Jialing Xiang

  • Professor of Biology
  • Chair of Biology Graduate Affairs Committee


M.D. Xuzhou Medical University
Ph.D. University of Alabama at Birmingham

Research Interests

The work in my laboratory is focused on answering the basic biological questions at the molecular level related to human diseases. The research areas include program cell death, signaling transduction, and cellular protein membrane trafficking. One of the major projects involves proapoptotic Bcl-2 family members, such as Bax and Bad. We identified a unique Bax isoform, which may serve as a prognostic marker for cancer chemotherapy. We also defined a broad signaling interplay between apoptotic pathway and other signaling pathways, involving many pathological events, such as hormone refractory and inflammation. We believe that study of the cellular signaling process will help our understanding of the molecular basis of human diseases and identify cellular targets for the effective treatment.


  • Yao Q, Zhang H, Zhao Y, Ye Z, Lee YJ, Xiang J (2018). The C-terminus of Ubl4A is critical for pro-death activity and association with the Arp2/3 complex. Biochem Biophys Res Commun. 2018 Sep 18;503(4):3192-3197. doi: 10.1016/j.bbrc.2018.08.123
  • Chen X, Wang L, Roozbahani GM, Zhang Y, Xiang J, Guan X (2018). Nanopore label-free detection of single-nucleotide deletion in Baxα/BaxΔ2
  • Electrophoresis. 2018 Jul 12. doi: 10.1002/elps.201800193. [Epub ahead of print]
  • Yan J, Zhang H, Xiang J, Zhao Y, Yuan X, Sun B, Lin A (2018). The BH3-only protein BAD mediates TNFα cytotoxicity despite concurrent activation of IKK and NF-κB in septic shock. Cell Res. 2018 Jul;28(7):701-718. doi: 10.1038/s41422-018-0041-7
  • Chen X, M Roozbahani G, Ye Z, Zhang Y, Ma R, Xiang J, Guan X (2018). Label-Free Detection of DNA Mutations by Nanopore Analysis.ACS Appl Mater Interfaces. 2018 Apr 11;10(14):11519-11528. doi: 10.1021/acsami.7b19774
  • Mañas A, Davis A, Lamerand S, Xiang J (2018). Detection of pro-apoptotic Bax∆2 proteins in the human cerebellum. Histochem Cell Biol. 2018 Jul;150(1):77-82. doi: 10.1007/s00418-018-1669-6
  • Mañas A, Chen W, Nelson A, Yao Q, Xiang J (2018). BaxΔ2 sensitizes colorectal cancer cells to proteasome inhibitor-induced cell death. Biochem Biophys Res Commun. 2018. 496(1):18-24. DOI: 10.1016/j.bbrc.2017.12.156
  • Mañas A, Wang S, Nelson A, Li J, Zhao Y, Zhang H, Davis A, Xie B, Maltsev N, Xiang J (2017). The functional domains for Bax∆2 aggregate-mediated caspase 8-dependent cell death. Exp Cell Res. 2017. 359(2):342-355. DOI: 10.1016/j.yexcr.2017.08.016
  • Zhao Y, Zhang H, Affonso C, Bonomo R, Mañas A, Xiang J (2017). Deficiency in ubiquitin-like protein Ubl4A impairs migration of fibroblasts and macrophages. Biochem Biophys Res Commun. 2017. 483(1):617-623. DOI: 10.1016/j.bbrc.2016.12.094
  • Zhao Y, Lin Y, Zhang H, Mañas A, Tang W, Zhang Y, Wu D, Lin A, Xiang J (2015). Ubl4A is required for insulin-induced Akt plasma membrane translocation through promotion of Arp2/3-dependent actin branching. Proc Natl Acad Sci USA. 2015. 112(31):9644-9649. PMID: 26195787, PMCID: PMC4534221
  • Zhang H, Tassone C, Lin N, Mañas A, Zhao Y, Xiang J (2015). Detection of Bax Microsatellite Mutations and BaxΔ2 Isoform in Human Buccal Cells. J Cell Sci Ther. 2015. 6(Suppl 8): 002. DOI: 10.4172/2157-7013.S8-002
  • Zhang H, Lin Y, Manas A, Zhao Y, Denning MF, Ma L, Xiang, J. (2014) Bax∆2 promotes apoptosis through caspase-8 activation in microsatellite unstable colon cancer. Mol. Cancer Res. 12(9), 1225-23.
  • Haferkamp, B., Zhang, H., Kissinger, S., Xin, W., Lin, Y., Schultz, M., Xiang, J. (2013) BaxΔ2 family alternative splicing salvages Bax microsatellite-frameshift mutations. Genes & Cancer. 4, 501-512.
  • Yan, J., Xiang, J., Lin, Y., Ma, J., Zhang, J., Zhang, H., Sun, J., Danial, N., Liu, J., Lin, A. (2013). Inactivation of BAD by IKK inhibits TNFα-induced apoptosis independently of NF-κB activation. Cell. 152(1), 304-315.
  • Lin, Y., Lu, Z., Kokontis, J., Xiang, J. (2013). Androgen receptor primes prostate cancer cells to apoptosis through down-regulation of basal p21 expression. Biochem. Biophys. Res. Commun. 430(1), 289-93.
  • Haferkamp, B., Zhang, H., Lin, Y., Yeap. X, Bounce, A., Sharpe, J., Xiang, J. (2012). BaxΔ2 is a novel Bax isoform unique to microsatellite unstable tumors. J. Biol. Chem. 287(41), 34722-9.
  • Godfrey, B., Lin, Y., and Xiang, J. (2010). Structure and function analysis of the pro-death domains of androgen receptor in prostate cancer cells. Cell Res. 20: 1138-1140.
  • Tang F, Kokontis J, Lin Y, Liao S, Lin A, Xiang, J. (2009).Androgen via p21 inhibits TNF-alpha-induced JNK activation and apoptosis. J. Biol. Chem. 284(47), 32353-8.
  • Deng, H., Yu, F., Chen, J., Zhao, Y., Xiang, J., Lin, A. (2008). Phosphorylation of bad at Thr201 by JNK1 promotes glycolysis through activation of phosphofructokinase-1. J. Biol. Chem. 283(30):20754-60.
  • Lin, Y., Fukuchi, J., Hiipakka, R., Kokontis, J., and Xiang, J. Up-regulation of Bcl-2 is required for the progression of prostate cancer cells from androgen-dependent to androgen-independent growth. Cell Res. 17(6), 531-536 (2007).
  • Lin, Y., Kokontis, J., Tang, F., Liao, S., Lin, A., Chen, C., and Xiang, J. Androgen and Its Receptor AR Promote BAX-mediated Apoptosis. Mol. Cell. Biol. 26(5), 1908 –1916 (2006).
  • Yu, C., Minemoto, Y., Zhang, J., Liu, J., Tang, F., Bui, T., Lin, A.* and Xiang, J*. Activation of the JNK pathway inhibits IL-3 withdrawal induced apoptosis in B-lymphocytes. Molecular Cell. 13, 329-340 (2004).
  • Xiang, J., Gomez-Navarro, J, Arafat, W., Liu B., Barker, S.D., Alvarez, R.D., Siegal G.P., and Curiel, D.T. Pro-apoptotic treatment with an adenovirus encoding bax enhances the effect of chemotherapy in ovarian cancer. J. Gene Medicine 2(2), 97-106 (2000).
  • Xiang, J., Chao, D.T., and Korsmeyer, S.J. Bax-induced cell death may not require interleukin 1 b-converting enzyme-like proteases. Proc. Natl. Acad. Sci. USA. 93, 14559-14563 (1996).


  • Molecular cell biology
  • Signaling network
  • Programmed cell death
  • Cancer biology
Jialing Xiang

Contact Information

312.567.3491 312.567.3494 294 Robert A. Pritzker Science Center