Pages that link to "Q73511577"
Jump to navigation
Jump to search
The following pages link to Microvillus inclusion disease: a genetic defect affecting apical membrane protein traffic in intestinal epithelium (Q73511577):
Displaying 45 items.
- Functional characterization of mutations in the myosin Vb gene associated with microvillus inclusion disease (Q24323378) (← links)
- The role of enterocyte defects in the pathogenesis of congenital diarrheal disorders (Q26770040) (← links)
- Haemochromatosis protein is expressed on the terminal web of enterocytes in proximal small intestine of the rat (Q28581175) (← links)
- chaoptin, prominin, eyes shut and crumbs form a genetic network controlling the apical compartment of Drosophila photoreceptor cells (Q30578072) (← links)
- Myosin Vb uncoupling from RAB8A and RAB11A elicits microvillus inclusion disease (Q30581661) (← links)
- Autophagocytosis of the apical membrane in microvillus inclusion disease (Q31109538) (← links)
- Mechanism of IFN-gamma-induced endocytosis of tight junction proteins: myosin II-dependent vacuolarization of the apical plasma membrane (Q34049874) (← links)
- Traffic jam: a compendium of human diseases that affect intracellular transport processes (Q34156525) (← links)
- Prominin: a story of cholesterol, plasma membrane protrusions and human pathology. (Q34180122) (← links)
- Myosin 5b loss of function leads to defects in polarized signaling: implication for microvillus inclusion disease pathogenesis and treatment (Q34519300) (← links)
- Loss-of-function of MYO5B is the main cause of microvillus inclusion disease: 15 novel mutations and a CaCo-2 RNAi cell model. (Q34617207) (← links)
- Intracellular redirection of plasma membrane trafficking after loss of epithelial cell polarity (Q34755368) (← links)
- Endocytosis of Epithelial Apical Junctional Proteins by a Clathrin-mediated Pathway into a Unique Storage Compartment (Q34786013) (← links)
- MYO5B mutations cause microvillus inclusion disease and disrupt epithelial cell polarity. (Q34812873) (← links)
- Isoforms of amino acid transporters in placental syncytiotrophoblast: plasma membrane localization and potential role in maternal/fetal transport (Q35174309) (← links)
- Acetylated sialic acid residues and blood group antigens localise within the epithelium in microvillous atrophy indicating internal accumulation of the glycocalyx (Q35597037) (← links)
- The zebrafish goosepimples/myosin Vb mutant exhibits cellular attributes of human microvillus inclusion disease. (Q36096812) (← links)
- An inducible mouse model for microvillus inclusion disease reveals a role for myosin Vb in apical and basolateral trafficking (Q36155098) (← links)
- Cargo-selective apical exocytosis in epithelial cells is conducted by Myo5B, Slp4a, Vamp7, and Syntaxin 3. (Q36266151) (← links)
- Loss of MYO5B in mice recapitulates Microvillus Inclusion Disease and reveals an apical trafficking pathway distinct to neonatal duodenum (Q36724921) (← links)
- Hepatocyte polarity (Q36972087) (← links)
- Polarized protein transport and lumen formation during epithelial tissue morphogenesis (Q37052115) (← links)
- Defects in retinal pigment epithelium cell proliferation and retinal attachment in mutant mice with p27(Kip1) gene ablation (Q37078875) (← links)
- Chapter 3: acquisition of membrane polarity in epithelial tube formation patterns, signaling pathways, molecular mechanisms, and disease. (Q37435101) (← links)
- Recycling endosomes in apical plasma membrane domain formation and epithelial cell polarity (Q37787522) (← links)
- Molecular motors and apical CFTR traffic in epithelia (Q38104258) (← links)
- An overview and online registry of microvillus inclusion disease patients and their MYO5B mutations. (Q38135356) (← links)
- Disrupted apical exocytosis of cargo vesicles causes enteropathy in FHL5 patients with Munc18-2 mutations. (Q38696809) (← links)
- Plasticity of the brush border - the yin and yang of intestinal homeostasis (Q38720389) (← links)
- Disruption of Rab8a and Rab11a causes formation of basolateral microvilli in neonatal enteropathy. (Q38735421) (← links)
- Rabs set the stage for polarity (Q39104860) (← links)
- Mechanisms of Cell Polarity-Controlled Epithelial Homeostasis and Immunity in the Intestine (Q39141494) (← links)
- MYO5B and bile salt export pump contribute to cholestatic liver disorder in microvillous inclusion disease (Q39283295) (← links)
- Inhibition and redistribution of NHE3, the apical Na+/H+ exchanger, by Clostridium difficile toxin B. (Q40567906) (← links)
- A novel cellular phenotype for familial hypercholesterolemia due to a defect in polarized targeting of LDL receptor (Q40801530) (← links)
- Towards understanding microvillus inclusion disease. (Q41838926) (← links)
- Identification of intestinal ion transport defects in microvillus inclusion disease (Q42008380) (← links)
- Apical Membrane Alterations in Non-intestinal Organs in Microvillus Inclusion Disease. (Q46194285) (← links)
- Abnormal Rab11-Rab8-vesicles cluster in enterocytes of patients with microvillus inclusion disease (Q46789322) (← links)
- Advances in Evaluation of Chronic Diarrhea in Infants. (Q52588795) (← links)
- Intestinal epithelial cell polarity defects in disease: lessons from microvillus inclusion disease. (Q52723533) (← links)
- Unusual ultrastructural features in microvillous inclusion disease: A report of two cases (Q83144968) (← links)
- Editing Myosin VB Gene to Create Porcine Model of Microvillus Inclusion Disease, With Microvillus-lined Inclusions and Alterations in Sodium Transporters (Q89951757) (← links)
- Recent advances in understanding and managing malabsorption: focus on microvillus inclusion disease (Q91869822) (← links)
- Physiology of Electrolyte Transport in the Gut: Implications for Disease (Q92677838) (← links)