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Kole T. Roybal

Researcher at University of California, San Francisco

Publications -  66
Citations -  5347

Kole T. Roybal is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Chimeric antigen receptor & T cell. The author has an hindex of 20, co-authored 58 publications receiving 3910 citations. Previous affiliations of Kole T. Roybal include University of Bristol & University of Texas Southwestern Medical Center.

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Mania-like behavior induced by disruption of CLOCK.

TL;DR: It is shown that mice carrying a mutation in the Clock gene display an overall behavioral profile that is strikingly similar to human mania, including hyperactivity, decreased sleep, lowered depression-like behavior, lower anxiety, and an increase in the reward value for cocaine, sucrose, and medial forebrain bundle stimulation.
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Precision Tumor Recognition by T Cells With Combinatorial Antigen-Sensing Circuits.

TL;DR: A combinatorially activated T cell circuit in which a synthetic Notch receptor for one antigen induces the expression of a CAR for a second antigen opens the door to immune recognition of a wider range of tumors.
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Engineering Customized Cell Sensing and Response Behaviors Using Synthetic Notch Receptors.

TL;DR: It is found that chimeric forms of Notch, in which both the extracellular sensor module and the intracellular transcriptional module are replaced with heterologous protein domains, can serve as a general platform for generating novel cell-cell contact signaling pathways.
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Remote control of therapeutic T cells through a small molecule-gated chimeric receptor

TL;DR: The ON-switch CAR exemplifies a simple and effective strategy to integrate cell-autonomous decision-making with exogenous, reversible user control and highlights the importance of developing optimized bio-inert, orthogonal control agents such as small molecules and light, together with their cellular cognate response components, in order to advance precision-controlled cellular therapeutics.
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CRISPR/Cas9-mediated PD-1 disruption enhances anti-tumor efficacy of human chimeric antigen receptor T cells.

TL;DR: In this paper, a protocol for combined Cas9 ribonucleoprotein (Cas9 RNP)-mediated gene editing and lentiviral transduction was developed to generate PD-1 deficient anti-CD19 CAR T cells.