Evidence map›Paper›PMID 36824858›Full record

ArticlebioRxiv : the preprint server for biology2023

Physiological reprogramming

Takeshi Katsuda, Jonathan Sussman, Kenji Ito, Andrew Katznelson, Salina Yuan, Jinyang Li, Allyson J Merrell, Naomi Takenaka, Hector Cure, Qinglan Li and 4 more

Open access · greenAbstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 2 institutions in 1 country.

Takeshi KatsudaPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Jonathan SussmanPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Kenji ItoPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Andrew KatznelsonPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Salina YuanPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Jinyang LiPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Allyson J MerrellPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Naomi TakenakaPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Hector CurePerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Qinglan LiPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Reyaz Ur RasoolPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Irfan A AsanganiPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Kenneth S ZaretPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Ben Z StangerPerelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Cancer Research Institute · USCalifornia Institute for Regenerative Medicine · US

Funding

TRANSGENIC AND CHIMERIC MOUSE COREP30DK050306 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI REBECCA G WELLS · 1997 to 2026
$32.5M
TRANS-ACTING FACTORS CAUSING CELL-SPECIFIC GENE CONTROLR01GM036477 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI ZARET, KENNETH · 1986 to 2023
$7.7M
Mechanisms of bile duct reprogrammingR01DK083355 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI GROMPE, MARKUS, STANGER, BEN Z · 2009 to 2020
$4.3M
Role of MED1 in the AR-dependent transcription in advanced prostate cancerR01CA249210 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ASANGANI, IRFAN AHMED · 2020 to 2024
$1.9M
NCI NIH HHS R01 CA249210NIDDK NIH HHS P30 DK050306NIDDK NIH HHS R01 DK083355NIGMS NIH HHS R01 GM036477
6 · The paper itself

Abstract

Tissue damage elicits cell fate switching through a process called metaplasia, but how the starting cell fate is silenced and the new cell fate is activated has not been investigated in animals. In cell culture, pioneer transcription factors mediate "reprogramming" by opening new chromatin sites for expression that can attract transcription factors from the starting cell's enhancers. Here we report that Sox4 is sufficient to initiate hepatobiliary metaplasia in the adult liver. In lineage-traced cells, we assessed the timing of Sox4-mediated opening of enhancer chromatin versus enhancer decommissioning. Initially, Sox4 directly binds to and closes hepatocyte regulatory sequences via a motif it overlaps with Hnf4a, a hepatocyte master regulator. Subsequently, Sox4 exerts pioneer factor activity to open biliary regulatory sequences. The results delineate a hierarchy by which gene networks become reprogrammed under physiological conditions, providing deeper insight into the basis for cell fate transitions in animals.

Identifiers

PMID36824858
PMCPMC9948957
OpenAlexW4320919658

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.