Products & Sercives
——
TurboMice™Custom Model Generation
Founders as little as 3-5 months

· TurboMice™ Knock-in Mice

· TurboMice™ Knock-out Mice

· TurboMice™ Conditional KO Mice

· TurboMice™ Point Mutation Mice ……

· TurboMice™ Humanized Mice ……


QuickMice™ Catalog Models
· QuickMice™ nuNPG Mice · QuickMice™ HPV Mice · QuickMice™ hHLA Mice · QuickMice™ LMNA Mice · QuickMice™ hPSCK9 Mice · QuickMice™ hACE2 Mice ……

Feeder Cells
· ICR MEF
· ICR Feeder
· CF1 Feeder
· CF1 MEF

Learn More  
Case Study
——
Highly cooperative chimeric super-SOX induces naive pluripotency across species

Our understanding of pluripotency remains limited: iPSC generation has only been established for a few model species, pluripotent stem cell lines exhibit inconsistent developmental potential, and germline transmission has only been demonstrated for mice and rats. By swapping structural elements between Sox2 and Sox17, we built a chimeric super-SOX factor, Sox2-17, that enhanced iPSC generation in five tested species: mouse, human, cynomolgus monkey, cow, and pig. A swap of alanine to valine at the interface between Sox2 and Oct4 delivered a gain of function by stabilizing Sox2/Oct4 dimerization on DNA, enabling generation of high-quality OSKM iPSCs capable of supporting the development of healthy all-iPSC mice. Sox2/Oct4 dimerization emerged as the core driver of naive pluripotency with its levels diminished upon priming. Transient overexpression of the SK cocktail (Sox+Klf4) restored the dimerization and boosted the developmental potential of pluripotent stem cells across species, providing a universal method for naive reset in mammals.

Journal：Cell stem cell    Sercives：TurboMice™ tetraploid complementation technology

Rapid generation of ACE2 humanized inbred mouse model for COVID-19 with tetraploid complementation

Journal：National Science Review Sercives：TurboMice™ tetraploid complementation technology

Dalbavancin binds ACE2 to block its interaction with SARS-CoV-2 spike protein and is effective in inhibiting SARS-CoV-2 infection in animal models


Infection with severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)has caused a pandemic worldwide.Currently,however,no effective drug or vaccine is available to treat or prevent the resulting coronavirus disease 2019(COVID-19).Here,we report our discovery of a promising an ti-COVID-19 drug can didate,the lipoglycopeptide antibiotic dalbava ncin,based on virtual screening of the FDA-approved peptide drug library combined with in vitro and in vivo functional antiviral assays.Our results showed that dalbavancin directly binds to human angiotensin-converting enzyme 2(ACE2)with high affinity,thereby blocking its interaction with the SARS-CoV-2 spike protein.Furthermore,dalbavancin effectively prevents SARS-CoV-2 replication in Vero E6 cells with an EC50 of~12 nM.In both mouse and rhesus macaque models,viral replication and histopathological injuries caused by SARS-CoV-2 infection are significantly inhibited by dalbavancin administration.Given its high safety and long plasma half-life(8-10 days)shown in previous clinical trials,our data indicate that dalbavancin is a promising anti-COVID-19 drug candidate.

Journal：Cell Research    Sercives：TurboMice™ tetraploid complementation technology


SARS-CoV-2 envelope protein causes acute respiratory distress syndrome (ARDS)-like pathological damages and constitutes an antiviral target

Cytokine storm and multi-organ failure are the main causes of SARS-CoV-2-related death. However, the origin of excessive damages caused by SARS-CoV-2 remains largely unknown. Here we show that the SARS-CoV-2 envelope (2-E) protein alone is able to cause acute respiratory distress syndrome (ARDS)-like damages in vitro and in vivo. 2-E proteins were found to form a type of pH-sensitive cation channels in bilayer lipid membranes. As observed in SARS-CoV-2-infected cells, heterologous expression of 2-E channels induced rapid cell death in various susceptible cell types and robust secretion of cytokines and chemokines in macrophages. Intravenous administration of purified 2-E protein into mice caused ARDS-like pathological damages in lung and spleen. A dominant negative mutation lowering 2-E channel activity attenuated cell death and SARS-CoV-2 production. Newly identified channel inhibitors exhibited potent anti-SARS-CoV-2 activity and excellent cell protective activity in vitro and these activities were positively correlated with inhibition of 2-E channel. Importantly, prophylactic and therapeutic administration of the channel inhibitor effectively reduced both the viral load and secretion of inflammation cytokines in lungs of SARS-CoV-2-infected transgenic mice expressing human angiotensin-converting enzyme 2 (hACE-2). Our study supports that 2-E is a promising drug target against SARS-CoV-2.

Journal：Cell Research    Sercives：TurboMice™ tetraploid complementation technology

Captopril alleviates lung inflammation in SARS-CoV-2-infected hypertensive mice

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent responsible for the global coronavirus disease 2019 (COVID-19) pandemic. Numerous studies have demonstrated that cardiovascular disease may affect COVID-19 progression. In the present study, we investigated the effect of hypertension on viral replication and COVID-19 progression using a hypertensive mouse model infected with SARS-CoV-2. Results revealed that SARS-CoV-2 replication was delayed in hypertensive mouse lungs. In contrast, SARS-CoV-2 replication in hypertensive mice treated with the antihypertensive drug captopril demonstrated similar virus replication as SARS-CoV-2-infected normotensive mice. Furthermore, antihypertensive treatment alleviated lung inflammation induced by SARS-CoV-2 replication (interleukin (IL)-1β up-regulation and increased immune cell infiltration). No differences in lung inflammation were observed between the SARS-CoV-2-infected normotensive mice and hypertensive mice. Our findings suggest that captopril treatment may alleviate COVID-19 progression but not affect viral replication.

Journal：Zoological Research    Sercives：TurboMice™ tetraploid complementation technology

Get in Touch
——
If you need immediate assistance, please contact Customer Service:
Tel
400-8388-113
Mail
sales@mingceler.com
Wechat
123456789
Adress
Guangzhou, Guangdong Province, China.