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The most two important receptors mediating tension "sensing" and myofibroblast activity are the αѴ β3 and α5 β1 integrin receptors.
Measuring mechanical forces at the cell surface does not require genetic encoding of the tension sensing element but can be performed using mechanically well-described polymers.
By inserting a tension sensing FRET element in Vinculin, it was shown that in integrin-based Focal Adhesions Vinculin itself is under actomyosin-based tension (Grashoff et al., 2010).
This may constitute the potential tension sensing mechanism performed by actin filaments.
One explanation is that tension sensing is an intrinsic property of the kinetochore (Campbell and Desai 2013).
Hence, it is possible that the low collagen III expression in the ECM will have an effect on myofibroblasts through changes in the "tension" sensing receptors.
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The FRET signal is high at disassembling or sliding focal adhesions near the trailing edge of migrating cells, implying that the tension sensed by the sensor is low (< 2.5 pN) where stress fibers are disassembled.
Another direction would be to make a more extensive use of traction force measurements to substantiate comments on stress fibers sensing tension.
However, given the difficulty AP propagation alone has explaining organ-level function, largely forgotten idea of mechanotransduction by pressure-tension sensing should be re-considered [ 40, 56].
Its expression was similar under both oxygen conditions, which could be a sign for low oxygen tension being sensed as normoxic by those stem cells.
When chromosomes are attached improperly, a signal of no tension is sensed to activate the spindle assembly checkpoint (SAC).
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