Arvind Reddy Kandi

You are already at the latest version Spinocerebellar Ataxia type 2 (SCA2) and Amyotrophic Lateral Sclerosis type 13 (ALS13) are triggered by polyglutamine expansion in Ataxin-2 (ATXN2). To understand these neurodegenerative disorders at the molecular level, the brains of 10-month-old Atxn2-CAG100-knockin mice were analyzed as microglial, astroglial and neuronal fractions via global RNA sequencing. Data were validated by comparison with spinal cord oligonucleotide microarray profile.

This version is not peer-reviewed. Jana Key  † ,Luis-Enrique Almaguer-Mederos  †,Arvind Reddy Kandi,Meike Fellenz,Suzana Gispert,Gabriele Köpf,David Meierhofer,Thomas Deller,Georg Auburger  * Jana Key  † ,Luis-Enrique Almaguer-Mederos  †,Arvind Reddy Kandi,Meike Fellenz,Suzana Gispert,Gabriele Köpf,David Meierhofer,Thomas Deller,Georg Auburger  * † Joint first authorship.

Abstract The cytoplasmic Ataxin-2 (ATXN2) protein associates with TDP-43 in stress granules (SG) where RNA quality control occurs. Mutations in this pathway underlie Spinocerebellar Ataxia type 2 (SCA2) and Amyotrophic Lateral Sclerosis. In contrast, Ataxin-2-like (ATXN2L) is predominantly nuclear, more abundant, and essential for embryonic life. Its sequestration into ATXN2 aggregates may contribute to disease. In this study, we utilized two approaches to clarify the roles of ATXN2L.