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Shah, H. V.

Publications and source records attributed to Shah, H. V..

2 recordsLinked to original sources

From Policy to Practice: Tracking an Open Science Funding Initiative

This is a critical moment in the open science landscape. Over the past few years there has been growing momentum to improve open research policies and require grantees to share all research outputs, from datasets to code to protocols, in FAIR (findable, accessible, interoperable and reusable [FAIR]) repositories with persistent identifiers attached. The Aligning Science Across Parkinsons (ASAP) initiative has made substantial investments in improving open science compliance monitoring for its grantees, requiring grantees to update their manuscripts if not all research outputs have been linked in the initial manuscript version. Here, we evaluate ASAPs effectiveness in improving research output sharing for all articles processed through the ASAP compliance workflow between March 1, 2022, and October 1, 2022. Our ultimate goal in sharing our findings is to assist other funders and institutions as they consider open science implementation. By normalizing the open science and compliance process across funding bodies, we hope to simplify and streamline researcher, institutional, and funder workflows, allowing researchers to focus on science by easily leveraging resources and building upon the work of others.

scientific communication and education↗

Selective autophagic clearance of protein aggregates is mediated by the autophagy receptor, TAX1BP1

Misfolded protein aggregates can disrupt cellular homeostasis and cause toxicity, a hallmark of numerous neurodegenerative diseases. Protein quality control by the ubiquitin proteasome system (UPS) and autophagy is vital for clearance of aggregates and maintenance of cellular homeostasis1. Autophagy receptor proteins bridge the interaction between ubiquitinated proteins and the autophagy machinery allowing selective elimination of cargo2. Aggrephagy is critical to protein quality control, but how aggregates are recognized and targeted for degradation is not well understood. Here we examine the requirements for 5 autophagy receptor proteins: OPTN, NBR1, p62, NDP52, and TAX1BP1 in proteotoxic stress-induced aggregate clearance. Endogenous TAX1BP1 is both recruited to and required for the clearance of stress-induced aggregates while overexpression of TAX1BP1 increases aggregate clearance through autophagy. Furthermore, TAX1BP1 depletion sensitizes cells to proteotoxic stress and Huntingtons disease-linked polyQ proteins, whereas TAX1BP1 overexpression clears cells of polyQ protein aggregates by autophagy. We propose a broad role for TAX1BP1 in the clearance of cytotoxic proteins, thus identifying a new mode of clearance of protein inclusions.

cell biology↗