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Pathology & Immunology

Houston, Texas

Pathology and Immunology
Pathology & Immunology
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Min Chen, Ph.D. - Faculty

Min Chen, Ph.D.Assistant Professor, Department of Pathology & Immunology

B.S., University of Science and Technology of China
Ph.D., University of Southern California
Postdoctoral fellow, National Institutes of Health

E-mail: minc@bcm.edu

Research Interests:

Molecular regulation of dendritic cell function - Dendritic cells, the most potent antigen-presenting cells, play pivotal roles in initiating and regulating the immune responses. Dendritic cells can produce a variety of cytokines that broadly engage all cells of the immune system. However, the inflammatory environment generated by dendritic cells is, if unchecked, as potentially damaging to the host cells as it is to invading pathogens. The immune system must therefore maintain a balance between the positive signals that activate dendritic cells, and the negative signals that inhibit their function. To understand how dendritic cell function is regulated, we are studying how temporal production of cytokines by dendritic cells are differentially regulated. We are interested in studying signal transduction pathways involved in dendritic cell activation, in particular those signaling molecules that can affect cytokine production by dendritic cells.

Autophagy in mitochondrial quality control and erythropoiesis - We are also studying the regulation of erythroid differentiation and mitochondrial quality control by autophagy. Autophagy is an evolutionally conserved cellular degradation process which can regulate both cell survival and cell death. Autophagy has been suggested to play an important role in removing damaged mitochondria and other organelles. Defective autophagy is associated with aging, cancer, and neurodegenerative diseases. We have recently identified a novel role for a Bcl-2 family member, Bnip3L/Nix, in regulating mitochondrial autophagy in reticulocytes. Loss of Nix causes defective sequestration of mitochondria into autophagosomes, elevated caspase activation and reduced lifespan of red blood cells in mice, leading to anemia. We are interested in further characterizing the molecular mechanisms for mitochondrial autophagy using the differentiating erythroid cells as a model. We are also interested in studying the role of autophagy in regulating functions of other cell types under both normal and disease settings.


Selected Publications:

  • Chen, M., Orozco, A., Spencer, D.M., and Wang, J. (2002). Activation of initiator caspases through a stable dimeric intermediate. J. Biol. Chem. 277:50761-50767.
  • Chen, M.*, Wang, Y.H., Wang, Y., Huang, L., Sandoval, H., Liu, Y.J., and Wang, J.* (2006) Dendritic cell apoptosis in the maintenance of immune tolerance. 311:1160-1164. Science 311:1160-1164.

  • Chen, M., Huang, L., Shabier, Z. and Wang, J. (2007) Regulation of the lifespan in dendritic cell subsets. Molecular Immunology 44:2558-2265.

  • Chen, M., Huang, L. and Wang, J. (2007) Deficiency of Bim in dendritic cells contributes to over-activation of lymphocytes and autoimmunity. Blood 109:4360-4367.

  • Chen, M.*, Guerrero, A.D., Huang, L., Shabier, Z., Pan, M., Tan, T.-H. and Wang, J.* (2007) Caspase-9-induced mitochondrial disruption through cleavage of anti-apoptotic Bcl-2 family members. J. Biol. Chem. 282:33888-33895.

  • Guerrero, A.D., Chen, M.*, and Wang, J.* (2008) Delineation of the caspase-9 signaling cascade. Apoptosis 13:177-186.

  • Sandoval, H., Thiagarajan, P., Dasgupta, S.K., Schumacher, A., Prchal, J.T., Chen, M.*, and Wang, J.* (2008) Essential roles for Nix in autophagic maturation of erythroid cells. Nature 454:232-235.

  • Chen, M.* and Wang, J. (2010) Programmed cell death of dendritic cells in immune regulation. Immunological Review 236:11-27.

    For a complete list of Dr. Chen's publications, visit PubMed.


    Contact Information:
Dr. Min Chen
Department of Pathology & Immunology
Baylor College of Medicine
One Baylor Plaza, BCM245
Houston, TX 77030

Phone: 713-798-6237
Fax: 713-798-3033
E-mail: minc@bcm.edu

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