Focal Adhesions: Transmembrane Junctions Between the Extracellular Matrix and the Cytoskeleton

Burridge, Keith; Fath, Karl R.; Kelly, Thomas J.; Nuckolls, Glen H.; Turner, Christopher E.

doi:10.1146/annurev.cb.04.110188.002415

Cited by 2,052 publications

(1,358 citation statements)

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“…Actin stress fibers contact the extracellular matrix at focal adhesions in the plasma membrane [10]. Astrocyte stellation is usually the result of actin stress fiber disassembly [22].…”

Section: Resultsmentioning

confidence: 99%

“…Astrocyte stellation is usually the result of actin stress fiber disassembly [22]. To demonstrate the involvement of stress fibers and focal adhesions in AICAR-induced stellation, we stained cells with phalloidin, a probe that specifically binds to F-actin [1], and vinculin, an actin-binding protein enriched at focal adhesions [10]. AICAR-induced stellation resulted in marked loss of stress fibers as evidenced by phalloidin staining (arrows, Fig.…”

Section: Resultsmentioning

confidence: 99%

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A pharmacological activator of AMP-activated protein kinase (AMPK) induces astrocyte stellation

Favero

Mandell

2007

Brain Research

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AMP-activated protein kinase (AMPK) represents a key energy-sensing molecule in many cell types. Because astrocytes are key mediators of metabolic signaling in the brain, we have initiated studies on the expression and activation of AMPK in these cells. Treatment of cultured rat cortical astrocytes with a pharmacological AMPK activator, AICA-riboside (AICAR) resulted in a time-and concentration-dependent increase in phosphorylation of AMPK and acetyl-CoA carboxylase (ACC), a direct substrate. AICAR treatment also induced a transition from epithelioid to stellate morphology in a time-and concentration-dependent manner. As stellation is indicative of actin cytoskeletal reorganization, the formation of stress fibers and focal adhesions in response to AICAR was assessed. AICAR-induced stellation correlated with F-actin disassembly and focal adhesion dispersal. Furthermore, transient transfection of an activated RhoA construct prevented AICAR-induced stellation, indicating a mechanism upstream of RhoA. Use of pharmacological inhibitor compound C prevented AICAR-induced stellation demonstrating necessity of AMPK activity for the response. Our findings suggest that AMPK mediates morphological alterations of astrocytes in response to energy depletion.

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“…Actin stress fibers contact the extracellular matrix at focal adhesions in the plasma membrane [10]. Astrocyte stellation is usually the result of actin stress fiber disassembly [22].…”

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

A pharmacological activator of AMP-activated protein kinase (AMPK) induces astrocyte stellation

Favero

Mandell

2007

Brain Research

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“…Here we have more directly explored the possible relationship between dystrophin and focal adhesions in cultured Xenopus muscle by localizing dystrophin relative to two other proteins. One is talin, a protein of focal adhesions in many cultured cells [8] and of the myotendinous junction in skeletal muscle [9,10]. The second is the 48 kDa [12] in this paper, is also a component of the myotendinous junction (as is dystrophin [13]) and talinpositive sites in cultured Xenopus muscle [12].…”

Section: Introductionmentioning

confidence: 82%

“…sites of closest contact between the ventral surface and the substrate at which force is transmitted from the cytoskeleton to the extracellular matrix [8]. This identification is possible because talin is a key component of focal adhesions in many cultured cells [8] and actin filaments (stress fibers) have been shown to project to talin-positive sites in cultured Xenopus muscle [12] as they do at focal adhesions in fibroblasts. The function of dystrophin at these sites is unknown.…”

Section: Discussionmentioning

confidence: 99%

Dystrophin as a focal adhesion protein

Kramarcy

Sealock

1990

FEBS Letters

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Monoclonal antibodies against dystrophin and the postsynaptic 58 kDa protein from Torpedo electric organ were used to localize homologs of these proteins in cultured skeletal muscle (Xenopus laevis). The Xenopus homolog is an Mr 48000 protein and, like dystrophin, is a sarcolemmal protein. Both proteins localized precisely to talin-positive sites, hence with each other, on the substrate-apposed sarcolemma. Therefore, the first sites of appearance of dystrophin on cultured muscle cells are focal adhesions, i.e. specific sites of cytoskeleton/extracellular matrix interaction.These data also add to evidence that dystrophin antt the 58 kDa act together.

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“…FA formation is modulated by traction forces on the adhesion and the size of the adhesion increases with force (Tan et al 2003;Balaban et al 2001). FAs are typically observed experimentally at the end of SF bundles (Burridge et al 1988) and disrupting SF contractility has been shown to cause FAs to disappear (Oakes et al 2012). Previous attempts to simulate FA dynamics have not considered the coupling between active SF contractility and FA assembly (Shemesh et al 2005;Bruinsma 2005).…”

Section: Introductionmentioning

confidence: 99%

Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion

Ronan

Deshpande

McMeeking

et al. 2013

Biomech Model Mechanobiol

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Publication InformationRonan, William, Deshpande, Vikram S., McMeeking, Robert M., & McGarry, J. Patrick. (2014). Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion. Biomechanics found to alter the range of substrate stiffness that cause the most significant changes in stress fibre and focal adhesion formation. Furthermore, stress fibre and focal adhesion formation evolve as a cell spreads on a substrate and leading to the formation of bands of fibres leading from the cell periphery over the nucleus. Inhibiting the formation of FAs during cell spreading is found to limit stress fibre formation. The predictions of this mutually dependent material-interface framework are strongly supported by experimental observations of cells adhered to elastic substrates and offer insight into the interdependent biomechanical processes regulating stress fibre and focal adhesion formation.

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Focal Adhesions: Transmembrane Junctions Between the Extracellular Matrix and the Cytoskeleton

Cited by 2,052 publications

References 205 publications

A pharmacological activator of AMP-activated protein kinase (AMPK) induces astrocyte stellation

A pharmacological activator of AMP-activated protein kinase (AMPK) induces astrocyte stellation

Dystrophin as a focal adhesion protein

Cellular contractility and substrate elasticity: a numerical investigation of the actin cytoskeleton and cell adhesion

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