The development of the B-lymphoid cell lineage is tightly controlled by the concerted action of a network of transcriptional and epigeneticregulators.EBF1,acentralcomponentofthisnetwork,isessentialforB-lymphoidspecificationandcommitmentaswell asforthemaintenanceoftheB-cellidentity.GeneticalterationscausinglossoffunctionoftheseB-lymphopoiesisregulatorshave beenimplicatedinthepathogenesisofB-lymphoidmalignancies,withparticularregardtoB-cellacutelymphoblasticleukaemias (B-ALLs),wheretheirpresenceisfrequentlydetected.TheactivityoftheB-cellregulatorynetworkmayalsobedisruptedbythe aberrantexpressionofinhibitorymolecules.Inparticular,twomulti-zincfingertranscriptioncofactorsnamedZNF423andZNF521 havebeencharacterisedaspotentinhibitorsofEBF1andareemergingaspotentiallyrelevantcontributorstothedevelopmentof B-cellleukaemias.Herewewillbrieflyreviewthecurrentknowledgeofthesefactorsanddiscusstheimportanceoftheirfunctional crosstalkwithEBF1inthedevelopmentofB-cellmalignancies.
ZNF423 and ZNF521: EBF1 antagonists of potential relevance in B-lymphoid malignancies.
Mesuraca M;Chiarella E;Scicchitano S;Codispoti B;Nappo G;Bond H;
2015-01-01
Abstract
The development of the B-lymphoid cell lineage is tightly controlled by the concerted action of a network of transcriptional and epigeneticregulators.EBF1,acentralcomponentofthisnetwork,isessentialforB-lymphoidspecificationandcommitmentaswell asforthemaintenanceoftheB-cellidentity.GeneticalterationscausinglossoffunctionoftheseB-lymphopoiesisregulatorshave beenimplicatedinthepathogenesisofB-lymphoidmalignancies,withparticularregardtoB-cellacutelymphoblasticleukaemias (B-ALLs),wheretheirpresenceisfrequentlydetected.TheactivityoftheB-cellregulatorynetworkmayalsobedisruptedbythe aberrantexpressionofinhibitorymolecules.Inparticular,twomulti-zincfingertranscriptioncofactorsnamedZNF423andZNF521 havebeencharacterisedaspotentinhibitorsofEBF1andareemergingaspotentiallyrelevantcontributorstothedevelopmentof B-cellleukaemias.Herewewillbrieflyreviewthecurrentknowledgeofthesefactorsanddiscusstheimportanceoftheirfunctional crosstalkwithEBF1inthedevelopmentofB-cellmalignancies.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
