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This triggers a  large change in TF binding activity and chromatin state at an enhancer cluster  spanning >150 kb, coinciding with subtle, long-range chromatin compaction and  robust AXIN2 up-regulation. Our results support a model in which the indel acts  as an AXIN2 VCM-activating TF nucleation event, which modulates CLL pathology.", "principals_allowed": {"view": ["system.Everyone"], "edit": ["group.admin"]}}, "pubs_using": [], "publications_of_set": [{"abstract": "Non-coding variants coordinate transcription factor (TF) binding and chromatin  mark enrichment changes over regions spanning >100 kb. These molecularly  coordinated regions are named \"variable chromatin modules\" (VCMs), providing a  conceptual framework of how regulatory variation might shape complex traits. To  better understand the molecular mechanisms underlying VCM formation, here, we  mechanistically dissect a VCM-modulating noncoding variant that is associated  with reduced chronic lymphocytic leukemia (CLL) predisposition and disease  progression. This common, germline variant constitutes a 5-bp indel that controls  the activity of an AXIN2 gene-linked VCM by creating a MEF2 binding site, which,  upon binding, activates a super-enhancer-like regulatory element. This triggers a  large change in TF binding activity and chromatin state at an enhancer cluster  spanning >150 kb, coinciding with subtle, long-range chromatin compaction and  robust AXIN2 up-regulation. 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