Bio

Honors & Awards


  • William Randolph Hearst Fund Postdoctoral Award, Harvard Medical School (2008)
  • Graduate Division Dissertation Year Fellowship, UCLA (2005-2006)
  • Corine Tyler Walker Prize, Campbell Student Book Collection Competition, UCLA (2005)
  • Phi Beta Kappa (Alpha Association) International Scholarship, Phi Beta Kappa (2004-2005)
  • UCLA Affiliates Hortense Fishbaugh Memorial Scholar, UCLA (2004-2005)
  • Dr. Ursula Mandel Scholarship, UCLA (2002-2004)
  • Graduate Division Fellowship, UCLA (2001-2002)
  • Institute for Biodiagnostics Award for Science Education, Institute for Biodiagnostics (1995)

Service, Volunteer and Community Work


  • Science Fair Judge (4/9/2012 - Present)

    Intel International Science and Engineering Fair, Synopsys Silicon Valley Science and Technology Championship

    Location

    California

  • Innovation Farm Team member, Stanford University (4/9/2012 - Present)

    The Stanford Innovation Farm Teams Project, Office of Technology and Licensing

    Location

    Stanford, CA

Publications

Journal Articles


  • Clinical Neuroproteomics and Biomarkers: From Basic Research to Clinical Decision Making NEUROSURGERY Shoemaker, L. D., Achrol, A. S., Sethu, P., Steinberg, G. K., Chang, S. D. 2012; 70 (3): 518-525

    Abstract

    Clinical neuroproteomics aims to advance our understanding of disease and injury affecting the central and peripheral nervous systems through the study of protein expression and the discovery of protein biomarkers to facilitate diagnosis and treatment. The general premise of the biomarker field is that in vivo factors present in either tissue or circulating biofluids, reflect pathological changes, and can be identified and analyzed. This approach offers an opportunity to illuminate changes occurring at both the population and patient levels toward the realization of personalized medicine. This review is intended to provide research-driven clinicians with an overview of protein biomarkers of disease and injury for clinical use and to highlight methodology and potential pitfalls. We examine the neuroproteomic biomarker field and discuss the hallmarks and the challenges of clinically relevant biomarker discovery relating to central nervous system pathology. We discuss the issues in the maturation of potential biomarkers from discovery to Food and Drug Administration approval and review several platforms for protein biomarker discovery, including protein microarray and mass spectrometry-based proteomics. We describe the application of microfluidic technologies to the evolution of a robust clinical test. Finally, we highlight several biomarkers currently in use for cancer, ischemia, and injury in the central nervous system. Future efforts using these technologies will result in the maturation of existing and the identification of de novo biomarkers that could guide clinical decision making and advance diagnostic and therapeutic options for the treatment of neurological disease and injury.

    View details for DOI 10.1227/NEU.0b013e3182333a26

    View details for Web of Science ID 000300781700008

    View details for PubMedID 21866062

  • Untangling the cortex: Advances in understanding specification and differentiation of corticospinal motor neurons BIOESSAYS Shoemaker, L. D., Arlotta, P. 2010; 32 (3): 197-206

    Abstract

    The mature cerebral cortex contains a staggering variety of projection neuron subtypes, and a number of complementary studies have recently begun to define their identity and embryonic origin. Among the different types of cortical projection neurons, subcerebral projection neurons, including corticospinal motor neurons (CSMN), have been extensively studied and some of the molecular controls over their differentiation have been elucidated. Here, we first provide an overview of the approaches used to purify and molecularly profile neuronal populations of the neocortex and, more broadly, of the central nervous system (CNS). Next, we specifically review recent progress in understanding the genes that define and control development of the CSMN population. Finally, we briefly discuss the relevance of this work to current questions regarding the mechanisms of the establishment of projection neuron subtype identity in the neocortex and its implications to direct the differentiation of CSMN for therapeutic benefit.

    View details for DOI 10.1002/bies.200900114

    View details for Web of Science ID 000275508900003

    View details for PubMedID 20108227

  • Identification of Differentially Expressed Proteins in Murine Embryonic and Postnatal Cortical Neural Progenitors PLOS ONE Shoemaker, L. D., Orozco, N. M., Geschwind, D. H., Whitelegge, J. P., Faull, K. F., Kornblum, H. I. 2010; 5 (2)

    Abstract

    The central nervous system (CNS) develops from a heterogeneous pool of neural stem and progenitor cells (NSPC), the underlying differences among which are poorly understood. The study of NSPC would be greatly facilitated by the identification of additional proteins that mediate their function and that would distinguish amongst different progenitor populations.To identify membrane and membrane-associated proteins expressed by NSPC, we used a proteomics approach to profile NSPC cultured as neurospheres (NS) isolated from the murine cortex during a period of neurogenesis (embryonic day 11.5, E11.5), as compared to NSPC isolated at a peak of gliogenesis (postnatal day 1, P0) and to differentiated E11.5 NS. 54 proteins were identified with high expression in E11.5 NS, including the TrkC receptor, several heterotrimeric G proteins, and the Neogenin receptor. 24 proteins were identified with similar expression in E11.5 and P0 NS over differentiated E11.5 NS, and 13 proteins were identified with high expression specifically in P0 NS compared to E11.5 NS. To illustrate the potential relevance of these identified proteins to neural stem cell biology, the function of Neogenin was further studied. Using Fluorescence Activated Cell Sorting (FACS) analysis, expression of Neogenin was associated with a self-renewing population present in both E11.5 and adult subventricular zone (SVZ) NS but not in P0 NS. E11.5 NS expressed a putative Neogenin ligand, RGMa, and underwent apoptosis when exposed to a ligand-blocking antibody.There are fundamental differences between the continuously self-renewing and more limited progenitors of the developing cortex. We identified a subset of differentially expressed proteins that serve not only as a set of functionally important proteins, but as a useful set of markers for the subsequent analysis of NSPC. Neogenin is associated with the continuously self-renewing and neurogenic cells present in E11.5 cortical and adult SVZ NS, and the Neogenin/RGMa receptor/ligand pair may regulate cell survival during development.

    View details for DOI 10.1371/journal.pone.0009121

    View details for Web of Science ID 000274442600019

    View details for PubMedID 20161753

  • Maternal embryonic leucine zipper kinase is a key regulator of the proliferation of malignant brain tumors, including brain tumor stem cells JOURNAL OF NEUROSCIENCE RESEARCH Nakano, I., Masterman-Smith, M., Saigusa, K., Paucar, A. A., Horvath, S., Shoemaker, L., Watanabe, M., Negro, A., Bajpai, R., Howes, A., Lelievre, V., Waschek, J. A., Lazareff, J. A., Freije, W. A., Liau, L. M., Gilbertson, R. J., Cloughesy, T. F., Geschwind, D. H., Nelson, S. F., Mischel, P. S., Terskikh, A. V., Kornblum, H. I. 2008; 86 (1): 48-60

    Abstract

    Emerging evidence suggests that neural stem cells and brain tumors regulate their proliferation via similar pathways. In a previous study, we demonstrated that maternal embryonic leucine zipper kinase (Melk) is highly expressed in murine neural stem cells and regulates their proliferation. Here we describe how MELK expression is correlated with pathologic grade of brain tumors, and its expression levels are significantly correlated with shorter survival, particularly in younger glioblastoma patients. In normal human astrocytes, MELK is only faintly expressed, and MELK knockdown does not significantly influence their growth, whereas Ras and Akt overexpressing astrocytes have up-regulated MELK expression, and the effect of MELK knockdown is more prominent in these transformed astrocytes. In primary cultures from human glioblastoma and medulloblastoma, MELK knockdown by siRNA results in inhibition of the proliferation and survival of these tumors. Furthermore, we show that MELK siRNA dramatically inhibits proliferation and, to some extent, survival of stem cells isolated from glioblastoma in vitro. These results demonstrate a critical role for MELK in the proliferation of brain tumors, including their stem cells, and suggest that MELK may be a compelling molecular target for treatment of high-grade brain tumors.

    View details for DOI 10.1002/jnr.21471

    View details for Web of Science ID 000252521000006

    View details for PubMedID 17722061

  • An Introduction to the Basic Principles and Concepts of Mass Spectrometry Protein Mass Spectrometry in Comprehensive Analytical Chemistry Series Faull KF, Dooley AN, Halgand F, Shoemaker LD, Norris A, Ryan CM, Laganowsky A, Johnson JV, Katz JE 2008; 52
  • Genomics, Proteomics and Neurology From Neuroscience to Neurology - Neuroscience, Molecular Medicine, and the Therapeutic Transformation of Neurology Shoemaker LD, Geschwind DH 2005
  • Immune response profiling identifies autoantibodies specific to Moyamoya patients ORPHANET JOURNAL OF RARE DISEASES Sigdel, T. K., Shoemaker, L. D., Chen, R., Li, L., Butte, A. J., Sarwal, M. M., Steinberg, G. K. 2013; 8

    Abstract

    Moyamoya Disease is a rare, devastating cerebrovascular disorder characterized by stenosis/occlusion of supraclinoid internal carotid arteries and development of fragile collateral vessels. Moyamoya Disease is typically diagnosed by angiography after clinical presentation of cerebral hemorrhage or ischemia. Despite unclear etiology, previous reports suggest there may be an immunological component.To explore the role of autoimmunity in moyamoya disease, we used high-density protein arrays to profile IgG autoantibodies from the sera of angiographically-diagnosed Moyamoya Disease patients and compared these to healthy controls. Protein array data analysis followed by bioinformatics analysis yielded a number of auto-antibodies which were further validated by ELISA for an independent group of MMD patients (n?=?59) and control patients with other cerebrovascular diseases including carotid occlusion, carotid stenosis and arteriovenous malformation.We identified 165 significantly (p?

    View details for DOI 10.1186/1750-1172-8-45

    View details for Web of Science ID 000318759100001

    View details for PubMedID 23518061

  • Potential application of hydrogen in traumatic and surgical brain injury, stroke and neonatal hypoxia-ischemia. Medical gas research Eckermann, J. M., Krafft, P. R., Shoemaker, L., Lieberson, R. E., Chang, S. D., Colohan, A. 2012; 2 (1): 11-?

    Abstract

    This article summarized findings of current preclinical studies that implemented hydrogen administration, either in the gas or liquid form, as treatment application for neurological disorders including traumatic brain injury (TBI), surgically induced brain injury (SBI), stroke, and neonatal hypoxic-ischemic brain insult (HI). Most reviewed studies demonstrated neuroprotective effects of hydrogen administration. Even though anti-oxidative potentials have been reported in several studies, further neuroprotective mechanisms of hydrogen therapy remain to be elucidated. Hydrogen may serve as an adjunct treatment for neurological disorders.

    View details for DOI 10.1186/2045-9912-2-11

    View details for PubMedID 22515516

  • Introduction to the Analysis of Protein Residues in Archaeological Ceramics Theory and Practice of Archaeological Residue Analysis Barnard, H., Shoemaker L, Rider M, Craig OE, Parr RE, Sutton MQ, Yohe RM 2007

Conference Proceedings


  • Report on the workshop "New Technologies in Stem Cell Research," Society for Pediatric Research, San Francisco, California, April 29, 2006. Cheng, J. C., Horwitz, E. M., Karsten, S. L., Shoemaker, L., Kornblum, H. I., Malik, P., Sakamoto, K. M. 2007: 1070-1088

    View details for PubMedID 17255523

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