Bu Yin

Bu Yin

Patent Agent

San Diego, (858) 720-7912


Tsinghua University (B.S., 2005)
University of Pennsylvania (Ph.D., 2010)

Bar Admissions

U.S. Patent & Trademark Office

Bu Yin is a patent agent in the firm’s San Diego office. Dr. Yin prepares and prosecutes domestic and international patent applications in biotechnology, pharmaceuticals and life sciences. He has experience in conducting due diligence assessments, freedom to operate analyses, and patentability analyses. He has also provided support for patent litigation, patent arbitration, and third-party preissuance submission.

Dr. Yin’s scientific expertise encompasses the fields of biochemistry, cell and molecular biology, and genetics/epigenetics. He is familiar with recombinant DNA and protein, therapeutic antibodies, neurodegenerative diseases, cancer diagnosis and therapy, vaccines and gene therapy, high-throughput drug discovery, and drug delivery systems, amongst other subject matters.

Dr. Yin was a Presidential Postdoctoral Fellow at the Novartis Institutes for Biomedical Research in Cambridge, Massachusetts. At Novartis, he developed high-throughput si/shRNA-based screening technologies to study cancer cell death. Dr. Yin earned his Ph.D. in Cell and Molecular Biology from the University of Pennsylvania, working in the Children’s Hospital of Philadelphia. His research focused on DNA damage and repair during B-cell and T-cell development, during antibody production and immune responses, and during tumorigenesis. Dr. Yin received his B.S. from Tsinghua University, Beijing, China, with training in bioinformatics at Uppsala University, Sweden. Prior to joining the firm, Dr. Yin was a registered patent agent at another international law firm.

Dr. Yin is an author of scientific publications in leading journals including Nature Immunology, Molecular Cell, and Journal of Clinical Investigation. He also serves as a reviewer for many international journals. He was a recipient of the Saul Winegrad Award for Outstanding Dissertation from the University of Pennsylvania, Emphasis in Tumor Immunology Training Grant from the Cancer Research Institute, New York, and the Aflac Inc. Scientist-in-training Award from the American Association for Cancer Research.

Dr. Yin is fluent in Mandarin Chinese.


  • “ATM deficiency augments constitutively nuclear cyclin D1-driven genomic instability and lymphomagenesis,” Oncogene [Epub ahead of print] (2013). 
  •  “Redundant and non-redundant functions of ATM and H2AX in maintenance of genomic stability during lymphocyte proliferation,” J. Immunol. 189:1372-1379 (2012) 
  • “Non-redundant functions of ATM and H2AX in maintenance of genomic stability during lymphocyte proliferation.” Yin B, Lee B, Yang-Iott KS, et al. Journal of Immunology, in press. 
  • “PRAME: from diagnostic marker and tumor antigen to promising target of RNAi therapy in leukemic cells,” Leuk. Res. 35:1159−1160 
  • “Focal adhesion kinase as a target in the treatment of hematological malignancies,” Leuk. Res. 35:1416−1418 
  •  “Ataxia telangiectasia mutated (Atm) and DNA-PKcs kinases have overlapping activities during chromosomal signal joint formation,” Proc. Natl. Acad. Sci. USA 108:2022−2027 
  •  “Cellular context-dependent effects of H2ax and p53 deletion on the development of thymic lymphoma,” Blood 117:75−85 
  •  “Distinct roles for PTEN in prevention of lymphoma and autoimmunity,” J. Clin. Invest. 120:2497−2507 
  •  “H2AX suppresses chromosome end separation and subsequent break/translocation formation in V(D)J recombination,” J. Exp. Med. 206:2625−2639 
  •  “V(D)J Recombination causes dangerous chromosome liaisons in developing thymocytes,” Cell Cycle 8:2486−2487 
  •  “Mice heterozygous for germline mutations in methylthioadenosine phosphorylase die prematurely of T-cell lymphoma,” Cancer Res. 69:5961−5969 
  •  “Formation of dynamic gamma-H2AX structures along broken DNA strands is distinctly regulated by ATM and MDC1 and dependent upon H2AX densities in chromatin,” Mol. Cell 34:298−310 
  •  “RAG1 and ATM co-ordinate mono-allelic recombination and nuclear positioning of Ig loci,” Nat. Immunol. 10:655−664 
  •  “ATR and H2AX cooperate in maintaining genome stability under replication stress,” J. Biol. Chem. 284:5994−6003 
  •  “The sticky business of H2AX in V(D)J recombination, maintenance of genomic stability, and suppression of lymphoma,” Immunol. Res. 42:29−40 
  •  “ATM prevents unattended DNA double strand breaks on site and in generations to come,” Cancer Biol. Ther. 6:1837−1839

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