High-throughput affinity proteomics (AP) technologies, such as Olink and SomaScan, are central to biomarker discovery and clinical studies, but unlike mass spectrometry (MS)-based proteomics, they have lacked a dedicated, standards-driven open-data repository. To address this gap, we introduce the PRIDE Affinity Proteomics Archive (PRIDE-AP), a centralized, open, technology-agnostic repository extending the PRIDE infrastructure to support submission, storage, and reuse of AP datasets in compliance with FAIR principles. Each dataset receives a stable PAD identifier and DOI and undergoes automated validation. We extended the HUPO-PSI SDRF-Proteomics format and the PRIDE controlled vocabulary for AP experiments, and integrated quality-control statistics via the open-source library pyprideap. As of May 2026, PRIDE-AP includes 20 public datasets spanning 14 human diseases, with evidence for over 10,000 proteins. By enabling AP and MS datasets to be jointly deposited and linked, with protein-centric exploration cross-referenced to UniProt, PRIDE-AP enables cross-technology proteome interrogation at scale.

Although the non-selective β-blocker, propranolol, improves bone density with PTH treatment in mice, the mechanism of this effect is unclear. To address this, we used a combination of in vitro and in vivo approaches to address how propranolol influences bone remodeling in the context of PTH treatment. In female C57BL/6J mice, intermittent PTH and propranolol had complementary effects in the trabecular bone of the distal femur and L5 vertebra, with combination treatment achieving micro-architectural parameters beyond that of PTH alone. Combined treatment improved the serum bone formation marker, P1NP, but did not impact other histomorphometric parameters relating to osteoblast function at the L5. In vitro , propranolol amplified the acute, PTH-induced, intracellular calcium signal in osteoblast-like cells. The most striking finding, however, was suppression of PTH-induced bone resorption. Despite this, PTH-induced receptor activator of nuclear factor kappa-B ligand (RANKL) mRNA and protein levels were unaltered by propranolol, which led us to hypothesize that propranolol could act directly on osteoclasts. Using in situ methods, we found Adrb2 expression in osteoclasts in vivo , suggesting β-blockers may directly impact osteoclasts. Taken together, this work suggests a strong anti-osteoclastic effect of non-selective β-blockers in vivo , indicating that combining propranolol with PTH could be beneficial to patients with extremely low bone density.

Exemplifying analysis of large-scale protein data from the 'Olink platform', primarily relative protein expression data that has been exported from 'Olink NPX Software', as well as QUANT data from 'Olink'. QUANT data is log-transformed. Materials focus on reading data, demonstrating data wrangling and quality control analysis, performing statistical analysis and generating figures to visualize the results of the statistical analysis. The goal of this package is to guide users extract biological insights from large-scale protein data run on the 'Olink platform'. More information on 'Olink' data can be found at .