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Here, using murine CPCs, we attempted to identify miRNAs that could be directly regulated by Bmi1.
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Therefore, in designing a semantic relation system for CPCs, we encounter the following problems: How many relations are needed to meet the completeness criterion, that is, are all semantic relations between CPCs covered by the proposed classification system?
Next, to study the potential function of Cdh2 in Isl1+ CPCs, we examined the expression of N-cadherin in AHF-CPCs.
To study the function of N-cadherin in Isl1+ CPCs, we performed conditional gene knockout using the Cre-loxP system.
Because Bmi1 knockdown reduces proliferation of mouse CPCs, we attempted to identify regulatory elements controlled by Bmi1.
To enhance the efficiency of CPC generation, we examined the influence of different culture conditions on culture output.
However, we characterized CPCs by CD34 and CD133 double-positivity, confirmative for an immature progenitor cell.
In an attempt to identify the components of the microenvironment of the Isl1+ CPCs in the AHF, we analyzed microarray data containing the transcriptional profiles of CPCs derived from mouse ES cells.
Temporal assessment performed as long as one month after injection into the infarcted region of the murine myocardium, demonstrated that the CPCs engrafted and differentiated into cardiomyocytes, as well as contributed to neovascularization in the infarcted region.
We're holding CPCs accountable city by city.
Furthermore, we investigated specific CPCs sub-populations previously described in the adult heart.
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