1. Hartnett EB, Zhou M, Gong YN*, Chen YC.* (2022) LANCE: a Label-Free Live Apoptotic and Necrotic Cell Explorer Using Convolutional Neural Network Image Analysis. Analytical Chemistry. https://doi.org/10.1021/acs.analchem.2c00878 (*Co-corresponding)
2. Wang W, Wu S, Cen Z, Zhang, Y, Chen Y, Huang Y, Cillo AR, Prokopec J, Quarato G, Vignali DA, Stewart-Ornstein J, Li S, Lu L*, and Gong YN.* (2022) Mobilizing Phospholipids on Tumor Plasma Membrane Reveals Phosphatidylserine Externalization Blockade for Cancer Immunotherapy. Cell Reports. https://doi.org/10.1016/j.celrep.2022.111582 (*Co-corresponding, lead contact, Y-N. Gong)
3. Weihong Wang, and Yi-Nan Gong. (2022) MLKL Ubiquitylation: More Than a Makeover. Cell Death and Differentiation. https://doi.org/10.1038/s41418-022-00934-z
4. Weihong Wang, Joshua S. Prokopec, Yixin Zhang, Maria Sukhoplyasova, Himaly Shinglot, Man-Tzu Wang, Andreas Linkermann, Jacob Stewart-Ornstein*, and Yi-Nan Gong*. (2022) Sensing plasma membrane pore-formation induces chemokine production in survivors of regulated necrosis. Developmental Cell. (*Co-corresponding) https://doi.org/10.1016/j.devcel.2021.12.015
5. Gong YN*, Crowfard, JC, Heckmann BL, and Green DR*. (2018) To the edge of cell death and back. FEBS Journal. (co-Corresponding)
6. Gong YN, Guy C, Crowfard, J and Green DR. (2017) The biological events downstream of MLKL activation during necroptosis. Cell Cycle. 19, 1748-60
7. Gong YN, Guy C, Olauson H, Becker JU, Yang M, Fitzgerald P, Linkermann A, Green DR. (2017) Components of the ESCRT-III machinery act downstream of MLKL to regulate necroptotic cell death and its consequence. Cell. 169, 286-300
8. Ge J*, Gong YN*, Xu Y, Shao F. (2012) Preventing bacterial DNA release and absent in melanoma 2 inflammasome activation by a Legionella effector functioning in membrane trafficking. Proc. Natl. Acad. Sci., 109, 6193-6398. (*Co-first author)
9. Gong YN, Wang X, Wang J, Yang Z, Li S, Yang J, Liu L, Lei X, Shao F.(2010)Chemical probing reveals insights into the signaling mechanism of inflammasome activation. Cell Res., 20:1289- 305.
Plasma membrane dynamics and signaling
Since the appearance of the first cells on Earth 4 billion years ago, the cell membrane serves the essential role of segregating the external environment and creating an internal environment, where genetic materials can reside, and biochemical reactions can take place. Meanwhile the cell membrane also faces a variety of external conditions that cause stress, including the compromise of the membrane integrity.
Given that the cell membranes are the first defenders against external (sometimes even internal) stress, in theory, perturbations that may disrupt the any type of cell membrane function should activate a multifactorial defend mechanism. We are studying how plasma membrane damage/repair and lipid mobilization affect both innate and adaptive immune system. We also explore how these signaling evolves during system development.
Tumor cell death re-programmer
To achieve a robust anti-tumor response, we will find novel ways to “kill” those tumors in an immune system favorable way. To reprogram the cell death, we will use multiple CRIPSR technologies, including genome-wide CRISPR screening and CROP-seq (CRISPR then scRNAseq). Our ultimate goal is to treat cancer by modulating cell death program.
Tumor cell death probing
Collaborating with physicians, our lab have collect probes to detect several major types of cell death in responding to all kinds of treatments, including those are still on the clinic trails. We can also set up real-time recording system for various tumor cell death. We provide insights into analyzing or predicting the therapeutic outcomes from a “cell death” angle.