.Zhang X, Y Yuan, L Jiang, J Zhang, J Gao, Z Shen, Y Zheng, T Deng, H Yan, W Li, WW Hou, J Lu, Y Shen, H Dai, WW Hu, Z Zhang and Z Chen. (2014). Endoplasmic reticulum stress induced by tunicamycin and thapsigargin protects against transient ischemic brain injury: Involvement of PARK2-dependent mitophagy. Autophagy 10:1801-13.
