Biology subjects

Hardy, J. C.

Publications and source records attributed to Hardy, J. C..

2 recordsLinked to original sources

bioRxiv2025

New Quantitative Cost-Impact Effectiveness Indexes to Assist in Publication Decisions by Researchers in the Open Access Era

Scientific publications have become the backbone of scientific communication since their foundation in 1665. The three main models for publishing are Traditional (or subscription-based), Open Access (OA), and Hybrid. As of July 1, 2025, the NIH requires that Author Accepted Manuscripts resulting from NIH-funded research be immediately publicly available. To comply with this new requirement, authors may be forced to pay an Article Processing Charge (APC) to publish Open Access, ranging from [~]$2000 to [~]$13,000 per article. With this change to the scientific publishing landscape, publishing costs shift from subscribers to authors causing authors to re-evaluate how they choose which journal to publish in. Here we analyze 75 popular biomedical journals to evaluate the publishing costs compared to the scientific impact (i.e. Impact Factor, CiteScore, SNIP) illustrated by three different Cost-Impact Effectiveness (CIE) metrics (APC/IF, APC/CS and APC/SNIP). To complement the new open access policy, our goal is to provide a resource to help the scientific community evaluate the impact-based cost effectiveness of different Open Access options during their journal selection process.

scientific communication and education↗

bioRxiv2023

Molecular Determinants and Signaling Effects of PKA RIα Phase Separation

Spatiotemporal regulation of intracellular signaling molecules, such as the 3,5-cyclic adenosine monophosphate (cAMP)-dependent protein kinase (PKA), ensures the specific execution of various cellular functions. Liquid-liquid phase separation (LLPS) of the ubiquitously expressed PKA regulatory subunit RI was recently identified as a major driver of cAMP compartmentation and signaling specificity. However, the molecular determinants of RI LLPS remain unclear. Here, we reveal that two separate dimerization interfaces combined with the cAMP-induced release of the PKA catalytic subunit (PKA-C) from the pseudosubstrate inhibitory sequence are required to drive RI condensate formation in cytosol, which is antagonized by docking to A-kinase anchoring proteins. Strikingly, we find that the RI pseudosubstrate region is critically involved in the formation of a non-canonical R:C complex, which serves to maintain low basal PKA activity in the cytosol by enabling the recruitment of active PKA-C to RI condensates. Our results suggest that RI LLPS not only facilitates cAMP compartmentation but also spatially restrains active PKA-C, thus highlighting the functional versatility of biomolecular condensates in driving signaling specificity.

cell biology↗