Felicia Zhao

Tel: 978-***-**** (C)

Email: acvstx@r.postjobfree.com

Education:

MS. Cell and Molecular Biology, Southern Connecticut State University

MD. Medicine, Third Military Medical School, Chongqing, China

Summary:

Over fifteen years of working experience in pharmaceutical industry. Broad skills and knowledge of immunology, cellular and molecular biology as well as therapeutic antibody drug in cancer and auto-immune diseases are developed. Familiarity with immune cellular and molecular biology assays including primary immune cell purification, culture and cell based assay for target validation and function study of therapeutic antibodies and small molecular, T cell activity and proliferation, cytokine profile, MDDC culture and ADCC. flow cytometry, FloJo Analysis, ELISA, MSD, SDS-PAGE, Western Blot, protein purification, immunocytochemistry, DNA and RNA purification, plasmid cloning, lentivirus based siRNA, and qRT-PCR.

Professional Experience:

Horizon Discovery, Cambridge, MA 2015-now

Principle associate scientist, Immune Oncology

Assay development to support immune oncology novel drug discovery. Purify PBMCs, T cell and monocyte. Performed the mammalian cell culture, primary T cells and monocyte cell culture and cell activation and proliferation. Purifying NK cells and performed NK mediated ADCC. Phenotyping NK and evaluate NK activity function by flow cytometry. Induced, cultured and phenotyping of MDDC for MLR (APC/T). Performed flow cytometry for assay development of NK mediated ADCC, bispecific antibody function, and T cell activation and proliferation (with SEB super antigen). Performed HTRF assay and ELISA to determine cytokines, IL-2; IFN granzyme-B. Isolated Tregs and performed Tregs function assay.

EMD Serono, Billerica, MA 2013 - 2015

Scientist I, Cellular & Translational Immunology

Validating novel targets in inflammatory and autoimmune disease for the development of innovative medicines. Performed flow cytometry to identify Foxp3 expression in human Tregs cells proliferation under the target genes over expression and lentivirus based siRNA silent. Performed cell based assay, T cell and B cell proliferation assay, MLR, MSD, ELISA, alphaLISA, Western blotting for identification of mechanisms driving disease pathogenesis and novel targets; bi-function drug signaling pathway, and compound screening

Validating biomarker of bi-specific function drug for auto-immune disease. Isolated and cultured PBMC. Purifying monocytes, B cells and T cells from human blood with Auto-MACS. Generated MDDC and performed MLR of MDDC with T cells. Analyzed samples by Wes (New Western Blotting System). Developed assays to identify and validate novel target in dendritic cells that directly phosphorylated a key protein of TLR signaling path.

Designed, developed and performed multi-assays to conform our hypothesis. The results confirmed that phosphorylation of the key protein by this target play a key role for T cell activity and proliferation. The assays developed was used for drug screening.

Induction of NETOsis from neutrophils of health and SLE patients. Produced NETOsis supernatant to identify whether the NETOsis supernatant induce RPTEC (or other cell line) secreting inflammation factors, for instance IL-6. Performed ELISA and alphaLISA to detect cytokines.

MIT (Massachusetts Institute Technology), Cambridge, MA 2010-2011

Scientist

Independently executed cellular and molecular assays to investigate signaling pathway involved in the protein transfer disorder disease. Executed cellular and molecular assays to investigate/identify a novel molecular which involved post-synaptic molecules translocation.

Maintained mammalian cell culture and primary neuron culture. Executed transfection and transduction on mammalian cell lines and primary neuron. Performed Western Blot, purified synoptic membrane protein, PCR, RT-PCR to support the investigation of post synoptic flexibility. We found that two transport protein mutations may affect the post synoptic signaling pathway and post synoptic membrane flexibility. Our results suggest that spontaneously negative mutation of the V gene causes the proteins transfer disorder and decreased the proteins/receptors density at post-synaptic which leads signal transduction disorder.

Merck Research Laboratories Boston, MA 2006 – 2009

Research Biologist, Neuroscience Drug Discovery

Targets validation and identification for novel drug discovery. Performed DNA and RNA purification. Designed and performed molecular cloning for target genes expression and silent. Executed mammalian cell culture and performed stable and transient transfection. Generated stable cell lines. Optimized condition of genes expression and protein products on mammalian cells. Isolated primary cell from tissue and executed primary cell culture and transduction. Executed immunocytochemistry and InCell assay, PCR and qRT-PCR, Western Blot, ELISA, enzyme activity assay and MSD to support target validation projects. Evaluated and confirmed target genes function and provided critical information that led to project Go/No go decision making.

Assays development for target validation. Developed immunoassay to identify immunotherapy antibody, vaccine and biomarker. Developed lentivirus based siRNA/miRNA gene silent assay; enzyme activity assay; TA sub-cloning assay for stable cell line; biochemistry assay to identify pathogenic target.

Developing therapeutic antibody and vaccine. Developed and optimized direct ELISA to detect antigen specific antibodies from immunized Tg animal. Mapping binding epitope. Performed immunoassay to determine biomarker.

Eli Lilly and Company (Pharmaceutic), Indianapolis, IN 1998-2005

Biologist, Department of Discovery

Discovering novel genes product which may be new target candidates for class-I medicine with modern technology. Generated gene engineered knock out (KO) and transgenic (Tg) animal models to elucidate the target genes function and the novel targets for drug discovery.

Generated m-LIGHT knock out (KO) construct to create m-LIGHT deficiency animal model. Catheterized KO mice of m-LIGHT, an immune modulator. Performed T cell proliferation and toxicity assay to evaluate m-Light function on CD4+ and CD8+ T cells. Performed Western and ELISA assay as requirement. Our data suggest that m-Light is an immune modulator. LIGHT-deficiency impairs CD8+ T cell expansion which may be a target for cancel treatment.

Yale Medical School, New Haven, CT 1993 – 1998

Post-Doctoral Associate

Study immune network theory. Created B-lymphocyte hybridoma cell and generated anti-idiotype monoclonal antibody to acetylcholine receptor (rabies virus receptor). Isolated B cells from spleen. Performed mouse B-lymphocytes and tumor cells fusion to generate hybridoma cell line. Affinity purify (Fab)2 fragment of the antibody. Executed ELISA, immunocytochemistry, and immunohistochemistry assay to characterize anti-idiotype monoclonal antibody. Examined and evaluated the effect of anti-idiotype monoclonal antibody in vitro and in vivo animal models.

Our study suggests that anti-idiotype antibody against AchR induces neutral antibody to rabies virus witch may be a candidate of rabies virus vaccine.

Research Associate

Isolated and characterized three novel protein tyrosine phosphotase (PTP) genes, STEP64; STEP38 and STEP20 from phage cDNA library. Sub-cloning STEP64 gene fragment and analysis gene sequence to identify full length gene and ORF. Sequencing analysis to identify function domains. Performed point mutation to identify PTP enzyme function domain. Generated and purified recombinant protein. Executed transfection, sucrose gradient, Western blot, immunocytochemistry and enzyme activity assay to characterize novel PTP, STEP. Results suggest that STEP is a family which consists of cytosol, trans-membrane and truncated isoforms. Gene alternative splicing generates theses isoforms.

Publications:

Kumar S, Zhao F, Myaskovsky A, Kifle L, McCarty M, France D, Steiger J, Ann F. Development of an in vitro screening platform for high-capacity evaluation of immunomodulatory drug candidates. Poster ACCR of 2016.

W. Frank An, Sujatha Kumar, Cristina Ghirelli, Kim Hoenderdos, Tabasum Huseni, Thibault Laurent, Lydia Kifle, Felicia Zhao, Simon Scrace, Chris Lowe, Anatoly Myaskovsky, Janine Steiger, Nicola McCarthy, and Jonathan Moore. An integrated immuno-oncology platform using high-throughput cell based assays, gene editing and genomic screens in immune cells, AACR Abstract.

Zhao F, Berengere Bouzou, Sarah J. Augood. Gene Expression Changes in Striatal neurons of a mouse model of Huntington's disease: A Combined LCM and Microarray Study, 2005.

Lu JQ, Schmidt CS, Zhao F, Okragly AJ, Glasebrook A, Fox N, Galbreath E, Zhang Q, Song HY, Na SQ and Yang DD. LIGHT-deficiency impairs CD8+ T cell expansion, but not effector function. 15(7): 861-870 Journal of immunology, 2003

Bogue CW, Ganea G, Sturm E, Zhao F, and Jacobs HC. Divergent homeobox gene Hex regulates promoter of the Na+-dependent bile acid cotransporter. Am J Physiol Gastrointest Liver Physiol 279: G347-G355, 2000

Bult A. Zhao F. Dirkx R. Raghunathan A. Solimena M. Lombroso PJ. STEP: a family of brain-enriched PTPs. Alternative splicing produces transmembrane, cytosolic and truncated isoforms. European Journal of Cell Biology. 72(4): 337-44, 1997

Zhao F. Bult A. Dirkx R Jr. Sharma E. Lukacsi E. Solimena M. Naegele JR. Lombroso PJ. STEP61: a member of a family of brain-enriched PTPs is localized to the endoplasmic reticulum. Journal of Neuroscience. 16(24): 7821-31, 1996 Dec 15.

Sharma E. Zhao F. Bult A. Lombroso PJ. Identification of two alternatively spliced transcripts of STEP: a subfamily of brain-enriched protein tyrosine phosphates. Brain Research. Molecular Brain Research. 32(1): 87-93, 1995

Hanham CA. Zhao F. Tignor GH. Evidence from the anti-idiotypic network that the acetylcholine receptor is a rabies virus receptor. Journal of Virology. 67(1): 530-42, 1993

Hanham CA. Zhao F. Monoclonal antibodies for the identification of new world leishmania. Transaction of the Royal Society of Tropical Medicine and Hygiene. 1993, 85:220-223

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