Evidence map›Paper›PMID 36640764›Full record

ArticleCell stem cell2023

A DLG1-ARHGAP31-CDC42 axis is essential for the intestinal stem cell response to fluctuating niche Wnt signaling.

David Castillo-Azofeifa, Tomas Wald, Efren A Reyes, Aaron Gallagher, Julia Schanin, Stephanie Vlachos, Nathalie Lamarche-Vane, Carolyn Bomidi, Sarah Blutt, Mary K Estes and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cell stem cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.4field-weighted citation impact, top 8% of its field
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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. CDC42 Regulatory Patterns Related To Inflammatory Bowel Disease and Hyperglycemia.Journal of bioinformatics and systems biology : Open access · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
4 · The record

Corrections and comments

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

12 authors at 4 institutions in 2 countries.

David Castillo-AzofeifaDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, San Francisco, CA, USA; Department of Regenerative Medicine, Genentech, Inc., South San Francisco, CA, USA.
Tomas WaldDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, San Francisco, CA, USA.
Efren A ReyesDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, San Francisco, CA, USA; Department of Pharmaceutical Chemistry and TETRAD Program, University of California, San Francisco, San Francisco, CA, USA.
Aaron GallagherDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, San Francisco, CA, USA.
Julia SchaninDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, San Francisco, CA, USA.
Stephanie VlachosDepartment of Anatomy, University of California, San Francisco, San Francisco, CA, USA.
Nathalie Lamarche-VaneCancer Research Program, Research Institute of the McGill University Health Centre, Montréal, QC, Canada; Department of Anatomy and Cell Biology, McGill University, Montréal, QC, Canada.
Carolyn BomidiDepartment of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA.
Sarah BluttDepartment of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA.
Mary K EstesDepartment of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX, USA.
Todd NystulDepartment of Anatomy, University of California, San Francisco, San Francisco, CA, USA.
Ophir D KleinDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, San Francisco, CA, USA; Department of Pediatrics and Institute for Human Genetics, University of California, San Francisco, San Francisco, CA, USA; Department of Pediatrics, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: ophir.klein@cshs.org.
University of California, San Francisco · USBaylor College of Medicine · USCedars-Sinai Medical Center · USMcGill University Health Centre · CA

Funding

Harnessing natural stem cell-based strategies for mammalian dental renewalR35DE026602 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KLEIN, OPHIR D · 2016 to 2023
$8.0M
Intestinal Stem Cell Consortium Coordinating CenterU01DK085532 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NILAND, JOYCE CAROL · 2009 to 2018
$6.5M
The roles of regional specialization, mechanical forces and epigenetic memory after perturbation and injury of the intestinal stem cell microenvironmentU01DK103147 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KLEIN, OPHIR D · 2014 to 2023
$5.4M
Intestinal Stem Cell Response to InfectionU01DK103168 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI ESTES, MARY KOLB · 2014 to 2023
$4.2M
Cell Fate Decisions in Epithelial Stem Cell LineagesR35GM136348 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Todd Nystul · 2020 to 2026
$3.9M
Limited Competition for the Continuation of the Intestinal Stem Cell Consortium Coordinating CenterU24DK085532 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI NILAND, JOYCE CAROL · 2019 to 2023
$2.3M
The roles of cell death and mechanical signaling in aging intestinal stem cellsK99AG071933 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CASTILLO-AZOFEIFA, DAVID · 2022 to 2022
$125k
NIA NIH HHS K99 AG071933NIDCR NIH HHS R35 DE026602NIDDK NIH HHS U01 DK085532NIDDK NIH HHS U01 DK103147NIDDK NIH HHS U01 DK103168NIDDK NIH HHS U24 DK085532NIGMS NIH HHS R35 GM136348
6 · The paper itself

Abstract

A central factor in the maintenance of tissue integrity is the response of stem cells to variations in the levels of niche signals. In the gut, intestinal stem cells (ISCs) depend on Wnt ligands for self-renewal and proliferation. Transient increases in Wnt signaling promote regeneration after injury or in inflammatory bowel diseases, whereas constitutive activation of this pathway leads to colorectal cancer. Here, we report that Discs large 1 (Dlg1), although dispensable for polarity and cellular turnover during intestinal homeostasis, is required for ISC survival in the context of increased Wnt signaling. RNA sequencing (RNA-seq) and genetic mouse models demonstrated that DLG1 regulates the cellular response to increased canonical Wnt ligands. This occurs via the transcriptional regulation of Arhgap31, a GTPase-activating protein that deactivates CDC42, an effector of the non-canonical Wnt pathway. These findings reveal a DLG1-ARHGAP31-CDC42 axis that is essential for the ISC response to increased niche Wnt signaling.

Indexed as

Intestinal MucosaWnt Signaling PathwayAnimalscdc42 GTP-Binding ProteinCell ProliferationDiscs Large Homolog 1 ProteinGTPase-Activating ProteinsIntestinesMiceStem Cell NicheStem Cellscdc42 GTP-Binding ProteinCdc42 protein, mouseDiscs Large Homolog 1 ProteinDlg1 protein, mouseGTPase-Activating ProteinsArhgap31Cdc42cell deathDlg1epitheliumintestineorganoidregenerationstem cellsWnt

Identifiers

PMID36640764
PMCPMC9922544
OpenAlexW4315874383

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.