This resume summarizes the qualifications of Jane Yang, a scientist with extensive experience in cancer biology, transcriptional and epigenetic regulation, and cell differentiation. She has over 15 years of research experience, including positions at Genentech and Stanford University where she led projects discovering new mechanisms of action for small molecule inhibitors and identifying protein complexes involved in cell fate decisions. Her publications include high-impact articles in journals such as Cell Death and Differentiation and Genes & Development. She has strong skills in molecular and biochemical techniques and has received competitive NIH funding and honors for her work.

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Jane Yang, PhD
261 La Cuesta Dr., Portola Valley, CA 94028 Ι janeyangzte@gmail.com Ι (206) 218-3796
http://www.linkedin.com/pub/jane-yang-phd/5/104/7a5
Scientist who thrives in a team-oriented environment and employs critical thinking and extensive hands-
on experience to advance challenging projects with competing priorities. Experimentalist, a proven
ability to rapidly devise practical tests of hypotheses using multidisciplinary approaches. Dot connector,
seeking out expertise and initiating collaborations in diverse fields. Good listener, mentored and trained
research associates on independent projects.
Core Competencies:
 Transcriptional and epigenetic regulation
 Cancer biology
 Cell differentiation and development
 Early discovery and mechanisms of action
 Chemical and genetic modulation of cell fate and behavior
 Publications and awarded competitive research grants.
Technical Skills:
 Molecular and biochemical methodologies
 Proteomic, genomic, and epigenetic approaches
 Mammalian and bacterial protein expression and purification
 Cell- and enzyme-based assays
 Multicolor flow cytometry and microscopy
 Tissue cultures, primary cells, mouse embryo work
PROFESSIONAL EXPERIENCE
Visiting Scientist 2/2015 – 9/2016
Early Discovery Biochemistry, Genentech, South San Francisco, CA
Discovered new mechanisms of action of two small molecule inhibitors in order to advance early stage
research and discovery programs in therapeutic targeting of bromodomains (manuscript in preparation).
 Identified erythroleukemia cells and primary erythroid precursors as model systems, leading to
two unique cell-based functional characterizations of the small molecules.
 Defined drug dosage range and temporal window of activity through identifying and analyzing
induction of apoptosis and expression of target genes and cell-fate surface markers.
 Designed, expressed, and purified one transcription factor heterodimer; devised in vitro and in
vivo acetylation assays for inter- and intra-team collaborations aimed at epigenetic inhibitors.
Research Scientist 3/2008 – 2/2015
Stanford University, Stanford, CA
Designed and applied genetic and chemical approaches to modulate cell fate and cell behavior in
response to genotoxic stress, somatic reprogramming to pluripotency, and Wnt signaling.
Project I: A multidisciplinary collaboration in discovering a previously unknown mechanistic link
between p53 and muscle differentiation in response to genotoxic stress, clarified a discrepancy in

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understanding p53 as a stress sensor in regulating muscle cell fate, and confirming existence of a
differentiation checkpoint control (Yang et al., 2015, a featured article with an editorial highlight).
 Designed and executed five independent cell-based assays and collected complex data sets to
study impact of genotoxic stress on cell fate and behavior during muscle differentiation.
 Led three technical innovations:
 Quantitatively tuning p53 protein levels to control cell fate output;
 Simultaneous characterization of cell cycle and a nuclear factor by flow cytometry;
 Visualization and quantification of post-mitotic nuclear integrity under genotoxic stress.
 Discovered one novel enhancer bound by stress-sensing p53 and active histone markers.
 Supported the PI in grant writing and preparation of manuscripts and guided research associates
in experimental design and data interpretation in a chemical engineering research environment.
Project II: Identified protein complexes of activation-induced cytidine deaminase (AID); Developed a
plasmid-based methylation-specific PCR and bisulfite sequencing of promoters of pluripotent genes.
Project III: Quantified cell polarity and migration of primary myoblasts in a chemotactic Wnt gradient.
Postdoctoral Research (NIH/NCI F32 National Research Service Award) 10/2003 - 3/2008
Fred Hutchinson Cancer Research Center, Seattle, WA
Applied large-scale genomic and proteomic datasets to identify and validate oncogenic factors,
discovered a novel mechanism of programming human rhabdomyosarcoma cells to terminal
differentiation; Opened new avenues for biomarker identification and design of differentiation therapy
(Yang et al., 2009) (Reviewed by F1000).
Staff Scientist – Gene Switch Project 7/2001 - 9/2003
Maxygen Inc., Redwood City, CA
Evolved Aspergillus nidulans transcriptional factor AlcR by constructing site-directed degenerate
libraries and family-shuffled DNA libraries based on fragmentation and homology-dependent
reassembly of orthologues; Exceeded project goal by improving AlcR transactivation by 15 fold.
Doctoral Research (NIH Biotechnology Training Grant Fellowship) 9/1996 - 6/2001
University of California at Davis, Davis, CA
Interrogated transcriptional regulation by thyroid hormone receptors (Yang et al., 2001 and 1999).
EDUCATION
Ph.D. Microbiology, University of California at Davis, CA. 2001
M.S. Plant Virology, University of Minnesota at Twin Cities, MN. 1995
B.S. Plant Pathology, China Agricultural University, P. R. China. 1992
HONORS AND AWARDS
 NIH/NCI F32 Ruth L. Kirschstein National Research Service Award (NRSA) (2006 - 2009)
 FHCRC/Amgen Interdisciplinary Training Grant (2005 - 2006)
 Fred Hutchinson Cancer Research Center Travel Grant (2006) and Course Award (2005-2006)
 NIH/Amgen Biotechnology Training Grant Fellowship, UC Davis (1998 - 2001)
 Excellent Undergraduate Scholarships at CAU, Beijing, China (1989 - 1992)

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PUBLICATIONS
 Yang, Z., Kenzelmann Broz, D., Noderer, W. L., Ferreira, J. P., Overton, K. W., Spencer, S. L.,
Meyer, T., Tapscott, S. J., Attardi, L. D., and Wang, C. L. (2015) p53 suppresses muscle
differentiation at myogenin step. Cell Death & Differentiation 22: 560-573.
Featured article with an editorial ‘Muscle gets stressed? p53 represses and protects’.
 Yang, Z., MacQuarrie, K., Analau, E., Tyler, A., Dilworth, F.J., Cao, Y., Diede, S., and Tapscott, S.
J. (2009) MyoD and E-protein heterodimers switch rhabdomyosarcoma cells from an arrested
myoblast phase to a differentiated state. Genes & Development 23: 694-707 (Reviewed by Faculty
1000).
 Olguin H. C., Yang, Z., Tapscott, S. J., and Olwin, B. B. (2007) Reciprocal inhibition between Pax7
and MRFs modulates myogenic cell fate determination. Journal of Cell Biology 177(5): 769-779.
 Yang, Z., Nicolaisen, M., Olszewski, N. E., and Lockhart, B. E. L. (2005) Sequencing, improved
detection, and a novel form of Kalanchoë top-spoting virus. Plant Disease 89 (3): 298-302.
 Hong, S.-H., Yang, Z., and Privalsky, M. L. (2001) Arsenic trioxide is a potent inhibitor of the
interaction of SMRT corepressor with its transcription factor partners, including the PML-RARα
oncoprotein found in human acute promyelocytic leukemia. Molecular and Cellular Biology 21(21):
7172-7182.
 Yang, Z. and Privalsky, M. L. (2001) Isoform-specific transcriptional regulation by thyroid hormone
receptors: hormone-independent activation operates through a steroid receptor-mode of coactivator
interaction. Molecular Endocrinology 15 (7): 1170-1185.
 Yang, Z., Hong, S.-H., and Privalsky, M. L. (1999) Transcriptional anti-repression: Thyroid hormone
receptor beta-2 recruits SMRT corepressor but interferes with subsequent assembly of a functional
corepressor complex. Journal of Biological Chemistry 274 (52): 37131-37138.