Altered trafficking and epithelial cell polarity in disease.
Establishment and maintenance of a polarized epithelium relies on the integration of signaling cascades, acquisition of specialized trafficking circuits and establishment of a unique cytoarchitecture. Defects in any of these processes can adversely affect cell polarity and cause defects in specific organs and systemic disease. Mutations that disrupt the proper transport of individual plasma membrane proteins, or inactivate components of the epithelial-specific trafficking machinery, have severe functional consequences. Links between renal diseases and defects in trafficking, differentiation or signaling, highlight the delicate balance between these parameters which, when altered, precipitates a loss of renal function.
Molecular Trafficking Laboratory, Dept of Pathology, University of New Mexico School of Medicine, Albuquerque 87131, NM, USA.
Mary
M
Stein
Angela
A
Wandinger-Ness
Tamara
T
Roitbak
D000199:Actins / Q000378:metabolism; D000818:Animals; D001692:Biological Transport; D016764:Cell Polarity; D004705:Endocytosis / Q000502:physiology; D004847:Epithelial Cells / Q000378:metabolism* / Q000502:physiology; D005786:Gene Expression Regulation; D030342:Genetic Diseases, Inborn / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D051379:Mice; D008954:Models, Biological; D016891:Polycystic Kidney, Autosomal Dominant / Q000378:metabolism; D017044:Polycystic Kidney, Autosomal Recessive / Q000378:metabolism; D015398:Signal Transduction
D000199:Actins