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B. Alver

Harvard University

ORCID: 0000-0002-5019-7652

Publishes on High-Energy Particle Collisions Research, Particle physics theoretical and experimental studies, Quantum Chromodynamics and Particle Interactions. 195 papers and 18.4k citations.

195Publications
18.4kTotal Citations

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Top publicationsby citations

HiGlass: web-based visual exploration and analysis of genome interaction maps
Peter Kerpedjiev, Nezar Abdennur, Fritz Lekschas et al.|Genome biology|2018
Cited by 2.3kOpen Access

We present HiGlass, an open source visualization tool built on web technologies that provides a rich interface for rapid, multiplex, and multiscale navigation of 2D genomic maps alongside 1D genomic tracks, allowing users to combine various data types, synchronize multiple visualization modalities, and share fully customizable views with others. We demonstrate its utility in exploring different experimental conditions, comparing the results of analyses, and creating interactive snapshots to share with collaborators and the broader public. HiGlass is accessible online at http://higlass.io and is also available as a containerized application that can be run on any platform.

The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers
B. Alver, Kimberly H. Kim, Ping Lu et al.|Nature Communications|2017
Cited by 436Open Access

Genes encoding subunits of SWI/SNF (BAF) chromatin remodelling complexes are collectively altered in over 20% of human malignancies, but the mechanisms by which these complexes alter chromatin to modulate transcription and cell fate are poorly understood. Utilizing mouse embryonic fibroblast and cancer cell line models, here we show via ChIP-seq and biochemical assays that SWI/SNF complexes are preferentially targeted to distal lineage specific enhancers and interact with p300 to modulate histone H3 lysine 27 acetylation. We identify a greater requirement for SWI/SNF at typical enhancers than at most super-enhancers and at enhancers in untranscribed regions than in transcribed regions. Our data further demonstrate that SWI/SNF-dependent distal enhancers are essential for controlling expression of genes linked to developmental processes. Our findings thus establish SWI/SNF complexes as regulators of the enhancer landscape and provide insight into the roles of SWI/SNF in cellular fate control.