Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing 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.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
8 authors.
Thomas Suter *Cellular and Molecular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA 92093.
Meyer J Friedman *Cellular and Molecular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA 92093.
Cagdas Tazearslan *Department of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461.
Daria MerkurjevCellular and Molecular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA 92093.
Kenny OhgiCellular and Molecular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA 92093.
Dario MeluzziCellular and Molecular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA 92093.
Michael G RosenfeldCellular and Molecular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA 92093.ORCID 0000-0002-1572-156X
Yousin SuhDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461.
Funding
Validation and characterization of the identified variants associated with human longevity in mouse modelsU19AG056278 · NIA · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI JAN VIJG · 2017 to 2026
$24.5M
HORMONAL AND DEVELOPMENTAL REGULATION OF GENE EXPRESSIONR01DK018477 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 1986 to 2025
$12.7M
REGULATION OF NEUROENDOCRINE SWITCHING EVENTSR37DK039949 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 1987 to 2020
$12.3M
Combinatorial Actions of Genetic Variants and Gender Bias of Alzherimer's DiseaseR01AG057706 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GAGE, FRED H, GLASS, CHRISTOPHER K · 2017 to 2021
$8.1M
Enhancer-based Immune and Beta Cell Dysregulation Underlying T1D RiskR01DK127778 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI EGLI, DIETER MEINRAD, ROSENFELD, MICHAEL G · 2020 to 2023
$4.5M
REGULATION OF NEUROENDOCRINE SWITCHING EVENTSR01DK039949 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 1996 to 2024
$2.4M
The Aging vs Disease Trajectory Trees of CNS Cell Types Based on Simultaneous Single Nuclear Global Genomic AnalysesR01AG061521 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G, SUH, YOUSIN · 2019 to 2021
$2.1M
Regulatory Landscape of the Aging Human OvaryR01AG069750 · NIA · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ROSENFELD, MICHAEL G, SUH, YOUSIN · 2020 to 2024
$1.7M
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) DK018477HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) DK039949HHS | NIH | National Institute on Aging (NIA) AG061521NIA NIH HHS R01 AG057706NIA NIH HHS R01 AG061521NIA NIH HHS R01 AG069750NIA NIH HHS U19 AG056278NIDDK NIH HHS R01 DK018477NIDDK NIH HHS R01 DK039949NIDDK NIH HHS R01 DK127778NIDDK NIH HHS R37 DK039949
6 · The paper itself
Abstract
Cellular senescence, a major contributor to aging and age-related pathologies, is characterized by irreversible proliferative arrest and a disease-linked, proinflammatory profile known as the Senescence Associated Secretory Phenotype (SASP). A critical unanswered question is whether these properties are regulated by specific enhancer subsets, potentially licensing strategies that selectively block deleterious SASP components. Here, we identify two functionally distinct and independently regulated enhancer programs underlying senescence that are controlled by different TGF-β family ligands. Whereas Activin A stimulates recruitment of nuclear factor IA/C (NFIA/C) and SMAD2/3 transcription factors to an enhancer network that induces proliferation arrest, TGF-β2 promotes SMAD2/3-mediated suppression of a p65-dependent enhancer cohort driving the SASP. We have also uncovered reciprocal SMAD2/3-super-enhancer-regulated feedback loops that govern expression of the TGF-β2 (
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.
Ligand-specific regulation of a binary enhancer code dictating cellular senescence. · full record | OpenQuestion