Post-transcriptional regulation of ULBP1 ligand for the activating immunoreceptor NKG2D involves 3′ untranslated region

Regulation of NKG2D-ligand cell surface expression by intracellular calcium after HDAC-inhibitor treatment

“…We have previously demonstrated a calcium dependency of HDAC-inhibitor induced MICA/B expression (Andresen et al, 2007) and show here that calcium is also important for the induction of ULBP2 expression. However, the calcium dependency of MICA/B and ULBP2 cell surface expression is distinct, supporting the current perception that MICA/B and ULBP2 expression is regulated by different signal transduction pathways (Andresen et al, 2007;Heinemann et al, 2012;Himmelreich et al, 2011;Vales-Gomez et al, 2008;Venkataraman et al, 2007;Wei et al, 2010).…”

“…Depending on the stress stimuli, MICA/B expression is controlled by Sp1, HSF-1, or HIF-1 promoter binding (Andresen et al, 2007;Venkataraman et al, 2007;Wei et al, 2010), whereas p53 activity controls ULBP2 expression (Textor et al, 2011). Furthermore, the expression level of MICA/B and ULBP2 is regulated by distinct cellular microRNAs (Heinemann et al, 2012;Himmelreich et al, 2011).…”

p38 MAPK differentially controls NK activating ligands at transcriptional and post-transcriptional level on multiple myeloma cells

“…Besides the involvement of transcriptional activity, the presence of ARE (AU-Rich Elements) regions in the 3 0 UTR of all human NKG2D ligands ( 43,47 ) suggests that mRNA stability could play an important role among the various levels of regulation. Our data demonstrate that VCR affects the stability of ULBP-1 but not MICA and PVR mRNA and are consistent with the evidence showing that the microtubule disruption can increase the binding to AU sequences of ELAV proteins involved in the stability of the mRNA ( 48 ).…”

c-Myc regulates expression of NKG2D ligands ULBP1/2/3 in AML and modulates their susceptibility to NK-mediated lysis

“…Various molecular pathways, including extracellular signal-regulated kinase (ERK), AKT, p53, and signal transducer and activator of transcription 3 have been reported to play a regulatory, both at the transcriptional or posttranscriptional level. [38][39][40][41][42][43][44][45][46][47][48] In this study, we investigated the molecular basis of cytarabine resistance in AML cells. We found that these cells exhibited increased susceptibility to NK lysis that correlates with an increase in c-Myc induction and the subsequent upregulation of ULBPs.…”