Evidence map›Paper›PMID 41720082›Full record

ArticleStem cell reports2026

Myosin VB is critical for progenitor cell identity and function in the intestine.

Andreanna Burman, Monica E Brown, Yilin Yang, Michael Momoh, Francisca Adeniran, Cynthia Ramos, Ken S Lau, Linda C Samuelson, Mitchell D Shub, Joseph T Roland and 1 more

Erratum issuedAbstract read
In one paragraph

Article in Stem cell reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors.

Andreanna BurmanDepartment of Cell & Developmental Biology, Vanderbilt University, Nashville, TN, USA; Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, TN, USA.
Monica E BrownDepartment of Cell & Developmental Biology, Vanderbilt University, Nashville, TN, USA; Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, TN, USA; Center for Computational Systems Biology, Vanderbilt University, Nashville, TN, USA.
Yilin YangDepartment of Cell & Developmental Biology, Vanderbilt University, Nashville, TN, USA; Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, TN, USA.
Michael MomohDepartment of Surgery, Vanderbilt University Medical Center, Nashville, TN, USA.
Francisca AdeniranDepartment of Surgery, Vanderbilt University Medical Center, Nashville, TN, USA.
Cynthia RamosDepartment of Surgery, Vanderbilt University Medical Center, Nashville, TN, USA.
Ken S LauDepartment of Cell & Developmental Biology, Vanderbilt University, Nashville, TN, USA; Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Surgery, Vanderbilt University Medical Center, Nashville, TN, USA; Center for Computational Systems Biology, Vanderbilt University, Nashville, TN, USA.
Linda C SamuelsonDepartment of Molecular & Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
Mitchell D ShubDepartment of Child Health, University of Arizona College of Medicine and Phoenix Children's, Phoenix, AZ, USA.
Joseph T RolandEpithelial Biology Center, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Surgery, Vanderbilt University Medical Center, Nashville, TN, USA.
Izumi KajiDepartment of Cell & Developmental Biology, Vanderbilt University, Nashville, TN, USA; Epithelial Biology Center, Vanderbilt University Medical Center, Nashville, TN, USA; Department of Surgery, Vanderbilt University Medical Center, Nashville, TN, USA. Electronic address: izumi.kaji@vumc.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microvillus inclusion disease (MVID) is a congenital diarrheal disorder, caused by inactivating mutations in myosin Vb (MYO5B). MYO5B-deficient mice and cell lines have demonstrated the importance of MYO5B in brush border development; however, the previous models lacked specificity to test intestinal stem cell functions. In the present study, we investigated the effects of progressive MYO5B deficiency originating in intestinal crypt cells utilizing mouse models. Our transcriptomic and multiplex immunostaining datasets demonstrate that MYO5B is critical for intestinal stem cell function. MYO5B-deficient crypts acquire a hyperproliferative phenotype with incomplete cell differentiation in vivo and an elevated organoid formation rate compared to control crypts. An evident disruption in mitochondrial structure and fatty acid metabolism likely underlies these crypt phenotypes. Consistent with mouse models, MVID patient biopsies demonstrate abnormal expansion of the proliferative zone along with villus blunting. These data reveal the direct role of MYO5B in intestinal epithelial progenitor cell functions.

Indexed as

Intestinal MucosaIntestinesMyosin Heavy ChainsMyosin Type VStem CellsAnimalsCell DifferentiationCell ProliferationHumansMalabsorption SyndromesMiceMicrovilliMitochondriaMucolipidosesMyo5B protein, mouseMyosin Heavy ChainsMyosin Type Vdifferentiationintestinal stem cellmicrovillus inclusion diseaseMVIDproliferation

Identifiers

PMID41720082
PMCPMC12985367

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.