Yuanyuan Liu, PhD

Dr. Yuanyuan Liu

Stadtman Tenure Track Investigator
Somatosensation and Pain Unit

NIH NIDCR
Building 35A Room 3E410
35A Convent Drive, MSC 3757
Bethesda, MD 20892
United States

(301) 496-4898
Research Interests

Descending supraspinal pathways integrate signals from multiple brain regions and are the neural basis by which our brain controls our body. As yet, the design principles for such top-down control remain elusive. The mission of our lab is: (1) To decipher supraspinal circuits in somatosensory perception. (2) To investigate the underlying mechanisms of top-down control in chronic pain states. To achieve these goals, we will use a multidisciplinary approach combining intersectional viral-mediated gene manipulation, in vivo imaging, and electrophysiological and single-cell sequencing techniques. Ultimately, our research will help explain how our mental states directly alter normal and pathological somatosensory perception in different contexts or mood states, and will uncover potential targets for treating pain.

Biographical Sketch

Dr. Yuanyuan (Kevin) Liu obtained his BS degree in biological pharmacy in Nanjing University, China. He received his PhD in Dr. Ben Szaro’s lab at the State University of New York, focusing on the role of an RNA binding protein in axon development and regeneration in Xenopus Laevis. He completed his postdoc training in Dr. Zhigang He’s lab at Boston Children’s Hospital, Harvard Medical School. During his postdoc career, he optimized an elegant, multi-step viral-based intersectional targeting tool, which he used to dissect the role of corticospinal neurons in controlling distinct spinal circuits involved in fine motor control and tactile sensation. He joined NIDCR/NCCIH in 2020 and will continue his work to decipher the supraspinal circuits which control somatosensory perception and pain.

Selected Publications
  1. Barak, B., Zhang, Z., Liu, Y., Nir, A., Trangle, S., Ennis, M., Levandowski, K., Wang, D., Quast, K., Boulting, G., Li, Y., Bayarsaihan, D., He, Z. and Feng, G. Neuronal deletion of Gtf2i, associated with Williams syndrome, causes behavioral and myelin alterations rescuable by a remyelinating drug. Nat. Neurosci. 22: 700-708 (2019).
  2. Liu, Y., Latremoliere, A., Li, X., Zhang, Z., Chen, M., Wang, X., Fang, C., Zhu, J., Alexandre, C., Gao, Z., Chen, B., Ding, X., Zhou, J., Chen, C., Wang, K., Woolf, C.J., and He, Z. Touch and tactile neuropathic pain sensitivity are set by corticospinal projections. Nature 561: 547–550 (2018).
  3. Wang, X.*, Liu, Y.*, Li, X., Zhang, Z., Yang, H., Zhang, Y., Williams, P.R., Alwahab, N.S.A., Kapur, K., Yu, B., Zhang, Y., Chen, M., Ding, H., Gerfen, C.R., Wang, K.H., and He, Z. Deconstruction of corticospinal circuits for goal-directed motor skills. Cell 171: 440-455 (2017). *Equal contribution.
  4. Liu, Y., Wang, X., Li, W., Zhang, Q., Li, Y., Zhang, Z., Zhu, J., Chen, B., Williams, P. R., Zhang, Y., Yu, B., and He, Z. A sensitized IGF1 treatment restores corticospinal axon-dependent functions. Neuron 95: 817-833 (2017).
  5. Jin, D., Liu, Y., Sun, F., Wang X., Liu, X., and He, Z. Restoration of skilled locomotion by sprouting corticospinal axons induced by co-deletion of PTEN and SOCS3. Nat. Commun. 6:8074 (2015).
  6. Liu, Y., Yu, H., Deaton, S.K., and Szaro, B.G. hnRNP K, an RNA-binding protein, is required for optic axon regeneration in Xenopus laevis. J. Neurosci. 32: 3563-3574 (2012).
  7. Liu, Y., and Szaro, B.G. hnRNP K post-transcriptionally co-regulates multiple cytoskeletal genes needed for axonogenesis. Development 138: 3070- 3090 (2011). 8)
  8. Liu, Y., Gervasi, C., and Szaro, B.G. A critical role for hnRNP K in axon development in Xenopus Laevis. Development 135: 3125-3135 (2008).
Last Reviewed on
January 2020