Su-Jung Park, PhD

Assistant Research Professor of Pediatrics


  • PhD:Cell Biology & Biochemistry University of InJe, south Korea


  • Pak2 regulates hematopoietic progenitor cell proliferation, survival, and differentiation .Zeng Y, Broxmeyer HE, Staser K, Chitteti BR, Park SJ, Hahn S, Cooper S, Sun Z, Jiang L, Yang X, Yuan J, Kosoff R, Sandusky G, Srour EF, Chernoff J, Clapp DW. Stem Cells. 2015 (5):1630-41. PMID: 25586960
  • Gehlhausen JR, Park SJ, Hickox AE, Shew M, Staser K, Rhodes SD, Menon K, Lajiness JD, Mwanthi M, Yang X, Yuan J, Territo P, Hutchins G, Nalepa G, Yang FC, Conway SJ, Heinz MG, Stemmer-Rachamimov A, Yates CW, Clapp DW. A murine model of neurofibromatosis type 2 that accurately phenocopies human schwannoma formation. Hum Mol Genet. 2015 Jan 1;24(1):1-8. PMCID: PMC4262489 [Available on 2016-01-01]
  • Social learning and amygdala disruptions in Nf1 mice are rescued by blocking p21-activated kinase. Molosh AI, Johnson PL, Spence JP, Arendt D, Federici LM, Bernabe C, Janasik SP, Segu ZM, Khanna R, Goswami C, Zhu W, Park SJ, Li L, Mechref YS, Clapp DW, Shekhar A. Nat Neurosci. 2014 (11):1583-90..
  • Staser K, Park SJ, Rhodes S, Zeng Y, He YZ, Shew M, Gehlhausen J, Cerabona D, Chen S, Sun Z, Nalepa G, Yang FC, Clapp DW. (2013). Normal hematopoiesis and neurofibromin-deficient myeloproliferative disease require Erk. Journal of Clinical Investigation, 123(1):329-34. PMCID: PMC3533306.

Current Research Interests:

As a member of the Clapp laboratory, I am currently studying unknown the ubiquitin-proteasome pathway (UPP) of NF1 tumor suppressor protein. Neurofibromatosis type 1 (NF1) is the most common genetic disease in human with a predisposition to cancer and is caused by mutations of NF1 tumor suppressor gene that functions as GAP for Ras. The molecular mechanism of NF1 haploinsufficiency has unknown, yet, primary mechanism of haploinsufficiency is due to insufficient protein level. Neurofibromin expression is not only diminished by genetic loss and epigenetic lesion but also the protein itself is a target for accelerated degradation. In light of the NF1 haploinsufficient degradation by Ubiquitin-Proteasome Pathway (UPP) is clinically importance. However little is known about the molecular mechanism for degradation of neurofibromin by Ubiquitin-Proteasome Pathway. The goal of study is to contribute to develop the new therapeutic approaches to treat NF1 syndrome where neurofibromin is chronically destabilized.

Su, PhD
Office: 317-274-2981
Address: 1044 West Walnut Street, R4-#414, Indianapolis, IN 46202