Following studies demonstrate that miR-21 enhances the expression of Foxp3 while miR-31 suppresses it in human Tregs [ 17]. miR-155, modulated by Foxp3, guarantees competitive fitness of Tregs to the IL-2 signal by targeting suppressor of cytokine signaling 1 (SOCS1) protein [ 18, 19].
Following studies have demonstrated that AICD regulates the transcription of genes, including LRP1, KAI1, GSK-3β, neprilysin and EGFR.
Interestingly, follow up studies demonstrated that increased plasma fl-OPN was associated with shorter survival of patients (p < 0.001).
Follow up studies demonstrated that changes in copy number of Stat5ab explained the altered immune and metabolic function.
Follow up studies demonstrated that the rate of subunit exchange is limited by the rate of tetramer dissociation; thus, the faster a TTR tetramer exchanges subunits with FT2·WT TTR, the less stable it is.
Following initial studies demonstrating the anti-allergic potential of gene vaccines, which clearly linked this capacity to the induction of Th1 immunity, apprehension was raised that this type of response might trigger pathological inflammation, particularly of the airways, and could even lead to development of autoimmunity.
The follow-up studies demonstrated that the pathological protein conversion and the deposition of the insoluble protein aggregates are associated with the development of other diseases, including Parkinson's, Huntington, fatal familial insomnia, ataxias, diabetes, and others9,15,16.
Follow-up studies demonstrated that a 50-gene signature (subsequently designated the PAM50) could recapitulate the initial studies by Perou and colleagues [ 9].
Follow-up studies demonstrated that a subset of these miRNAs have essential roles in cell cycle regulation and self-renewal of ESCs.
