Our recently expanded Proteomics Shared Resource offers cancer researchers at the HICCC direct access to the cutting-edge proteomics technology to conduct discovery-based proteomics and targeted proteomics. During the last decade, the field of proteomics has evolved rapidly to overcome technical limitations to improve the dynamic range and reproducibility of large-scale analyses. In particular, advances in mass spectrometry (MS) instrumentation and bioinformatics for "bottom-up" or "shotgun" proteomic approaches have been at the core of new developments to meet the challenge of biological complexity. These methods are striving to provide a more comprehensive view of the multi-factorial processes occurring during normal development or disease progression. At the protein level, distinct changes occur during the transformation of a healthy cell into a neoplastic cell, including altered expression, differential protein modification, changes in specific activity, and aberrant subcellular localization, all ofwhich can affect cellular function. Included in this SR at CUM(J are start-to-finish protein identification and characterization services, including current quantification methods such as SILAC, which require sensitive and expensive MS-centered equipment with on-site expertise in experimental design, and state of the art informatics.

Public Health Relevance

In contrast to the genome, the proteome is rapidly dynamic, depending on the status and progression of a disease. The inherent advantage studying proteomics opposed to the genome is that the identified proteins are themselves the biological endpoint. Identifying changes of protein abundance and modifications is the underlying theme in cancer proteomics. The Proteomics Share Resource provides investigators access to state ofthe art proteomics technology and offer consultation on experimental design.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
2P30CA013696-40
Application #
8753119
Study Section
Subcommittee G - Education (NCI)
Project Start
1997-07-04
Project End
2019-06-30
Budget Start
2014-07-17
Budget End
2015-06-30
Support Year
40
Fiscal Year
2014
Total Cost
$84,983
Indirect Cost
$31,869
Name
Columbia University (N.Y.)
Department
Type
DUNS #
621889815
City
New York
State
NY
Country
United States
Zip Code
10032
Bassuk, Alexander G; Sujirakul, Tharikarn; Tsang, Stephen H et al. (2014) A novel RPGR mutation masquerading as Stargardt disease. Br J Ophthalmol 98:709-11
Li, Yao; Wu, Wen-Hsuan; Hsu, Chun-Wei et al. (2014) Gene therapy in patient-specific stem cell lines and a preclinical model of retinitis pigmentosa with membrane frizzled-related protein defects. Mol Ther 22:1688-97
Wert, Katherine J; Sancho-Pelluz, Javier; Tsang, Stephen H (2014) Mid-stage intervention achieves similar efficacy as conventional early-stage treatment using gene therapy in a pre-clinical model of retinitis pigmentosa. Hum Mol Genet 23:514-23
Shen, Sherry; Sujirakul, Tharikarn; Tsang, Stephen H (2014) Next-generation sequencing revealed a novel mutation in the gene encoding the beta subunit of rod phosphodiesterase. Ophthalmic Genet 35:142-50
Palomero, Teresa; Couronné, Lucile; Khiabanian, Hossein et al. (2014) Recurrent mutations in epigenetic regulators, RHOA and FYN kinase in peripheral T cell lymphomas. Nat Genet 46:166-70
Higuchi-Sanabria, Ryo; Pernice, Wolfgang M A; Vevea, Jason D et al. (2014) Role of asymmetric cell division in lifespan control in Saccharomyces cerevisiae. FEMS Yeast Res 14:1133-46
Lam, A T; Curschellas, C; Krovvidi, D et al. (2014) Controlling self-assembly of microtubule spools via kinesin motor density. Soft Matter 10:8731-6
Olszak, Torsten; Neves, Joana F; Dowds, C Marie et al. (2014) Protective mucosal immunity mediated by epithelial CD1d and IL-10. Nature 509:497-502
Murtomaki, Aino; Uh, Minji K; Kitajewski, Chris et al. (2014) Notch signaling functions in lymphatic valve formation. Development 141:2446-51
Nong, Eva; Lee, Winston; Merriam, Joanna E et al. (2014) Disease progression in autosomal dominant cone-rod dystrophy caused by a novel mutation (D100G) in the GUCA1A gene. Doc Ophthalmol 128:59-67

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