Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Fangzhu ZhaoDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.ORCID 0000-0002-3172-1340
Alex InagueDepartment of Molecular and Cell Biology, University of California Berkeley, Berkeley, CA 94720.ORCID 0000-0001-7410-9226
Trenton M Peters-ClarkeDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.ORCID 0000-0002-9153-2525
Yifei ChenDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.ORCID 0009-0005-8754-5779
Snehal D GanjaveDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.
Yun ZhangDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.
Kun MiaoDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.
Zi YaoDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.
Yan WuDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.ORCID 0000-0003-2596-1943
Madison K C SetoDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.ORCID 0000-0002-7900-5685
Kevin K LeungDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.ORCID 0000-0002-2087-4974
James A OlzmannDepartment of Molecular and Cell Biology, University of California Berkeley, Berkeley, CA 94720.ORCID 0000-0001-7751-8316
James A WellsDepartment of Pharmaceutical Chemistry, University of California San Francisco, San Francisco, CA 94158.ORCID 0000-0001-8267-5519
Funding
Surfaceomic technologies and antibodies to probe cell surface proteomes and their interactomes at unprecedented small scale and high-resolutionR35GM122451 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAMES A WELLS · 2017 to 2026
$5.3M
MYCN drives a ferroptotic vulnerability in neuroblastomaR01CA276207 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Anthony Charles Faber, JAMES A OLZMANN · 2023 to 2026
$2.9M
New protein engineering-based tools and technologies for characterizing cell surface proteolysis in cancer cells for novel neo-epitope biomarkers and drug targetsR01CA248323 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI JAMES A WELLS · 2020 to 2026
$2.6M
Toward Understanding the Functional Landscape of Proteolysis at the Cell SurfaceF32CA298768 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Trenton Peters-Clarke · 2025 to 2026
$155k
HHS | NIH | National Cancer Institute (NCI) F32CA298768HHS | NIH | National Cancer Institute (NCI) R01CA248323HHS | NIH | National Cancer Institute (NCI) R01CA276207HHS | NIH | National Institute of General Medical Sciences (NIGMS) R35GM122451NCI NIH HHS F32 CA298768NCI NIH HHS R01 CA248323NCI NIH HHS R01 CA276207NIGMS NIH HHS R35 GM122451NSF | NSF Graduate Research Fellowship Program (GRFP) 2445150
6 · The paper itself
Abstract
Tumor reliance on antioxidant defenses creates a vulnerability to ferroptosis, yet strategies to therapeutically disable these systems remain limited. Here, we identify targeted degradation of the selenium uptake receptor lipoprotein receptor-related protein 8 (LRP8) as an effective approach to decrease the abundance of the ferroptosis-protective enzyme glutathione peroxidase 4 (GPX4). Using bispecific cytokine receptor-targeting chimeras (KineTACs) that couple LRP8 to cytokine receptor internalization pathways, we selectively direct LRP8 to the lysosome for degradation. LRP8 degradation reduces the abundance of several selenoproteins, including GPX4, lowering the cellular threshold for lipid peroxidation and sensitizing cancer cells to ferroptosis. These findings establish receptor-mediated selenium uptake as a critical, targetable node in ferroptosis resistance and demonstrate that extracellular protein degradation can be leveraged to reprogram intracellular translational dependencies in cancer cells. More broadly, this work provides a framework for exploiting nutrient acquisition pathways to overcome therapy resistance.
Indexed as
FerroptosisLDL-Receptor Related ProteinsNeoplasmsTumor Suppressor ProteinsAnimalsCell Line, TumorHumansLipid PeroxidationLysosomesPhospholipid Hydroperoxide Glutathione PeroxidaseProteolysisProteolysis Targeting ChimeraSeleniumSelenoproteinsLDL-Receptor Related Proteinslow density lipoprotein receptor-related protein 8Phospholipid Hydroperoxide Glutathione PeroxidaseProteolysis Targeting ChimeraSeleniumSelenoproteinsTumor Suppressor Proteinsantibody engineeringferroptosisLRP8targeted protein degradation
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Targeted extracellular degradation of LRP8 promotes ferroptosis in cancer cells. · full record | OpenQuestion