While such small alterations putatively induced by miR-125b in proteins that regulate cell survival may not be significant under steady state conditions, they could provide growth advantage during periods of growth factor deprivation.
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Hsa-mir-125b-2 is highly expressed in childhood ETV6/RUNX1 (TEL/AML1) leukemias and confers survival advantage to growth inhibitory signals independent of p53.
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