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

Myosin 5b deficiency alters liver proliferation, zonation, and bile acid composition.

Microvillus Inclusion Disease: Successful Treatment of Severe Hyponatremia With High-Dose Fludrocortisone via a Possible Gut-Mediated Mechanism.

Syntaxin 3 regulates apical membrane integrity in proximal tubule epithelial cells and prevents Fanconi syndrome development.

Microvillus inclusion disease: a short review of literature.

Odevixibat therapy in progressive familial intrahepatic cholestasis with MYO5B variants: a retrospective case series.

LPAR5 as a prospective therapeutic target for treating microvillus inclusion disease.

A liver-specific mouse model for MYO5B-associated cholestasis reveals a toxic gain-of-function as underlying disease mechanism.

Altered chaperone-nonmuscle myosin II interactions drive pathogenicity of the UNC45A c.710T>C variant in osteo-oto-hepato-enteric syndrome.

Diagnostic dilemma in infantile refractory diarrhea: a rare case of IPEX syndrome.

Microvillus inclusion disease-causing MYO5B point mutations exert differential effects on motor function.

SLC26A3 (DRA, the Congenital Chloride Diarrhea Gene): A Novel Therapeutic Target for Diarrheal Diseases.

Massive bowel resection for children with non-short bowel syndrome intestinal failure.

Alterations in cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation.

Altered cellular metabolic pathway and epithelial cell maturation induced by MYO5B defects are partially reversible by LPAR5 activation.

Pediatric Chronic Intestinal Failure: Something Moving?

Intracellular Trafficking Defects in Congenital Intestinal and Hepatic Diseases.

An Adult Case of Benign Recurrent Intrahepatic Cholestasis Due to MYO5B Deficiency.

[Analysis of a child with Microvillus inclusion disease due to variants of MYO5B gene and a literature review].

Sonographic findings of transient marked proximal bowel dilatation in a growth-restricted fetus at 35 weeks' gestation.

Uncovering the Relationship Between Genes and Phenotypes Beyond the Gut in Microvillus Inclusion Disease.

CODE Think! Rare Mutations of STX3 Causing Microvillus Inclusion Disease.

Approach to Congenital Diarrhea and Enteropathies (CODEs).

Patient-derived enteroids provide a platform for the development of therapeutic approaches in microvillus inclusion disease.

Not all enteropathies are coeliac disease! Report of an infant with microvillus inclusion disease.

Clinicopathologic Features of IDEDNIK (MEDNIK) Syndrome in a Term Infant: Histopathologic Features of the Gastrointestinal Tract and Report of a Novel AP1S1 Variant.

Microvillus Inclusion Disease Caused by MYO5B: Different Presentation and Phenotypes Despite Same Mutation.

Generation of induced pluripotent stem cells (iPSCs) from a microvillus inclusion disease patient with a homozygous missense mutation in UNC45A.

Therapy Development for Microvillus Inclusion Disease using Patient-derived Enteroids.

Compound Heterozygous MYO5B Mutation, a Cause of Infantile Cholestasis: A Case Report.

A CRISPR screen in intestinal epithelial cells identifies novel factors for polarity and apical transport.

Weight loss and metabolic acidosis in a neonate: Answers.

Fetal Bowel Abnormalities Suspected by Ultrasonography in Microvillus Inclusion Disease: Prevalence and Clinical Significance.

Loss of Serum Glucocorticoid-Inducible Kinase 1 SGK1 Worsens Malabsorption and Diarrhea in Microvillus Inclusion Disease (MVID).

Case Report: MYO5B Homozygous Variant c.2090+3A>T Causes Intron Retention Related to Chronic Cholestasis and Diarrhea.

Altered MYO5B Function Underlies Microvillus Inclusion Disease: Opportunities for Intervention at a Cellular Level.

UNC45A deficiency causes microvillus inclusion disease-like phenotype by impairing myosin VB-dependent apical trafficking.

A Functional Relationship Between UNC45A and MYO5B Connects Two Rare Diseases With Shared Enteropathy.

MYO5B Gene Mutations: A Not Negligible Cause of Intrahepatic Cholestasis of Infancy With Normal Gamma-Glutamyl Transferase Phenotype.

Microvillus inclusion disease with prenatal ultrasound findings and postpartum confirmed.

A Novel Homozygous Mutation in the MYO5B Gene Associated With Normal-Gamma-Glutamyl Transferase Progressive Familial Intrahepatic Cholestasis.

Two cases of microvillus inclusion disease caused by MYO5B deficiency with prenatal abnormalities.

Novel MYO5B mutation in microvillous inclusion disease of Syrian ancestry.

MYO5B-associated diseases: Novel liver-related variants and genotype-phenotype correlation.

Monogenic mutations in four cases of neonatal-onset watery diarrhea and a mutation review in East Asia.

Risk and Clinical Significance of Idiopathic Preterm Birth in Microvillus Inclusion Disease.

Late Manifestation of Massive Jejunal and Cecal Varices Post Liver and Small Bowel Transplantation in a Patient With Microvillus Inclusion Disease.

Cell differentiation is disrupted by MYO5B loss through Wnt/Notch imbalance.

Expanding the clinical spectrum in trichohepatoenteric syndrome.

Pathogenic STX3 variants affecting the retinal and intestinal transcripts cause an early-onset severe retinal dystrophy in microvillus inclusion disease subjects.

Advanced Microscopy for Liver and Gut Ultrastructural Pathology in Patients with MVID and PFIC Caused by MYO5B Mutations.

Microvillous inclusion disease as a cause of severe congenital diarrhea in a newborn.

Recruitment of Polarity Complexes and Tight Junction Proteins to the Site of Apical Bulk Endocytosis.

Microvillus inclusion disease with novel MYO5B pathogenic variants.

Congenital Diarrhea and Cholestatic Liver Disease: Phenotypic Spectrum Associated with MYO5B Mutations.

Pharmacological and Parenteral Nutrition-Based Interventions in Microvillus Inclusion Disease.

[Congenital microvillus inclusion disease in a child].

The Rab11 effectors Fip5 and Fip1 regulate zebrafish intestinal development.

SNAREs and developmental disorders.

Challenges of Microvillus Inclusion Disease in the NICU.

Microvillus Inclusion Disease: A Rare Mutation of STX3 in Exon 9 Causing Fatal Congenital Diarrheal Disease.

The Endosomal Recycling Pathway-At the Crossroads of the Cell.

Exploiting Alternative Brush Border Trafficking Routes to Treat Microvillous Inclusion Disease.

Unequal Effects of Myosin 5B Mutations in Liver and Intestine Determine the Clinical Presentation of Low-Gamma-Glutamyltransferase Cholestasis.

Lysophosphatidic Acid Increases Maturation of Brush Borders and SGLT1 Activity in MYO5B-deficient Mice, a Model of Microvillus Inclusion Disease.

MYO5B Pathogenic Variants Found to Cause Intestinal Symptoms Without Microvillus Inclusion Disease in a Child Who Previously Underwent Liver Transplantation for PFIC-like Cholestasis.

Editing Myosin VB Gene to Create Porcine Model of Microvillus Inclusion Disease, With Microvillus-Lined Inclusions and Alterations in Sodium Transporters.

Recent advances in understanding and managing malabsorption: focus on microvillus inclusion disease.

Glucocorticoids and myosin5b loss of function induce heightened PKA signaling in addition to membrane traffic defects.

The challenge of personalized cell biology: The example of microvillus inclusion disease.

Loss of myosin Vb promotes apical bulk endocytosis in neonatal enterocytes.

Congenital diarrhea in a newborn infant: A case report.

A V0-ATPase-dependent apical trafficking pathway maintains the polarity of the intestinal absorptive membrane.

Microvillous Inclusion Disease as a Cause of Protracted Diarrhea.

Microvillus inclusion disease, a diagnosis to consider when abnormal stools and neurological impairments run together due to a rare syntaxin 3 gene mutation.

Dynamic Formation of Microvillus Inclusions During Enterocyte Differentiation in Munc18-2-Deficient Intestinal Organoids.

An Intravenous Fish Oil-Based Lipid Emulsion Successfully Treats Intractable Pruritus and Cholestasis in a Patient with Microvillous Inclusion Disease.

Hyaline fibromatosis syndrome: Clinical update and phenotype-genotype correlations.

Loss of MYO5B Leads to Reductions in Na+ Absorption With Maintenance of CFTR-Dependent Cl- Secretion in Enterocytes.

Weibel-Palade Body Localized Syntaxin-3 Modulates Von Willebrand Factor Secretion From Endothelial Cells.

Intestinal epithelial cell polarity defects in disease: lessons from microvillus inclusion disease.

The Endosomal Protein Endotubin Is Required for Enterocyte Differentiation.

Microvillus Inclusion Disease Variant in an Infant with Intractable Diarrhea.

MYO5B, STX3, and STXBP2 mutations reveal a common disease mechanism that unifies a subset of congenital diarrheal disorders: A mutation update.

Apical Membrane Alterations in Non-intestinal Organs in Microvillus Inclusion Disease.

[Clinical features and MYO5B mutations of a family affected by microvillus inclusion disease].

Kinetic signatures of myosin-5B, the motor involved in microvillus inclusion disease.

Congenital Fatal Diarrhea in Newborns.

Disrupted apical exocytosis of cargo vesicles causes enteropathy in FHL5 patients with Munc18-2 mutations.

A Case Study of Intractable Diarrhea Due to Neonatal Microvillous Inclusion Disease.

Abnormal Rab11-Rab8-vesicles cluster in enterocytes of patients with microvillus inclusion disease.

Trafficking Ion Transporters to the Apical Membrane of Polarized Intestinal Enterocytes.

Concise Review: The Potential Use of Intestinal Stem Cells to Treat Patients with Intestinal Failure.

New Mouse Models for Microvillus Inclusion Disease (MVID): Where Do the Inclusions Come From and Are They Cause or Consequence?

[Microvillous inclusion disease as a cause of severe congenital diarrhea. Case report].

Defects in myosin VB are associated with a spectrum of previously undiagnosed low γ-glutamyltransferase cholestasis.

[Phenotypic and genetic analysis of a family affected with microvillus inclusion disease].

Nonobstructive Diffuse Dilated Bowel Loops: Prenatal Diagnosis, Fetal Characteristics and Neonatal Outcomes.

Racecadotril May Reduce Diarrhoea in Microvillous Inclusion Disease.

Congenital Microvillus Inclusion Disease in the Differential Diagnosis of Intractable Metabolic Acidosis.

MYO5B mutations cause cholestasis with normal serum gamma-glutamyl transferase activity in children without microvillous inclusion disease.

The zebrafish goosepimples/myosin Vb mutant exhibits cellular attributes of human microvillus inclusion disease.

Microvillus inclusion disease: a subtotal enterectomy as a bridge to transplantation.

Generation of intestinal surface: an absorbing tale.

Identification of intestinal ion transport defects in microvillus inclusion disease.

RAB and RHO GTPases regulate intestinal crypt cell homeostasis and enterocyte function.

Loss of MYO5B in mice recapitulates Microvillus Inclusion Disease and reveals an apical trafficking pathway distinct to neonatal duodenum.

Endocytosis in enterocytes.

Identifying Mutations of the Tetratricopeptide Repeat Domain 37 (TTC37) Gene in Infants With Intractable Diarrhea and a Comparison of Asian and Non-Asian Phenotype and Genotype: A Global Case-report Study of a Well-Defined Syndrome With Immunodeficiency.

Multilabel immunofluorescence and antigen reprobing on formalin-fixed paraffin-embedded sections: novel applications for precision pathology diagnosis.

Towards understanding microvillus inclusion disease.

The role of enterocyte defects in the pathogenesis of congenital diarrheal disorders.

Cargo-selective apical exocytosis in epithelial cells is conducted by Myo5B, Slp4a, Vamp7, and Syntaxin 3.

The localisation of the apical Par/Cdc42 polarity module is specifically affected in microvillus inclusion disease.

An inducible mouse model for microvillus inclusion disease reveals a role for myosin Vb in apical and basolateral trafficking.

Myo5b knockout mice as a model of microvillus inclusion disease.

Peripheral Avascular Retina in a Term Male Neonate With Microvillus Inclusion Disease and Pancreatic Insufficiency.

Analysis of the interactions between Rab GTPases and class V myosins.