Sally Temple, Ph.D.

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Natalia Lowry, MD, Ph.D.

Natalia Lowry’s career path has taken her from treating children at the Institute of Pediatric Hematology in Moscow, Russia to teaching anatomy to medical students half a world away. Following the advice of her Russion mentor Dr. Lowry immigrated to the United States and entered the Albany Medical College graduate student program. Dr. Lowry focused her graduate studies on biochemistry and obtained her doctoral degree investigating transcription regulation in microorganisms. She applied her knowledge and skills in molecular biology to transcription regulation of neural stem cells while serving as a post-doctoral research fellow in Dr. Temple’s laboratory. Dr. Lowry’s current investigations include neural stem and progenitor cells for the treatment of spinal cord injury using fetal and adult animal models. “We treat the cells with different chemicals and implant them alone or in biodegradable microspheres that hold growth factors,” she explains. “Injury sites treated with neural stem cells improve dramatically”, she says. “We are studying self-renewal in neural stem cells, because for future applications in regenerative medicine we are going to need to need an efficient way to generate a large source of nerve cells.”

Select Publications: 

Multipotent embryonic spinal cord stem cells expanded by endothelial factors and Shh/RA promote functional recovery after spinal cord injury. Lowry N, Goderie SK, Adamo M, Lederman P, Charniga C, Gill J, Silver J, Temple S. Exp Neurol. 2008 Feb;209(2):510-22.

Stage-specific changes in gene expression in acutely isolated mouse CNS progenitor cells. Abramova N, Charniga C, Goderie SK, Temple S. Dev Biol. 2005 Jul 15;283(2):269-81.

Identifying the perpetrator in medulloblastoma: Dorian Gray versus Benjamin Button. Lowry NA, Temple S. Cancer Cell. 2009 Feb 3;15(2):83-5.

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Anne Messer, Ph.D.

Anne Messer received her PhD in Molecular Biology from the Univ. Oregon Institute of Molecular Biology, studying the genetics of membrane permeation in E. coli.  She made the transition to neurogenetics as a Helen Hay Whitney postdoctoral fellow with Dr. Richard Sidman, Harvard Medical School. Although her major project was with cerebellar development mutants of mice, there was also an active program in retinal disease mutants, with many parallels and interests. During her tenure as an independent neurogenetics research scientist at the Wadsworth Center of the NY State Department of Health (directing the Molecular Genetics Program, and the Laboratory of Human Genetics), and professor of Biomedical Sciences, Univ. at Albany (founding chair of the neuroscience track), she has published over 100 papers on genetics, mechanisms, and therapeutics for neurodevelopmental and neurodegenerative diseases, including papers in Nature, Nature Genetics, Proceedings of the National Academy of Sciences, Molecular Therapy, and major neuroscience journals. She has been funded by multiple NIH grants and several disease foundations, while reviewing grants for over 25 NIH study sections, and 12 national and international funding agencies. In the late 1990s, she pioneered the use of engineered antibody fragments (nanobodies and intrabodies) to counteract the cellular effects of misfolding proteins in stressed and aging cells. Since then, she has amassed a body of publications applying this technology to Huntington’s and Parkinson’s disease, ranging from antibody engineering and nanobody selection to in vivo delivery by novel gene therapies. There are many commonalities between the neurodegenerative diseases that have been her primary focus and the breakdown of cellular function in Age-related Macular Degeneration. Therefore, she recently moved her most relevant technology and extensive expertise to NSCI, to bring this powerful approach to the exciting stem cell work being done by her long-term colleagues, Drs. Sally Temple and Jeff Stern.

Selected Publications:

1. Lecerf, J.M., T.L. Shirley, Q. Zhu, A. Kazantsev, P. Amersdorfer, D.E. Housman, A. Messer and J.S. Huston (2001) Human single- chain Fv intrabodies counteract in situ huntingtin aggregation in cellular models of Huntington’s Disease. Proc Natl Acad Sci USA 98, 4764-4769. PMCID: PMC31908

2. Butler, D.C and Messer, A., (2011) Bifunctional anti-huntingtin proteasome-directed intrabodies mediate efficient degradation of mutant huntingtin exon 1 protein fragments. PLoS One. 2011;6(12):e29199. Epub 2011 Dec 22.

3. Joshi, SN, David C. Butler retargeting sequence increases soluble cytoplasmic expression and efficacy of diverse anti-synuclein intrabodies. mAbs, 2012: Aug 28;4(6). [Epub ahead of print]PMID:22929188

4.Messer A, Joshi SN, Intrabodies as Neuroprotective Therapeutics. Neurotherapeutics. 2013 May 7. [Epub ahead of print] PMID: 23649691, DC, Messer, A., Fusion to a highly charged proteasomal

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Barbara Corneo, Ph.D.

Dr. Corneo has been trained in human embryonic stem (hES) cell research through her experience as post-doc in Dr. Gordon Keller’s lab, where she acquired knowledge in hES cell culture and differentiation into definitive endoderm, the germ layer that gives rise to pancreas and liver.  She brings her experience to Dr. Temple’s lab in the effort to differentiate hES cells and induced pluripotent stem (iPS) cells into cell lineages of the eye for both cell therapy and eye disease modeling.

Select Publications: 

Corneo B and Temple S. (2009). Sense and serendipity aid in RPE generation. Cell Stem Cell. 5(4):347-8.Corneo B, Wendland RL, Deriano L, Cui X, Klein IA, Wong SY, ArnalS, Holub AJ, Weller GR, Pancake BA, Shah S, Brandt VL, Meek K, Roth DB. (2007).

Rag mutations reveal robust alternative end joining. Nature 449(7161):483-6. Corneo B, Benmerah A, Villartay JP. (2002).

A short peptide at the C terminus is responsible for the nuclear localization of RAG2. Eur J Immunol. 32:2068-73. Moshous D., Callebaut I., de Chasseval R., Corneo B., Cavazzana-Calvo M., Le Deist F., Tezcan I., Sanal O., Bertrand Y., Philippe N., Fischer A. and de Villartay J.P. (2001)

Artemis, a novel DNA double strand break repair/V(D)J recombination protein, is mutated in human severe combined immune deficiency. Cell 105: (177-186). CorneoB., MoshousD., GüngorT., Wulffraat  N., Philippet  P., Le DeistF., Fischer  A., and de VillartayJ.P. (2001)

Identical mutations in RAG1 or RAG2 genes leading to defective V(D)J recombinase activity can cause either T-B-SCID or Omenn syndrome. Blood 97 (9) : 2772-2776. Corneo B., Moshous D., Callebaut I., de Chasseval R., Fischer A., de Villartay J.P.  (2000)

Three-dimensional clustering of human Rag2 gene mutations in severe combined immunodeficiencyJ. Biol . Chem. 275 (17) :12672-12675.

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