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Entropic and energetic elasticity in controlling catch-to-slip bonds in cell-adhesion molecules

机译:控制细胞 - 粘附分子中的捕捞滑粘键的熵和能量弹性

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We develop a physical model to describe the kinetic behavior in cell-adhesion molecules. Unbinding of non-covalent biological bonds is decomposed into entropic and energetic controlled debonding. Such a treatment on debonding processes is a space decomposition of bond breaking events. Entropy controlled dissociation under thermal fluctuation is non-directional in a 3-dimensional space, and its energy barrier to escape may be not influenced by a tensile force but the microstates which can lead to dissociation are changed by the tensile force; An applied force effectively lowers the energy barrier to escape along the force direction. Such energetic effect will accelerate dissociate mainly along directions parallel to the loading direction. The lifetime of the biological bond, due to the superimposition of two concurrent off-rates, may grow with increasing tensile force to moderate amount and decrease with further increasing load, as debonding events dominated by entropy transit to those controlled by an applied force. We hypothesize that a catch-to-slip bond transition is a generic feature in biological bonds. The model also predicts that catch bonds in compliant molecular structure have longer lifetimes and may be activated at lower forces [1].
机译:我们开发一种物理模型来描述细胞粘附分子中的动力学行为。非共价生物键的解散成熵和精力量控制的剥离。这种对剥离过程的治疗是债券破坏事件的空间分解。在热量波动下的熵控制解离在三维空间中是非定向的,并且其能量屏障逃逸可能不受拉伸力的影响,而是可以通过拉伸力改变可以导致解离的微稳压;施加的力有效地降低了能量屏障沿着力方向逸出。这种能量效果将加速主要沿着平行于装载方向的方向解散。由于两种并发速率的叠加,生物键的寿命可以随着抗拉力的增加而增加,并且随着通过进一步增加的载荷而减少,因为由熵过渡到由施加的力控制的剥离事件。我们假设储存债券过渡是生物键的通用特征。该模型还预测符合分子结构的捕获键具有更长的寿命,并且可以在较低力[1]下激活[1]。

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