Education

博士后研究员
哈佛医学院和波士顿儿童医院,2019年
博士后研究员
Seoul National University, South Korea, 2012
Ph.D.
University of California, Irvine, 2010

Areas of Interest

Research Interests

Mechanoregulation of cellular adhesion and migration

Research Information

Cellular adhesion and migration require an intricate orchestration of membrane receptors and the cytoskeleton to transduce bidirectional force from extracellular substrates. When dysregulated, a myriad of pathologies can emerge from decreased immune extravasation (leukocyte adhesion deficiency), aberrant immune infiltration (rheumatoid arthritis, psoriasis, inflammatory bowel disease and atherosclerosis) and tumor metastasis via epithelial-mesenchymal transition. While the importance of the forces generated between cell-cell/ECM and the cytoskeleton are appreciated in cellular regulation, it is unknown how force sensing surface receptors and adhesion complexes dynamically respond to forces and transduce mechanical information. Integrins are one such family of cell surface mechanoreceptors.

整联蛋白信号传导很复杂,因为它们可以从其细胞外配体结合域进行双向传输信号,传达有关底物可用性和刚度的信息,以及从与信号转导途径相关的细胞质域。这些细胞内信号通路将信息从趋化因子受体传输,以调节整联蛋白的激活状态并表示规范的内而外信号传导。最近的证据支持内而外信号的另一个分支,涉及机械成分和肌动蛋白细胞骨架的作用。整联蛋白的激活取决于它们在肌动蛋白细胞骨架和固定或细胞表面结合的配体之间传递机械力的能力。显然,这种力转导充当变构效应子,导致整联蛋白构象变化和亲和力的相关变化,但是驱动整联蛋白激活及其在细胞水平的调节的分子机制仍然不清楚,对于理解整联蛋白的功能如何介导动态是至关重要的细胞粘附和迁移。

整联蛋白激活的这种细胞骨架力模型固有地将细胞极化和肌动蛋白细胞骨架与整合素激活在细胞内的同一位置联系起来,从而防止了异常整合素介导的粘附,仅通过将活性整合蛋白限制在细胞可以获得牵引力的位置。为了阐明肌动蛋白对整联蛋白激活的机制的机制,将需要功能研究和开发新方法,以定量测量肌动蛋白细胞骨架和整联蛋白动力学。我们将利用超分辨率显微镜,计算图像分析,基因组修饰和蛋白质化学来了解细胞骨架与整联蛋白的链接,并直接测量细胞表面上整联蛋白构象,从而促进我们对细胞粘附性和迁移调节的理解。

Publications

Publication Information

Travis I Moore,杰西·亚伦(Jesse Aaron),坦·莱恩(Teng-Leong Chew)和蒂莫西(Timothy)(2018)。用超分辨率显微镜在细胞表面测量整联蛋白构象变化。Cell Reports, 22 (7), 1903–1912.

Pontus Nordenfelt*,Travis I Moore*,Shalin B Mehta*, Joseph K Matthew**, Vinay Swaminathan**, Koga Nobuyasu, Talley J Lambert, David Baker, Jennifer C Waters, Rudolf Oldenbourg, Tomomi Tani, Satyajit Mayor, Clare M Waterman and Timothy A Springer. (2017). Direction of Actin Flow Dictates Integrin LFA-1 Orientation During Leukocyte Migration.Nature Communications, 8(1), 673.*, **这些作者做出了同样的贡献。

Vinay Swaminathan*, Joseph K Matthew*,Shalin B Mehta*, Pontus Nordenfelt**,Travis I Moore**, Koga Nobuyasu, Talley J Lambert, David Baker, Jennifer C Waters, Rudolf Oldenbourg, Tomomi Tani, Satyajit Mayor, Timothy A Springer and Clare M Waterman. (2017). Actin Retrograde Flow Actively Aligns and Orients Ligand-engaged Integrins in Focal Adhesions.PNAS, 114(40) 40648-10653.*, **这些作者做出了同样的贡献。

Ching-Shan Chou*,Travis I Moore*、清聂Tau-Mu易建联。(2015)。其他移动电话l polarity behaviors arise from bifurcations in G-protein spatial dynamics.IET Systems Biology, 9(2) 52-63.*这些作者做出了同样的贡献。

Travis I Moore, Hiromasa Tanaka, Hyung Joon Kim, Noo Li Jeon, and Tau-Mu Yi. (2013). Yeast G-proteins mediate directional sensing and polarization behaviors in response to changes in pheromone gradient direction.摩尔生物细胞, 24(4) 521-534.

Gabriel A Quinones,Travis I Moore, Katrina Nicholes, Hyunjae Lee, Laura Sun, Noo Li Jeon, Jean-Philippe Stephan. (2013). New Wall-less Plate Technology Enabling Cell-based Investigations.Blood, 21(7) 25-35.

Ching-Shan Chou*,Travis I Moore*, Steven Chang, Qing Nie, and Tau-Mu Yi. (2012). Signaling regulated endocytosis and exocytosis lead to mating pheromone concentration dependent morphologies in yeast.FEBS letters586(23), 4208-14.*这些作者做出了同样的贡献。

Travis I Moore, Ching-Shan Chou, Noo Li Jeon, Qing Nie, and Tau-Mu Yi. (2008). Robust spatial sensing of mating pheromone gradients by yeast cells.PLoS One3, e3865.

Ron Waksman, Pauline E McEwan,Travis I Moore, Frank D Kolodige, David G Hellinga, Rufus C Seabron, Steven Rychnovsky, Jefferey Vasek, Robert W Scott, Renu Virmani. (2008). PhotoPoint photodynamic therapy promotes stabilization of atherosclerotic plaques and inhibits plaque progression.J Am College Cardiology52, 1024-1032.

Jonathan A Deane, Michael G Kharas, Jean S Oak, Linda N Stiles, Ji Luo,Travis I Moore, Hong Ji, Christian Rommel, Lewis C Cantley, Thomas E Lane, and David A Fruman. (2007). T-cell function is partially maintained in the absence of class IA phosphoinositide 3-kinase signaling.Blood109,2894-2902。

Kristen L Hess, Amber C Donahue, Kwan L Ng,Travis I Moore, Jean Oak, and David A Fruman. (2004). Frontline: The p85alpha isoform of phosphoinositide 3-kinase is essential for a subset of B cell receptor-initiated signaling responses.European J Immunology34, 2968-2976.