Evidence map›Paper›PMID 32686657›Full record

ArticleJCI insight2020

Elevating EGFR-MAPK program by a nonconventional Cdc42 enhances intestinal epithelial survival and regeneration.

Xiao Zhang, Sheila Bandyopadhyay, Leandro Pires Araujo, Kevin Tong, Juan Flores, Daniel Laubitz, Yanlin Zhao, George Yap, Jingren Wang, Qingze Zou and 9 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.5field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. International journal of molecular sciences · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. CDC42 Regulatory Patterns Related To Inflammatory Bowel Disease and Hyperglycemia.Journal of bioinformatics and systems biology : Open access · 2025
    Article
  13. Article
  14. Tuft cells in the intestine, immunity and beyond.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  15. CTHRC1 Attenuates Tendinopathy via Enhancing EGFR/MAPK Signaling Pathway.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

19 authors at 4 institutions in 2 countries.

Xiao ZhangDepartment of Biological Sciences, Division of Life Sciences, School of Arts and Sciences, Rutgers University, Newark, New Jersey, USA.
Sheila BandyopadhyayDepartment of Biological Sciences, Division of Life Sciences, School of Arts and Sciences, Rutgers University, Newark, New Jersey, USA.
Leandro Pires AraujoDepartment of Microbiology and Immunology, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York, USA.
Kevin TongDepartment of Genetics, Division of Life Sciences, School of Arts and Sciences, Rutgers University, New Brunswick, New Jersey, USA.
Juan FloresDepartment of Biological Sciences, Division of Life Sciences, School of Arts and Sciences, Rutgers University, Newark, New Jersey, USA.
Daniel LaubitzDepartment of Pediatrics, University of Arizona, Tucson, Arizona, USA.
Yanlin ZhaoCenter for Immunity and Inflammation, Rutgers New Jersey Medical School, Newark, New Jersey, USA.
George YapCenter for Immunity and Inflammation, Rutgers New Jersey Medical School, Newark, New Jersey, USA.
Jingren WangDepartment of Mechanical and Aerospace Engineering, School of Engineering, Rutgers University, Piscataway, New Jersey, USA.
Qingze ZouDepartment of Mechanical and Aerospace Engineering, School of Engineering, Rutgers University, Piscataway, New Jersey, USA.
Ronaldo FerrarisDepartment of Pharmacology, Physiology and Neuroscience, Rutgers New Jersey Medical School, Newark, New Jersey, USA.
Lanjing ZhangDepartment of Biological Sciences, Division of Life Sciences, School of Arts and Sciences, Rutgers University, Newark, New Jersey, USA.
Wenwei HuRutgers Cancer Institute of New Jersey, New Brunswick, New Jersey, USA.
Edward M BonderDepartment of Biological Sciences, Division of Life Sciences, School of Arts and Sciences, Rutgers University, Newark, New Jersey, USA.
Pawel R KielaDepartment of Pediatrics, University of Arizona, Tucson, Arizona, USA.
Robert CoffeyDivision of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, and Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Michael P VerziDepartment of Genetics, Division of Life Sciences, School of Arts and Sciences, Rutgers University, New Brunswick, New Jersey, USA.
Ivaylo I IvanovDepartment of Microbiology and Immunology, Vagelos College of Physicians and Surgeons, Columbia University, New York, New York, USA.
Nan GaoDepartment of Biological Sciences, Division of Life Sciences, School of Arts and Sciences, Rutgers University, Newark, New Jersey, USA.
Rutgers, The State University of New Jersey · USColumbia University · USUniversity of Arizona · USVanderbilt University Medical Center · US

Funding

TRANSCRIPTIONAL PROFILINGP30CA072720 · NCI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI Tracie Saunders · 1997 to 2026
$94.5M
Translational Analysis CoreP30DK058404 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RICHARD M. PEEK · 2002 to 2026
$29.9M
Vanderbilt-Ingram Cancer Center SPORE in Gastrointestinal CancerP50CA236733 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Robert J. Coffey · 2019 to 2026
$19.6M
Integrated approach to study early and late events in colonic neoplasia: mouse to manR35CA197570 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Robert J. Coffey · 2017 to 2026
$9.4M
Role of intestinal commensal-induced Th17 cells and mucosal immunity in metabolic diseaseR01DK098378 · NIDDK · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Ivaylo Ivanov Ivanov · 2013 to 2026
$6.5M
Transcriptional Mechanisms of Tumor SuppressionR01CA190558 · NCI · RUTGERS, THE STATE UNIV OF N.J. · PI MICHAEL P. VERZI · 2015 to 2026
$3.6M
Paneth cell heterogeneity in infection and inflammationR01DK132885 · NIDDK · RUTGERS THE STATE UNIV OF NJ NEWARK · PI Nan Gao · 2022 to 2026
$2.4M
Non-redundant functions of type 3 innate lymphoid cells in mucosal immunityR01AI144808 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI IVANOV, IVAYLO IVANOV · 2019 to 2022
$1.9M
Research Supplements to Promote Diversity in Health-Related ResearchR01DK119198 · NIDDK · RUTGERS THE STATE UNIV OF NJ NEWARK · PI GAO, NAN, KIELA, PAWEL R · 2019 to 2023
$1.9M
Endosomal Control of Microbe-Host HomeostasisR01DK102934 · NIDDK · RUTGERS THE STATE UNIV OF NJ NEWARK · PI GAO, NAN · 2014 to 2018
$1.8M
Mucosal modulation by LGG and R. gnavus specific tryptophan metabolitesR01AT010243 · NCCIH · RUTGERS THE STATE UNIV OF NJ NEWARK · PI FERRARIS, RONALDO PARAOAN, GAO, NAN · 2018 to 2021
$1.6M
New mechanism of commensal bacteria interaction with host immunityR21AI126305 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI IVANOV, IVAYLO IVANOV · 2017 to 2018
$440k
NCCIH NIH HHS R01 AT010243NCI NIH HHS F32 CA235829NCI NIH HHS K99 CA245123NCI NIH HHS P30 CA072720NCI NIH HHS P50 CA236733NCI NIH HHS R01 CA190558NCI NIH HHS R21 CA178599NCI NIH HHS R35 CA197570NIAID NIH HHS R01 AI144808NIAID NIH HHS R21 AI126305NIAID NIH HHS R21 AI146817NIDDK NIH HHS F31 DK121428NIDDK NIH HHS P30 DK058404NIDDK NIH HHS R01 DK098378NIDDK NIH HHS R01 DK102934NIDDK NIH HHS R01 DK119198NIDDK NIH HHS R01 DK132885
6 · The paper itself

Abstract

The regulatory mechanisms enabling the intestinal epithelium to maintain a high degree of regenerative capacity during mucosal injury remain unclear. Ex vivo survival and clonogenicity of intestinal stem cells (ISCs) strictly required growth response mediated by cell division control 42 (Cdc42) and Cdc42-deficient enteroids to undergo rapid apoptosis. Mechanistically, Cdc42 engaging with EGFR was required for EGF-stimulated, receptor-mediated endocytosis and sufficient to promote MAPK signaling. Proteomics and kinase analysis revealed that a physiologically, but nonconventionally, spliced Cdc42 variant 2 (V2) exhibited stronger MAPK-activating capability. Human CDC42-V2 is transcriptionally elevated in some colon tumor tissues. Accordingly, mice engineered to overexpress Cdc42-V2 in intestinal epithelium showed elevated MAPK signaling, enhanced regeneration, and reduced mucosal damage in response to irradiation. Overproducing Cdc42-V2 specifically in mouse ISCs enhanced intestinal regeneration following injury. Thus, the intrinsic Cdc42-MAPK program is required for intestinal epithelial regeneration, and elevating this signaling cascade is capable of initiating protection from genotoxic injury.

Indexed as

Alternative SplicingAnimalscdc42 GTP-Binding ProteinCell SurvivalEndocytosisErbB ReceptorsHEK293 CellsHumansIntestinal MucosaMAP Kinase Signaling SystemMice, KnockoutMice, TransgenicRegenerationcdc42 GTP-Binding ProteinCdc42 protein, mouseEGFR protein, mouseErbB ReceptorsAdult stem cellsGastroenterologyMouse modelsStem cells

Identifiers

PMID32686657
PMCPMC7455142
OpenAlexW3043034559

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.