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Long Cheng

Long Cheng, Ph.D., Post-doctoral Research Fellow

Long joined the Engle lab in December 2006 as a postdoctoral research fellow. He came from the Cellular and Molecular Physiology Department of Penn State University College of Medicine, where he did research on enzymes involved in lipid synthesis and the development of diabetes and obesity-related retinopathy. Prior to that, Long did post-doctoral research in the State Key Laboratory of Biomembrane and Membrane Biotechnology in Tsinghua University School of Medicine investigating the molecular mechanisms of cell signaling transduction pathways. In 2003, he received his Ph.D. from the Department of Neuroanatomy at Beijing University of Chinese Medicine. His thesis research concerned how cerebral lesions cause neural stem cells to proliferate and migrate, and differentiate, developing into mature neurons, and some factors that promote these processes. He is focusing on identifying Kif21a cargoes and on the function of the Kif21a motor protein in neuronal development

Publications (selected): research conducted in other labs:

  1. Cheng L, Zhu P, Si Y, Wu H, Xu H. The expression of bFGF and PCNA in the forebrain of adult rats with cortical devascularization, and the effects of total saponin from Panax notoginseng on it. Chinese Archives of Traditional Chinese Medicine. 2003, 21(5):687-689. (In Chinese)
  2. Si Y, Cheng L, Zhu P. Effect on neural stem cells in hippocampal dentate gyrus of adult rats after cortical devascularization. Chinese J Rehabilitation. 2004, 8(31):7016-7018. (In English)
  3. Zhu P, Cheng L, Si Y, Huang B, Wu H, Xu H. The progenitor cells in the anterior subventricular zone increase proliferation and migration from the migratory pathway to the lesioned site in the adult rat after cortical devascularization (1) the subependymal ventricular zone as a source of proliferating and migrating progenitors. Chinese J Neuroanat. 2005, 21(6);583-591. (In Chinese)
  4. Zhu P, Cheng L, Si Y, Huang B, Wu H, Xu H. The progenitor cells in the anterior subventricular zone increase proliferation and migration from that migratory pathway to the lesioned site in the adult rat after cortical devascularization (2) progenitors derived from the dorsolateral subventricular zone follow a migratory pathway through the corpus callosum to the lesioned site. Chinese J Neuroanat. 2006, 22 (1):21-26. (In Chinese)
  5. Rong Y, Cheng L, Ning H, Zou J, Zhang Y, Xu F, Liu L, Chang Z, Fu XY. Wilms' tumor 1 and signal transducers and activators of transcription 3 synergistically promote cell proliferation: a possible mechanism in sporadic Wilms' tumor. Cancer Res. 2006; 66(16):8049-8057.
  6. Ren Y*, Cheng L*, Rong Z, Li Z, Li Y, Li H, Wang Z, Chang Z. hSef co-localizes and interacts with Ras in the inhibition of Ras/MAPK signaling pathway. Biochem Biophys Res Commun. 2006, 347 (4), 988-993. (* Co-first author)
  7. Rong Z, Ren Y, Cheng L, Li Z, Li Y, Sun Y, Li H, Xiong S, Chang Z. Sef-S, an alternative splice isoform of the sef gene, inhibits NIH3T3 cell proliferation via a mitogen-activated protein kinase p42 and p44 (ERK1/2)-independent mechanism. Cellular Signaling. 2007; 19(1):93-102.
  8. Cao J, Cheng L, Shi Y. Catalytic properties of MGAT3, a putative triacylglycerol synthase. J Lipid Research. 2007; 48(3):583-591.
  9. Ren Y, Li Z, Rong Z, Cheng L, Li Y, Wang Z, Chang Z. Tyrosine 330 in hSef is critical for the localization and the inhibitory effect on FGF signaling. Biochem Biophys Res Comm. 2007; 354(3):741-746.
  10. Rong Z, Cheng L, Ren Y, Li Z, Li Y, Li X, Li H, Fu XY, Chang Z. Interleukin-17F signaling requires ubiquitination of interleukin-17 receptor via TRAF6. Cellular Signalling. 2007 (7):1514-1520.
  11. Ren Y, Rong Z, Li Z, Cheng L, Li Y, Wang Y, Ren F, David M, Chang Z. c-Cbl mediated ubiquitination and degradation of hSef. Progress Biochem Biophys. 2008, 35(1): 43-49.
  12. Ren Y*, Cheng L*, Rong Z, Li Z, Li Y, Zhang X, Xiong S, Hu J, Fu XY, Chang Z. hSef potentiates EGF-mediated MAPK signaling through affecting EGFR trafficking and degradation. Cellular Signalling. 2008; 20(3):518-533. (* Co-first author)
  13. Rong Z, Wang A, Li Z, Ren Y, Cheng L, Li Y, Wang Y, Ren F, Zhang X, Hu J, Chang Z. L-17RD (Sef or IL-17RLM) interacts with IL-17 receptor and mediates IL-17 signaling. Cell Res. 2009;19(2):208-215.
  14. Cheng L, Han X, Shi Y. A regulatory role of LPCAT1 in the synthesis of inflammatory lipids, PAF and LPC, in the retina of diabetic mice. Am J Physiol Endocrin Metab. 2009; 297(6):E1276-1282.

Publications in the Engle lab:

Miyake N, Chilton J, Psatha M, Cheng L, Andrews C, Chan WM, Law K, Crosier M, Lindsay S, Cheung M, Allen J, Gutowski NJ, Ellard S, Young E, Iannaccone A, Appukuttan B, Stout JT, Christiansen S, Ciccarelli ML, Baldi A, Campioni M, Zenteno JC, Davenport D, Mariani LE, Sahin M, Guthrie S, Engle EC. Human CHN1 mutations hyperactivate α2-chimaerin and cause Duane's Retraction Syndrome. Science. 2008; 321(5890):839-843.

Contact information:

Long Cheng, Ph.D.
Division of Neurology
CLS 14030.6
Children’s Hospital Boston
300 Longwood Avenue
Boston, MA, 02115
E-mail: lcheng@enders.tch.harvard.edu

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