Figures & data
Figure 1. Schematic presentation of tight junction (TJ) regulation. A summary of the possible pathways of TJ regulation. Phosphorylation of the myosin light chain II leads to actin stress fiber formation and opens the TJ by its contractile forces [123,124]. This process is highly regulated by the balance between myosin light-chain kinase (MLCK) and myosin light-chain phosphatase (MLCP) [125]. A presumed mechanism for MLCP inhibition by PKC is via the small protein CPI-17 [126]. Furthermore, RhoA and its downstream effectors rho-associated protein kinases 1 and 2 can phosphorylate the myosin phosphatase targeting protein 1 subunit of MLCP [127]. Rho A, whose activity is regulated by protein kinase A (a cAMPdependent protein kinase), is a part of the superfamily of small GTPases [127]. The figure contains six examples of receptormediated TJ regulation.
![Figure 1. Schematic presentation of tight junction (TJ) regulation. A summary of the possible pathways of TJ regulation. Phosphorylation of the myosin light chain II leads to actin stress fiber formation and opens the TJ by its contractile forces [123,124]. This process is highly regulated by the balance between myosin light-chain kinase (MLCK) and myosin light-chain phosphatase (MLCP) [125]. A presumed mechanism for MLCP inhibition by PKC is via the small protein CPI-17 [126]. Furthermore, RhoA and its downstream effectors rho-associated protein kinases 1 and 2 can phosphorylate the myosin phosphatase targeting protein 1 subunit of MLCP [127]. Rho A, whose activity is regulated by protein kinase A (a cAMPdependent protein kinase), is a part of the superfamily of small GTPases [127]. The figure contains six examples of receptormediated TJ regulation.](/cms/asset/6934704d-655b-4040-955a-6ad3b049e6b8/iedc_a_1088181_f0001_b.jpg)