Article in Nature chemical biology, 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.
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
10 authors.
Ran Lin *Laboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY, USA. rlin@rockefeller.edu.ORCID 0000-0003-4201-1333
Yan Mo *Sanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.
Douglas Barrows *Bioinformatics Resource Center, The Rockefeller University, New York, NY, USA.
Wenbin MeiLaboratory of Systems Cancer Biology, The Rockefeller University, New York, NY, USA.
Takashi OnikuboLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY, USA.
Jianfeng SunLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY, USA.
Zhiguo ZhangInstitute for Cancer Genetics, Columbia University Irving Medical Center, New York, NY, USA.ORCID 0000-0002-9451-2685
Effie ApostolouSanford I. Weill Department of Medicine, Sandra and Edward Meyer Cancer Center, Weill Cornell Medicine, New York, NY, USA.ORCID 0000-0002-8111-0863
Sohail F TavazoieLaboratory of Systems Cancer Biology, The Rockefeller University, New York, NY, USA.
Robert G RoederLaboratory of Biochemistry and Molecular Biology, The Rockefeller University, New York, NY, USA. roeder@rockefeller.edu.ORCID 0000-0003-3865-8572
Funding
Functions and mechanisms of transcriptional coactivator OCA-B in B cell development and lymphomagenesisR01AI148387 · NIAID · ROCKEFELLER UNIVERSITY · PI SOHAIL MALIK · 2022 to 2023
$1.5M
Mechanisms of transcriptional control of adipocyte formation and function through nuclear receptor coactivatorsR01DK144459 · ROCKEFELLER UNIVERSITY · 2025 to 2025
$773k
Mechanistic studies of transcription initiation and elongation functions of an RNA polymerase II variant, Pol II(G), that is implicated in development and cancerR01CA273709 · ROCKEFELLER UNIVERSITY · 2025 to 2025
$388k
NCI NIH HHS R01 CA273709NIAID NIH HHS R01 AI148387NIDDK NIH HHS R01 DK144459U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) CA202245U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) CA234575U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) AI148387
6 · The paper itself
Abstract
Cells fine-tune gene expression in response to cellular stress, a process critical for tumorigenesis. However, mechanisms governing stress-responsive transcription remain incompletely understood. This study shows that the MED1 subunit of the Mediator coactivator complex is acetylated in its intrinsically disordered region (IDR). Under stress, SIRT1 associates with the super elongation complex to deacetylate MED1 in promoter-proximal regions. The deacetylated (or acetylation-defective mutant) MED1 amplified stress-activated cytoprotective genes and rescued stress-suppressed growth-supportive genes in estrogen-receptor-positive breast cancer (ER
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 Socratic graph.
MED1 IDR deacetylation controls stress responsive genes through RNA Pol II recruitment. · full record | Socratic