Evidence map›Paper›PMID 21763241›Full record

ArticleGastroenterology2011

Krüppel-like factor 5 is important for maintenance of crypt architecture and barrier function in mouse intestine.

Beth B McConnell, Samuel S Kim, Ke Yu, Amr M Ghaleb, Norifumi Takeda, Ichiro Manabe, Asma Nusrat, Ryozo Nagai, Vincent W Yang

Open access · bronzeAbstract read
In one paragraph

Article in Gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
3.1field-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

64 citing papers in PubMed, 88 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Cells · 2025
    Review
  5. Article
  6. Review
  7. Human enteroids as a tool to study conventional and ultra-high dose rate radiation.Integrative biology : quantitative biosciences from nano to macro · 2023
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. KLF5 Governs Stemness in the Adult Intestinal Stem Cell Niche.Cellular and molecular gastroenterology and hepatology · 2020
    Article
  20. Article

4 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 2 countries.

Beth B McConnellDepartment of Medicine, Emory University School of Medicine, Atlanta, Georgia, USA.
Samuel S Kim
Ke Yu
Amr M Ghaleb
Norifumi Takeda
Ichiro Manabe
Asma Nusrat
Ryozo Nagai
Vincent W Yang
Emory University · USThe University of Tokyo · JP

Funding

Regulation of intestinal epithelial barrier function by intercellular junction proteins in health and diseaseR01DK059888 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ASMA NUSRAT · 2001 to 2026
$10.5M
REGULATION OF INTESTINAL EPITHELIAL CELL PROLIFERATIONR01DK052230 · NIDDK · STATE UNIVERSITY NEW YORK STONY BROOK · PI Vincent W Yang · 1997 to 2026
$8.7M
Intestinal Mucosal Wound Resealing in IBDR01DK055679 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ASMA NUSRAT · 2004 to 2026
$8.1M
MECHANISMS OF INTESTINAL TUMORIGENESISR01CA084197 · NCI · STATE UNIVERSITY NEW YORK STONY BROOK · PI YANG, VINCENT W · 2000 to 2020
$7.5M
Emory Epithelial Pathobiology Research Development CenterR24DK064399 · NIDDK · EMORY UNIVERSITY · PI PARKOS, CHARLES A · 2003 to 2012
$5.3M
Proliferative Responses to Enteric Bacterial Pathogens in Intestinal TissuesK01DK076742 · NIDDK · EMORY UNIVERSITY · PI MCCONNELL, BETH B · 2007 to 2011
$667k
INTESTINAL MUCOSAL WOUND RESEALING IN SURGICAL DISEASESR29DK055679 · NIDDK · EMORY UNIVERSITY · PI NUSRAT, ASMA · 1998 to 2002
$324k
Role of Kruppel-Like Factor 4 in Wnt and Notch Signaling in the Intestinal TractF32CA130308 · NCI · EMORY UNIVERSITY · PI GHALEB, AMR · 2008 to 2010
$172k
Factors Contributing to Wound Healing in the ColonR03DK089131 · NIDDK · EMORY UNIVERSITY · PI MCCONNELL, BETH B · 2010 to 2011
$83k
NCI NIH HHS CA084197NCI NIH HHS CA130308NCI NIH HHS F32 CA130308NCI NIH HHS R01 CA084197NIDDK NIH HHS DK052230NIDDK NIH HHS DK055679NIDDK NIH HHS DK059888NIDDK NIH HHS DK0644399NIDDK NIH HHS DK076742NIDDK NIH HHS DK089131NIDDK NIH HHS K01 DK076742NIDDK NIH HHS R01 DK052230NIDDK NIH HHS R01 DK055679NIDDK NIH HHS R01 DK059888NIDDK NIH HHS R03 DK089131NIDDK NIH HHS R24 DK064399NIDDK NIH HHS R29 DK055679
6 · The paper itself

Abstract

BACKGROUND &

aimsKrüppel-like factor 5 (KLF5) is transcription factor that is expressed by dividing epithelial cells of the intestinal epithelium. KLF5 promotes proliferation in vitro and in vivo and is induced by mitogens and various stress stimuli. To study the role of KLF5 in intestinal epithelial homeostasis, we examined the phenotype of mice with conditional deletion of Klf5 in the gut.

methodsMice were generated with intestinal-specific deletion of Klf5 (Vil-Cre;Klf5fl/fl). Morphologic changes in the small intestine and colon were examined by immunohistochemistry, immunoblotting, and real-time polymerase chain reaction.

resultsKlf5 mutant mice were born at a normal Mendelian ratio but had high mortality compared with controls. Complete deletion of Klf5 from the intestinal mucosa resulted in neonatal lethality that corresponded with an absence of epithelial proliferation. Variegated intestinal-specific deletion of Klf5 in adult mice resulted in morphologic changes that included a regenerative phenotype, impaired barrier function, and inflammation. Adult mutant mice exhibited defects in epithelial differentiation and migration. These changes were associated with reduced expression of Caudal type homeobox (Cdx) 1, Cdx2, and Eph and ephrin signaling proteins. Concomitantly, Wnt signaling to β-catenin was reduced. Proliferation in regenerative crypts was associated with increased expression of the progenitor cell marker Sox9.

conclusionsDeletion of Klf5 in the gut epithelium of mice demonstrated that KLF5 maintains epithelial proliferation, differentiation, and cell positioning along the crypt radial axis. Morphologic changes that occur with deletion of Klf5 are associated with disruption of canonical Wnt signaling and increased expression of Sox9.

Indexed as

Intestinal AbsorptionAnimalsbeta CateninBlotting, WesternCDX2 Transcription FactorCell DifferentiationCell MovementCell ProliferationColonEphrinsEpithelial CellsGenotypeHomeodomain ProteinsIleumImmunohistochemistryIntestinal Mucosabeta CateninCdx1 protein, mouseCdx2 protein, mouseCDX2 Transcription FactorCTNNB1 protein, mouseEphrinsHomeodomain ProteinsKlf5 protein, mouseKruppel-Like Transcription FactorsReceptors, Eph FamilySox9 protein, mouseSOX9 Transcription FactorTranscription FactorsWnt Proteins

Identifiers

PMID21763241
PMCPMC3186863
OpenAlexW2071012973

What OpenQuestion 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 OpenQuestion graph.