Solution NMR backbone assignments of disordered Olduvai protein domain CON1 employing Hα-detected experiments

Olduvai protein domains, encoded by the NBPF gene family, are responsible for the largest increase in copy number of any protein-coding region in the human genome. This has spawned various genetics studies which have linked these domains to human brain development and divergence from our primate anc...

Full description

Saved in:
Bibliographic Details
Published in:Biomolecular NMR assignments Vol. 16; no. 1; pp. 113 - 119
Main Authors: Paukovich, Natasia, Henen, Morkos A., Hussain, Alya, Issaian, Aaron, Sikela, James M., Hansen, Kirk C., Vögeli, Beat
Format: Journal Article
Language:English
Published: Dordrecht Springer Netherlands 01.04.2022
Springer Nature B.V
Subjects:
ISSN:1874-2718, 1874-270X, 1874-270X
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Olduvai protein domains, encoded by the NBPF gene family, are responsible for the largest increase in copy number of any protein-coding region in the human genome. This has spawned various genetics studies which have linked these domains to human brain development and divergence from our primate ancestors, as well as currently relevant cognitive diseases such as schizophrenia and autism spectrum disorder (ASD). There are six separate Olduvai domains which together form the majority of the various protein products of the NBPF genes. The six domains include three conserved domains (CON1-3), and three human-lineage-specific domains (HLS1-3) which occur in triplet. Here, we present the solution nuclear magnetic resonance backbone assignments for the CON1 domain, which has been linked to the severity of ASD. The data confirm that CON1 is an intrinsically disordered protein (IDP). Additionally, we use innovative H α -detected experiments which allow us to not only assign the H α atoms and N atoms of proline residues, but also to assign residues where H N -experiments suffered from peak overlap or broadening.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ISSN:1874-2718
1874-270X
1874-270X
DOI:10.1007/s12104-022-10068-5