Biochemical and Structural Characterization of HDAC8 Mutants Associated with Cornelia de Lange Syndrome Spectrum Disorders-Reference-Cited by-同舟云学术

Biochemical and Structural Characterization of HDAC8 Mutants Associated with Cornelia de Lange Syndrome Spectrum Disorders

Published:2015-10-14 Issue:42 Volume:54 Page:6501-6513
ISSN:0006-2960
Container-title:Biochemistry
language:en
Short-container-title:Biochemistry

Author:

Decroos Christophe¹,Christianson Nicolas H.¹,Gullett Laura E.¹,Bowman Christine M.¹,Christianson Karen E.¹,Deardorff Matthew A.²³,Christianson David W.¹⁴

Affiliation:

1. Roy and Diana Vagelos Laboratories, Department of Chemistry, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6323, United States

2. Division of Human Genetics and Molecular Biology, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania 19104, United States

3. Department of Pediatrics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, United States

4. Radcliffe Institute for Advanced Study, Harvard University, Cambridge, Massachusetts 02138, United States

Funder

University of Pennsylvania

Radcliffe Institute for Advanced Study, Harvard University

National Institute of General Medical Sciences

Publisher

American Chemical Society (ACS)

Subject

Biochemistry

Link

https://pubs.acs.org/doi/pdf/10.1021/acs.biochem.5b00881

Reference52 articles.

1. Cornelia de Lange syndrome, cohesin, and beyond

2. On the Molecular Etiology of Cornelia de Lange Syndrome

3. Mutations in Cohesin Complex Members SMC3 and SMC1A Cause a Mild Variant of Cornelia de Lange Syndrome with Predominant Mental Retardation

4. De NovoHeterozygous Mutations inSMC3Cause a Range of Cornelia de Lange Syndrome-Overlapping Phenotypes

5. RAD21 Mutations Cause a Human Cohesinopathy

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