We report exceptionally large tunnel magnetoresistance (TMR) for biomolecular tunnel junctions based on ferritins immobilized between Ni and EGaIn electrodes. Ferritin stores iron in the form of ferrihydrite nanoparticles (NPs) and fulfills the following roles: (a) it dictates the tunnel barrier, (b) it magnetically decouples the NPs from the ferromagnetic (FM) electrode, (c) it stabilizes the NPs, and (d) it acts as a spin filter reducing the complexity of the tunnel junctions since only one FM electrode is required. The mechanism of charge transport is long-range tunneling which results in TMR of 60 10% at 200 K and 25 5% at room temperature. We propose a magnon-assisted transmission to explain the substantially larger TMR switching fields (up to 1 Tesla) than the characteristic coercive fields (a few Gauss) of ferritin ferrihydrite particles at T < 20 K. These results highlight the genuine potential of biomolecular tunnel junctions in designing functional nanoscale spintronic devices.

我们报告了基于固定在 Ni 和 EGaIn 电极之间的铁蛋白的生物分子隧道结的异常大隧道磁阻 (TMR)。铁蛋白以水铁矿纳米粒子 (NPs) 的形式储存铁并发挥以下作用：(a) 它决定了隧道势垒，(b) 它将 NPs 与铁磁 (FM) 电极磁性分离，(c) 它稳定了 NPs (d) 它充当自旋过滤器，降低隧道结的复杂性，因为只需要一个 FM 电极。电荷传输的机制是长程隧穿，导致 TMR 在 200 K 时为 60 ± 10%，在室温下为 25 ± 5%。我们提出了一个磁振子辅助传输来解释比铁蛋白水铁蛋白粒子的特征矫顽场（几个高斯）大得多的 TMR 开关场（高达 1 特斯拉）T < 20 K。这些结果突出了生物分子隧道结在设计功能性纳米级自旋电子器件方面的真正潜力。