Publisher Correction: BRD4 interacts with NIPBL and BRD4 is mutated in a Cornelia de Lange–like syndrome

Olley, Gabrielle; Study, Deciphering Developmental Disorders; Ansari, Morad; Bengani, Hemant; Grimes, Graeme R.; Rhodes, James; Kriegsheim, Alex von; Blatnik, Ana; Stewart, Fiona; Wakeling, Emma; Carroll, Nicola; Ross, Alison; Park, Soo‐Mi; Bickmore, Wendy A.; Pradeepa, Madapura M.; FitzPatrick, David R.

doi:10.1038/s41588-019-0448-1

Cited by 5 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Recent work has identified a non-canonical role for BRD4 upstream of cohesin loading 25, 33, 34 . To investigate this role, we first set out to completely deplete BRD4 from cells, including centromeres.…”

Section: Introductionmentioning

confidence: 99%

The bromodomain inhibitor JQ1 is a molecular glue targeting centromeres

Corless

Singh

Benabdallah

et al. 2023

Preprint

View full text Add to dashboard Cite

Centromeres are essential for cell proliferation and a promising target for anti-cancer therapies, yet no drugs have been identified that specifically target centromeric chromatin. To identify candidates, we analysed chromatin proteins at repetitive loci using a novel big-data approach and discovered the bromodomain protein BRD4 localises to centromeres, a localisation enhanced by the bromodomain inhibitor JQ1. While bromodomain inhibitors typically prevent BRD4 from binding chromatin, we found that JQ1 stabilises an interaction between BRD4 and the centromere protein CENP-B. Degradation of BRD4 caused centromere cohesion defects, whereas JQ1-treatment preserved centromere structure in a CENP-B dependent manner. Strikingly, JQ1-resistant cells became reliant on CENP-B for proliferation. Our results identify a non-canonical role for BRD4 in centromere cohesion and establish JQ1 as a molecular-glue targeting centromeric chromatin.

show abstract

Section: Introductionmentioning

confidence: 99%

The bromodomain inhibitor JQ1 is a molecular glue targeting centromeres

Corless

Singh

Benabdallah

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…The following supporting information can be downloaded at: . See [ 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 , 95 , 96 , 97 , 98 , 99 , 100 ].…”

unclassified

Complex Diagnostics of Non-Specific Intellectual Developmental Disorder

Levchenko

Дадали

Bessonova

et al. 2022

IJMS

View full text Add to dashboard Cite

Intellectual development disorder (IDD) is characterized by a general deficit in intellectual and adaptive functioning. In recent years, there has been a growing interest in studying the genetic structure of IDD. Of particular difficulty are patients with non-specific IDD, for whom it is impossible to establish a clinical diagnosis without complex genetic diagnostics. We examined 198 patients with non-specific IDD from 171 families using whole-exome sequencing and chromosome microarray analysis. Hereditary forms of IDD account for at least 35.7% of non-specific IDD, of which 26.9% are monogenic forms. Variants in the genes associated with the BAF (SWI/SNF) complex were the most frequently identified. We were unable to identify phenotypic features that would allow differential diagnosis of monogenic and microstructural chromosomal rearrangements in non-specific IDD at the stage of clinical examination, but due to its higher efficiency, exome sequencing should be the diagnostic method of the highest priority study after the standard examination of patients with NIDD in Russia.

show abstract