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Scott J. Bultman

Researcher at University of North Carolina at Chapel Hill

Publications -  69
Citations -  17000

Scott J. Bultman is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: SWI/SNF & Butyrate. The author has an hindex of 33, co-authored 69 publications receiving 14203 citations. Previous affiliations of Scott J. Bultman include Case Western Reserve University.

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Dissecting molecular steps in chromatin domain activation during hematopoietic differentiation.

TL;DR: A hierarchical order of GATA-1-triggered events at a complex locus is defined and a novel mechanism of long-range gene regulation is established to establish a novel way of hematopoiesis and transcriptional activation is established.
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BRG1 co-localizes with DNA replication factors and is required for efficient replication fork progression

TL;DR: It is demonstrated that the BRG1 catalytic subunit of mammalian SWI/SNF-related complexes co-localizes with origin recognition complexes, GINS complexes, and proliferating cell nuclear antigen at sites of DNA replication on extended chromatin fibers, suggesting it does not participate in origin selection but is involved in the firing of origins and the process of replication elongation.
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Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

Daniel J. Klionsky, +2522 more
- 01 Jan 2016 - 
TL;DR: Author(s): Klionsky, DJ; Abdelmohsen, K; Abe, A; Abedin, MJ; Abeliovich, H; A Frozena, AA; Adachi, H, Adeli, K, Adhihetty, PJ; Adler, SG; Agam, G; Agarwal, R; Aghi, MK; Agnello, M; Agostinis, P; Aguilar, PV; Aguirre-Ghis
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Functional Redundancy of SWI/SNF Catalytic Subunits in Maintaining Vascular Endothelial Cells in the Adult Heart

TL;DR: It is demonstrated for the first time that Brm functionally compensates for Brg1 in vivo and that there are significant changes in the relative importance of BRG1- and BRM-catalyzed SWI/SNF complexes during the development of an essential cell lineage.
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SWI/SNF complexes are required for full activation of the DNA-damage response

TL;DR: The results suggest that SWI/SNF tumor-suppressor activity involves a role in the DNA-damage response (DDR) to attenuate replicative stress and genomic instability.