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Therefore, VavNULL mice provided us with a unique tool to interrogate the importance of ITAM-dependent signals in neutrophil motility, as VavNULL neutrophils show a nearly complete block in ITAM signaling, but can still undergo integrin activation via inside-out signaling and undergo chemotaxis in response to chemotactic gradients [8].
The viability of Rps27l −/− ;Trp53 +/− mice provided us an opportunity to study the role of Rps27l in spontaneous tumorigenesis.
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Analysis of IgE binding epitopes in mice provides us with potential strategies for design of specific immunotherapy.
Furthermore, our current mice provide us with the potential of breeding new mouse models to better understand the increased risk of FTD observed in those with both an APOE4 allele and mutant VCP phenotype [38].
Clonal experiments in mice provide us with richer datasets than those available in human samples due to the defined time courses and greater numbers of replicates.
The TM-IEC C1galt1 −/− mice provide us with a model of IBD that has a defined molecular defect, as opposed to complicated and poorly understood immunological mechanisms such as cytokine knockouts, or HLA-B27 transgene expression.
Although these genetically modified mice have provided us with a superior model of spontaneous tumor development, the non-invasive imaging of these tumors continues to pose a problem.
The molecular cloning of seven v-rDNAs (Tseng et al., 2007, submitted) and the construction of the basonuclin-null mouse model provided us with the first opportunity to test the notion that a transcription factor could regulate a subset of rDNA.
Although with a limited translability to the human setting, these mouse models have provided us with the ability to probe over time the fundamental mechanisms promoting cholestatic disease progression.
Neither Dr. O'Shea nor his collaborator at NIH, who also maintains a colony of these mice, could provide us with sufficient mice.
Now, future tumor promotion studies using Gadd45b−/− and Jnk−/− mice may provide us with clues to understand the molecule mechanism of how CAR regulates PB promotion of HCC development.
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