訂購信息

服務(wù)詳情

病毒類型

• VSV-G假病毒化的第三代慢病毒（默認(rèn)）
• VSV-G假病毒化的第二代慢病毒
• 非整合慢病毒
• 使用其他膜蛋白進(jìn)行假病毒化的慢病毒（如使用冠狀病毒刺突蛋白）
• 無膜蛋白的表面光禿的慢病毒（可用于轉(zhuǎn)導(dǎo)時的陰性對照）

交付內(nèi)容

對照病毒

為了更好地開展您的實驗，我們按照“對照病毒與定制病毒的生物學(xué)應(yīng)用相匹配”的原則給您贈送或者推薦對照病毒。例如，如果定制病毒表達(dá)一個基因，則推薦的對照病毒表達(dá)熒光蛋白EGFP。如果定制病毒表達(dá)打靶某個基因的shRNA，則對照病毒表達(dá)一個Scramble shRNA。推薦的對照病毒信息如下表所示：

輔助病毒

為了更好地開展您的實驗，我們按照“輔助病毒與定制病毒的生物學(xué)應(yīng)用相匹配”的原則給您推薦輔助病毒。例如，如果定制病毒是一個只含TRE啟動子的TetOn慢病毒，則需要一個表達(dá)rtTA的輔助病毒，才能進(jìn)行誘導(dǎo)表達(dá)實驗。推薦的輔助病毒信息如下表所示：

運(yùn)輸/儲存

我們的慢病毒存儲在HBSS緩沖液中，并采用干冰運(yùn)輸。收到慢病毒后，立即放置于-80℃，長期貯存至少6個月。慢病毒的保質(zhì)期約為一年。請避免反復(fù)凍融，因為這會導(dǎo)致慢病毒滴度大幅下降。

生產(chǎn)/質(zhì)控

注意：第三代慢病毒包裝系統(tǒng)只能包裝第三代的慢病毒轉(zhuǎn)移載體。但是第二代慢病毒包裝系統(tǒng)既能包裝第二代，也能包裝第三代的慢病毒轉(zhuǎn)移載體。第三代慢病毒轉(zhuǎn)移載體上的5’ LTR中的U3元件是被一個外源啟動子替代（如CMV啟動子或者RSV啟動子），使其不依賴Tat蛋白進(jìn)行HIV RNA基因組的轉(zhuǎn)錄，故第三代慢病毒包裝系統(tǒng)的包裝質(zhì)粒不含Tat蛋白。第二代慢病毒轉(zhuǎn)移載體上的5’ LTR是野生型的LTR，含有U3、R和U5元件，依賴Tat蛋白轉(zhuǎn)錄HIV RNA基因組，故第二代慢病毒包裝系統(tǒng)的包裝質(zhì)粒含有Tat蛋白。

滴度保證

我們的滴度保證僅適用于這樣的轉(zhuǎn)移載體

• 載體上的慢病毒基因組（從5’ LTR的R元件的第一個堿基到3’ LTR的R元件的最后一個堿基）長度小于承載限度長度9.2 kb（～野生型HIV-1基因組長度）。超過該范圍，載體上的病毒基因組也許會被包裝進(jìn)病毒，但會造成病毒滴度降低。

對于如下這樣的轉(zhuǎn)移載體，我們不能保證滴度：

• 包含對包裝過程有不利影響的序列，例如毒性基因（如促凋亡基因、針對HIV的host factors）；破壞包裝細(xì)胞完整性的基因（如導(dǎo)致細(xì)胞聚集的膜蛋白）、破壞慢病毒RNA基因組完整性的序列（如含有polyA信號序列）、易于重排或者產(chǎn)生二級結(jié)構(gòu)的序列（如重復(fù)序列或者高GC含量序列）。
• 用戶提供的載體，因為我們無法控制載體質(zhì)量。

交付周期

交付周期是指訂單接收到發(fā)貨之間的時間，不包括需要客戶提供任何物料（如病毒載體）的等待時間。對于不含有熒光標(biāo)記，但是含有藥篩標(biāo)記的病毒載體，如果您需要獲得細(xì)胞藥篩效果的質(zhì)檢結(jié)果，由于細(xì)胞生長狀態(tài)需要較長時間觀察，周期將額外增加8-10天。

客戶提供載體

如需客戶提供慢病毒載體，則請按照外來物品接收指南將載體寄送給我們。請嚴(yán)格按照我們的指南來進(jìn)行裝運(yùn)以免造成物品的任何延誤和損壞。客戶提供的所有材料均需經(jīng)過QC檢測，每一份材料附加檢測費(fèi)用。請注意，客戶提供物品接收并通過QC之后生產(chǎn)才正式開始。

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慢病毒轉(zhuǎn)導(dǎo)

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慢病毒體內(nèi)應(yīng)用

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常見問題解答

精選文獻(xiàn)

FALCON systematically interrogates free fatty acid biology and identifies a novel mediator of lipotoxicity

Cell Metabolism, 2023, doi: 10.1016/j.cmet.2023.03.018

使用的云舟生物產(chǎn)品或服務(wù)：

• Lentivirus Packaging
• Vector Cloning

Abstract: Cellular exposure to free fatty acids (FFAs) is implicated in the pathogenesis of obesity-associated diseases. However, there are no scalable approaches to comprehensively assess the diverse FFAs circulating in human plasma. Furthermore, assessing how FFA-mediated processes interact with genetic risk for disease remains elusive. Here, we report the design and implementation of fatty acid library for comprehensive ontologies (FALCON), an unbiased, scalable, and multimodal interrogation of 61 structurally diverse FFAs. We identified a subset of lipotoxic monounsaturated fatty acids associated with decreased membrane fluidity. Furthermore, we prioritized genes that reflect the combined effects of harmful FFA exposure and genetic risk for type 2 diabetes (T2D). We found that c-MAF-inducing protein (CMIP) protects cells from FFA exposure by modulating Akt signaling. In sum, FALCON empowers the study of fundamental FFA biology and offers an integrative approach to identify much needed targets for diverse diseases associated with disordered FFA metabolism.

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Identification of natural compounds as SARS-CoV-2 entry inhibitors by molecular docking-based virtual screening with bio-layer interferometry

Dingqi Zhang, et al.

Pharmacological Research, 2021, doi: 10.1016/j.phrs.2021.105820

使用的云舟生物產(chǎn)品或服務(wù)：

• Lentivirus Packaging
• Lentivirus Pseudotyped with Coronavirus Spike (S) Protein
• Vector Cloning

Abstract: Coronavirus Disease 2019 (COVID-19) is caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), which enter the host cells through the interaction between its receptor binding domain (RBD) of spike glycoprotein with angiotensin-converting enzyme 2 (ACE2) receptor on the plasma membrane of host cell. Neutralizing antibodies and peptide binders of RBD can block viral infection, however, the concern of accessibility and affordability of viral infection inhibitors has been raised. Here, we report the identification of natural compounds as potential SARS-CoV-2 entry inhibitors using the molecular docking-based virtual screening coupled with bilayer interferometry (BLI). From a library of 1871 natural compounds, epigallocatechin gallate (EGCG), 20(R)-ginsenoside Rg3 (RRg3), 20(S)-ginsenoside Rg3 (SRg3), isobavachalcone (Ibvc), isochlorogenic A (IscA) and bakuchiol (Bkc) effectively inhibited pseudovirus entry at concentrations up to 100 μM. Among these compounds, four compounds, EGCG, Ibvc, salvianolic acid A (SalA), and isoliensinine (Isl), were effective in inhibiting SARS-CoV-2-induced cytopathic effect and plaque formation in Vero E6 cells. The EGCG was further validated with no observable animal toxicity and certain antiviral effect against SARS-CoV-2 pseudovirus mutants (D614G, N501Y, N439K & Y453F). Interestingly, EGCG, Bkc and Ibvc bind to ACE2 receptor in BLI assay, suggesting a dual binding to RBD and ACE2. Current findings shed some insight into identifications and validations of SARS-CoV-2 entry inhibitors from natural compounds.

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Glioblastoma remodelling of human neural circuits decreases survival

Saritha Krishna, et al.

Nature, 2023, doi: 10.1038/s41586-023-06036-1

使用的云舟生物產(chǎn)品或服務(wù)：

• Lentivirus Packaging
• Vector Cloning

Abstract: Gliomas synaptically integrate into neural circuits. Previous research has demonstrated bidirectional interactions between neurons and glioma cells, with neuronal activity driving glioma growth and gliomas increasing neuronal excitability. Here we sought to determine how glioma-induced neuronal changes infuence neural circuits underlying cognition and whether these interactions infuence patient survival. Using intracranial brain recordings during lexical retrieval language tasks in awake humans together with site-specifc tumour tissue biopsies and cell biology experiments, we fnd that gliomas remodel functional neural circuitry such that task-relevant neural responses activate tumour-infltrated cortex well beyond the cortical regions that are normally recruited in the healthy brain. Site-directed biopsies from regions within the tumour that exhibit high functional connectivity between the tumour and the rest of the brain are enriched for a glioblastoma subpopulation that exhibits a distinct synaptogenic and neuronotrophic phenotype. Tumour cells from functionally connected regions secrete the synaptogenic factor thrombospondin-1, which contributes to the diferential neuron–glioma interactions observed in functionally connected tumour regions compared with tumour regions with less functional connectivity. Pharmacological inhibition of thrombospondin-1 using the FDA-approved drug gabapentin decreases glioblastoma proliferation. The degree of functional connectivity between glioblastoma and the normal brain negatively afects both patient survival and performance in language tasks. These data demonstrate that high-grade gliomas functionally remodel neural circuits in the human brain, which both promotes tumour progression and impairs cognition.

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