The Par3/Par6/aPKC complex and epithelial cell polarity.

نویسندگان

  • Jia Chen
  • Mingjie Zhang
چکیده

Apical-basal polarity is the basic organizing principle of epithelial cells, and endows epithelial cells to function as defensive barriers and as mediators of vectorial transport of nutrients in and out of organisms. Apical-basal polarity is controlled by a number of conserved polarity factors that regulate cytoskeletal organizations, asymmetric distributions of cellular components, and directional transports across cells. Polarity factors often occupy specific membrane regions in response to the adhesion forces generated by cell-cell and cell-extracellular matrix interactions. Both internal polarity factors and the external extracellular matrices play fundamental roles in epithelial cell polarity establishment and maintenance. This review focuses on recent developments of the Par3/Par6/aPKC complex and its interacting proteins in epithelial cell polarity.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

KIBRA Suppresses Apical Exocytosis through Inhibition of aPKC Kinase Activity in Epithelial Cells

Epithelial cells possess apical-basolateral polarity and form tight junctions (TJs) at the apical-lateral border, separating apical and basolateral membrane domains. The PAR3-aPKC-PAR6 complex plays a central role in TJ formation and apical domain development during tissue morphogenesis. Inactivation and overactivation of aPKC kinase activity disrupts membrane polarity. The mechanism that suppr...

متن کامل

The polarity protein Par6 induces cell proliferation and is overexpressed in breast cancer.

The polarity protein complex Par6/atypical protein kinase (aPKC)/Cdc42 regulates polarization processes during epithelial morphogenesis, astrocyte migration, and axon specification. We, as well as others, have shown that this complex is also required for disruption of apical-basal polarity during the oncogene ErbB2-induced transformation and transforming growth factor beta-induced epithelial-me...

متن کامل

Loss of Podocyte aPKC / Causes Polarity Defects and Nephrotic Syndrome

Atypical protein kinase C (aPKC) is a central component of the evolutionarily conserved Par3-Par6aPKC complex, one of the fundamental regulators of cell polarity. We recently demonstrated that these proteins interact with Neph-nephrin molecules at the slit diaphragm of the glomerular filtration barrier. Here, we report that podocyte-specific deletion of aPKC / in mice results in severe proteinu...

متن کامل

Phosphorylation-Dependent Binding of 14-3-3 to the Polarity Protein Par3 Regulates Cell Polarity in Mammalian Epithelia

The mammalian homologs of the C. elegans partitioning-defective (Par) proteins have been demonstrated to be necessary for establishment of cell polarity. In mammalian epithelia, the Par3/Par6/aPKC polarity complex is localized to the tight junction and regulates its formation and positioning with respect to basolateral and apical membrane domains. Here we demonstrate a previously undescribed ph...

متن کامل

Numb regulates cell–cell adhesion and polarity in response to tyrosine kinase signalling

Epithelial-mesenchymal transition (EMT), which can be caused by aberrant tyrosine kinase signalling, marks epithelial tumour progression and metastasis, yet the underlying molecular mechanism is not fully understood. Here, we report that Numb interacts with E-cadherin (E-cad) through its phosphotyrosine-binding domain (PTB) and thereby regulates the localization of E-cad to the lateral domain o...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Experimental cell research

دوره 319 10  شماره 

صفحات  -

تاریخ انتشار 2013