[2] Stress fibers have been shown to play an important role in cellular contractility, providing force for a number of functions such as cell adhesion, migration and morphogenesis.

The Rho family of GTPases regulate many aspects of actin cytoskeletal dynamics, including stress fiber formation.

[4] When bound to GTP, Rho activates Rho-associated coiled-coil forming kinase (ROCK) and mammalian homologue of Drosophila diaphanous (mDia).

[6] This will lead to the accumulation of activated myosin motor proteins, which bind the actin filaments that were polymerized by mDia, to create stress fibers.

[7] LIM-kinase will in turn phosphorylate and inactivate cofilin, which will prevent the breakdown and recycling of actin filaments, maintaining the integrity of the stress fibers.

[11] Stress fibers play an important role in the maintenance of cadherin-dependent and nexin-dependent cell-cell contacts,[12] and the Rho-family GTPases have been found to regulate the structure and integrity of adherens junctions.

[19] Tight junctions, or zona occludens, are the most important cellular element for the formation of semi-permeable barriers within or between tissues.

[22] As the naming or their layers implies, focal adhesions play a large role in mechanotransduction and cell migration.

[23] An essential feature of many cells is their ability to migrate towards certain mechanical (Durotaxis) or chemical (Chemotaxis) stimuli.

[33] The mechanical force transmitted to focal adhesions by stress fibers can also alter the conformation of mechanosensitive focal adhesion proteins, such as p130Cas[34] and talins,[35] suggesting that stress fiber contractility may translate mechanical signals into biochemical cues.

There are also a small subset of focal adhesion-associated integrins that terminate in the perinuclear actin cap (at the top of the nucleus), and are anchored there by the LINC complex.

[38] Stress fibers in motile and non-motile cells are similar in that they both contain actin filaments which are cross-linked by α-actinin and myosin II, however the spatial orientation of individual actin filaments within the stress fiber differ between motile and non-motile cells.

[40] Stress fibers in the ventral regions of non-motile cells show a periodic polarity that is similar to the organization of the sarcomere.