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In vascular smooth muscle cells, surface expression of Fas [ 44] and molecules involved in signaling the apoptotic process, such as caspase-8 and caspase-3, appear to be regulated and provide another level of cellular control of apoptosis [ 45].
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The same enzyme detects the energy imbalance in a muscle cell that exercises where its activation also leads to the insertion of Glut4 onto the muscle cell surface.
To test whether muscle cell surface projections were affected when muscle elongation was perturbed, embryos were electroporated with sna>Bix and Tbx6b>PH-YFP (Figure 6M P and Movie S10).
To gain insight into the molecular nature of the muscle cell surface projections we employed additional fluorescent protein fusions that demarcate components of the cytoskeleton.
Muscle cell surface projections were most abundant at the neurula stage (Figure 6A,I; 2.1±0.8 projections/cell, n = 28), decreased in number by the early tailbud stage (Figure 6B,J; 1.5±0.1 projections/cell, n = 12), and were almost entirely absent by the mid tailbud (Figure 6C,K) and late tailbud stages (Figure 6D,L).
This effect in smooth muscle cells is mediated by extracellular TG2 binding to LRP5/6 on the smooth muscle cell surface and this reported interaction does not require transamidation activity.
Tsp4b and Lam bind Itgs (orange) on the muscle cell surface, activating FAK (green) and recruiting Pxn (yellow) and Ilk (purple) to promote muscle specific Itg signaling and stabilize myofiber attachment.
To achieve this strength, extracellular matrix proteins bind to one another and to receptors on the muscle cell surface that are linked to its internal scaffolding, thereby organizing other proteins into a structure called a myotendinous junction.
Physiologically, it has been suggested that the loss of local contractile stimulation induced through sitting leads to both the suppression of skeletal muscle lipoprotein lipase (LPL) activity (which is necessary for triglyceride uptake and HDL cholesterol production) and reduced glucose uptake through blunted translocation of GLUT4 glucose transporters to the skeletal muscle cell surface (15, 16).
The second type of fibre often runs along the common oviduct (Fig. 6A), and has branches running circularly parallel to the myofibres (Fig. 6A, marked c), (though it is possible that some of the finer parts result from immunoreaction with the muscle cell surface).
Using the replating method, this time onto coated 100mm culture dishes, we observed that cellular Rac1 is activated within 8h of plating, before the appearance of AChR complex clusters on the adherent muscle cell surface (Fig. 3), demonstrating the utility of this method for biochemical signaling assays associated with AChR aggregation by immobilized ECM components.
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