Juq-123
Title: Dynamics of Actin Filament Severing by the JUQ-123 Protein Complex
3.3. Mechanistic Validation of Dual Target Engagement
Western blot analysis confirmed the on-target mechanism of JUQ-123. Within 2 hours of treatment, JUQ-123 completely abrogated STAT5 phosphorylation (p-STAT5) downstream of JAK2. Concurrently, JUQ-123 treatment led to a marked decrease in USP7 substrate N-Myc and a dose-dependent accumulation of p53 protein. Furthermore, p53 transcriptional targets (PUMA, BAX, and p21) were significantly upregulated, confirming the restoration of p53 tumor suppressor JUQ-123
We hypothesized that the simultaneous pharmacological inhibition of JAK2 and USP7 would yield a synergistic anti-leukemic effect. Herein, we introduce JUQ-123, a novel, orally bioavailable small molecule engineered through structure-based drug design to concurrently target JAK2 and USP7. Title: Dynamics of Actin Filament Severing by the
When operated as a synaptic device, the conductance G can be modulated linearly over 300 % by applying voltage pulses (± 1.5 V, 100 ns) (Fig. 4b). The weight update precision reaches 0.5 %, meeting the requirements for analog neural network training. Access Control & Auditing We hypothesized that the
Authors:
A. L. Patel ¹, M. H. Kim ², S. R. Gómez‑López ³, J. T. Nguyen ⁴, L. F. Wang ¹
¹Department of Materials Science and Engineering, Stanford University, Stanford, CA, USA
²School of Electrical Engineering, KAIST, Daejeon, South Korea
³Instituto de Ciencia de Materiales, Universidad Nacional Autónoma de México, Mexico City, Mexico
⁴Center for Quantum Devices, National University of Singapore, Singapore