Hans Gerd Nothwang

Featured ArticleResearch Articles, Cellular/Molecular Constanze Krohs, Christoph Körber, Lena Ebbers, Faiza Altaf, Giulia Hollje, Simone Hoppe, Yvette Dörflinger, Haydn M. Prosser and Hans Gerd Nothwang Journal of Neuroscience 11 August 2021, 41 (32) 6796-6811; DOI: https://doi.org/10.1523/JNEUROSCI.0139-20.2021 Abstract A point mutation in miR-96 causes non-syndromic progressive peripheral hearing loss and alters structure and physiology of the central auditory system.

See original article: Cordshagen et al. 293 (44): 16984. VOLUME 293 (2018) PAGES 16984–16993 The KCC2 isoform that was used in this study was misidentified. The potassium chloride cotransporter KCC2 exists in two isoforms, KCC2a (NM_001355480.1) and KCC2b (NM_020333.2). These isoforms differ in the first exon that encodes the first part of the N terminus. In this article, the authors incorrectly referred to KCC2b. The constructs that were presented in this article were generated on KCC2a.

The pivotal role of K+-Cl− cotransporter 2 (KCC2) in inhibitory neurotransmission and severe human diseases fosters interest in understanding posttranslational regulatory mechanisms such as (de)phosphorylation. Here, the regulatory role of the five bona fide phosphosites Ser31, Thr34, Ser932, Thr999, and Thr1008 was investigated by the use of alanine and aspartate mutants.