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Arvind Reddy Kandi on Muck Rack

Arvind Reddy Kandi

As seen in: PLOS, MDPI, BioRxiv
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Articles

Astro-Versus Microglia-Enriched Transcriptomes from Aged Atxn2-CAG100-knockin Mice Suggest Underlying Pathology of RNA Processing at Ribosomes, and Possibly at U-Bodies

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By Georg Auburger, Arvind Reddy Kandi, Rajkumar Vutukuri
| preprints.org
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.
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Conditional ATXN2L-Null in Adult Frontal Cortex CamK2a+ Neurons Does Not Cause Cell Death, but Restricts Spontaneous Mobility, and Affects the Alternative Splicing Pathway

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By Jana Key, Arvind Reddy Kandi, Luis-Enrique Almaguer-Mederos, Meike Fellenz
| preprints.org
This version is not peer-reviewed.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.
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ATXN2L primarily interacts with NUFIP2, the absence of ATXN2L results in NUFIP2 depletion, and the ATXN2-polyQ expansion triggers NUFIP2 accumulation

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By Jana Key, Luis Enrique Almaguer-Mederos, Arvind Reddy Kandi, Nesli Ece Sen
| BioRxiv
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.
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