ArticleMolecular biology of the cell2007
Par1b promotes hepatic-type lumen polarity in Madin Darby canine kidney cells via myosin II- and E-cadherin-dependent signaling.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Generation ofRegenerative therapy · 2024Review
- Article
- Persistent cell contacts enable E-cadherin/HMR-1- and PAR-3-based symmetry breaking within a developing C. elegans epithelium.Developmental cell · 2023Article
- MARK2 regulates directed cell migration through modulation of myosin II contractility and focal adhesion organization.Current biology : CB · 2022Article
- Low Rho activity in hepatocytes prevents apical from basolateral cargo separation during trans-Golgi network to surface transport.Traffic (Copenhagen, Denmark) · 2020Article
- PKA-independent vasopressin signaling in renal collecting duct.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- From a common progenitor to distinct liver epithelial phenotypes.Current opinion in cell biology · 2018Review
- The role of microtubules in the regulation of epithelial junctions.Tissue barriers · 2018Review
- Laminins in Epithelial Cell Polarization: Old Questions in Search of New Answers.Cold Spring Harbor perspectives in biology · 2017Review
- Rab11-FIP1 phosphorylation by MARK2 regulates polarity in MDCK cells.Cellular logistics · 2017Article
- Partitioning-Defective 1a/b Depletion Impairs Glomerular and Proximal Tubule Development.Journal of the American Society of Nephrology : JASN · 2016Article
- Proglucagon Promoter Cre-Mediated AMPK Deletion in Mice Increases Circulating GLP-1 Levels and Oral Glucose Tolerance.PloS one · 2016Article
- Structural and functional hepatocyte polarity and liver disease.Journal of hepatology · 2015Review
- Induction of lateral lumens through disruption of a monoleucine-based basolateral-sorting motif in betacellulin.Journal of cell science · 2015Article
- The unique polarity phenotype of hepatocytes.Experimental cell research · 2014Review
- Phosphorylation of the E3 ubiquitin ligase RNF41 by the kinase Par-1b is required for epithelial cell polarity.Journal of cell science · 2014Article
- Role of tight junctions in signal transduction: an update.EXCLI journal · 2014Review
- Par1b links lumen polarity with LGN-NuMA positioning for distinct epithelial cell division phenotypes.The Journal of cell biology · 2013Article
- Build them up and break them down: Tight junctions of cell lines expressing typical hepatocyte polarity with a varied repertoire of claudins.Tissue barriers · 2013Article
- Hepatocyte polarity.Comprehensive Physiology · 2013Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Kidney-derived Madin Darby canine kidney (MDCK) cells form lumina at their apices, and target luminal proteins to an intracellular vacuolar apical compartment (VAC) when prevented from polarizing. Hepatocytes, by contrast, organize their luminal surfaces (the bile canaliculi; BC) between their lateral membranes, and, when nonpolarized, they display an intracellular luminal compartment that is distinct from the VACs of MDCK cells. Overexpression of the serine/threonine kinase Par1b/EMK1/MARK2 induces BC-like lateral lumina and a hepatic-type intracellular luminal compartment in MDCK cells, suggesting a role for Par1b in the branching decision between kidney- and hepatic-type epithelial phenotypes. Here, we report that Par1b promotes lateral lumen polarity in MDCK cells independently of Ca(2+)-mediated cell-cell adhesion by inhibiting myosin II in a rho kinase-dependent manner. Polarization was inhibited by E-cadherin depletion but promoted by an adhesion-defective E-cadherin mutant. By contrast, apical surface formation in control MDCK cells required Ca(2+)-dependent cell-cell adhesion, but it occurred in the absence of E-cadherin. We propose that E-cadherin, when in an adhesion-incompetent state at the lateral domain, serves as targeting patch for the establishment of lateral luminal surfaces. E-cadherin depletion also reverted the hepatic-type intracellular luminal compartment in Par1b-MDCK cells to VACs characteristic of control MDCK cells, indicating a novel link between E-cadherin and luminal protein targeting.
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Registered trials
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.