SIGNAL TRANSDUCTION IN SMOOTH MUSCLE

血管平滑肌对复杂的神经和神经的不适当反应 控制收缩的激素机制或控制生长的因素 生长和复制发生在大多数情况下的发病率和死亡率 美国。高血压和血管痉挛是失败的例子 动脉粥样硬化和血管成形术后收缩的调节 再狭窄反映了不适当的生长反应。经常接受治疗 靶向连接受体的信号转导事件中的关键步骤 在血管细胞膜中传递到细胞内的第二信使 支配生物的变构或共价调节机制 细胞蛋白质或遗传物质的活性。 该计划的广泛目标是识别信号并确定 调节收缩、生长和运动的信号转导事件 平滑肌的复制。这些方法主要是分子方面的，但 代表生物化学、生物物理学和细胞生物学的学科。 程序中统一的焦点是流畅的信号级联 由激动剂-受体复合体形成诱导的肌肉。这些信号 级联信号通路包括参与调节细胞内钙离子敏感性的通路。 收缩、交叉桥磷酸化调控和核糖体基因 抄写。所有这些信号级联都有共同的启动事件 在发散之前，可能会表现出某种程度的串音。 作为正式的结果，每个项目之间会出现类似的串扰 协作和共同的信号转导事件。

Inappropriate responses by vascular smooth muscle to the complex neural and hormonal mechanisms governing contraction or to growth factors governing growth and replication occur in most cases of morbidity and mortality in the United States. Hypertension and vasospasm are example of failures of regulation of contraction, while atherosclerosis and post-angioplasty restenosis reflect inappropriate growth responses. Therapy frequently targets critical steps in the signal transduction events linking receptors in the vascular cell membranes to intracellular second messengers and allosteric or covalent regulatory mechanisms that govern the biological activity of cellular proteins or genetic material. The broad objective of the program is to identify the signals and determine the signal transduction events that regulate contraction, growth and replication of smooth muscle. The approaches are largely molecular, but represent the disciplines of biochemistry, biophysics, and cell biology. The unifying focus in the program are the signaling cascades in smooth muscle induced by agonist-receptor complex formation. These signaling cascades include those involved in modulation of the Ca++-sensitivity of contraction, regulation of crossbridge phosphorylation, and ribosomal gene transcription. All these signaling cascades have common initiation events before diverging while presumably exhibiting some degree of cross-talk. Comparable cross-talk occurs between each project as a result of formal collaborations and common signal transduction events.