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Thus, this work exemplifies how clinical observations can be dissected mechanistically via basic investigations in murine and cell models.
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We previously established genetically precise murine and cell-based models for JNCL, Cln3Δex7/8 mice and CbCln3Δex7/8 cerebellar cells [20], [32].
When BCL2 was overexpressed in cultured murine and human cell lines, cell spreading, adhesion, and motility were impaired.
We therefore changed to murine and rat cell lines and employed murine CT26 and CMT93 and rat DHD/K12KTRb colon carcinoma cells for further tests of CRN5-specific shRNAs.
Classically, endogenous MLVs are categorised on the basis of their envelope gene sequence and their cognate receptor polymorphism into ecotropic (replicating only in murine cells), xenotropic (replicating in multiple mammalian cells, including human but not murine cells), polytropic and modified polytropic (able to grow in murine and nonmurine cells) [1].
Also there may be differences in the use of signaling molecules between murine and human cells.
DP1 receptors are found on murine and dendritic cells and DP2 on Th2, eosinophils and basophils.
These observations are in accord with similar intracellular signaling responses in murine and human cells.
Upon CMV infection, TS levels were upregulated in both murine and human cells.
Both murine and human cells could be successfully genetically modified using the engineered trigenic retroviral vectors.
This study investigated their mechanism of action and compared their effectiveness in relation to estramustine in vitro against a panel of human and murine cell lines and in vivo against two murine colon tumour models (MAC).
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