The mission of the Epigenomics Core is to assist investigators in performing specialized epigenomics assays and comprehensive data analyses of these large datasets. Through collaborative efforts with the other Cores of the DRTC, the effects of defined pharmacological, dietary, environmental and genetic alterations are thoroughly characterized for their effects on glucose homeostasis, insulin action, and metabolism. The role of genetic modifications in relevant tissues, such as neurons, hepatocytes, skeletal muscle, adipocytes, beta and immune cells that are related to glucose homeostasis can be directly compared by thorough and definitive experimentation in rodent models. Identification of candidate targets can be functionally confirmed or refuted by the generation of specific mouse models and validated in human populations by comparative analyses in multiple cohorts/populations. Although this is a rapidly developing field, the broad expertise assembled at Einstein's Center for Epigenomics including molecular genetics, bioinformatics and computational biology expertise allows the Epigenomics Core to provide services to DRTC investigators with a wide range of specialized, high quality methodologies and tools relevant to understanding metabolic disease processes. To accomplish these goals, the Epigenomics Core will: 1) make available to investigators specialized high-throughput molecular technological resources including microarray and massively-parallel sequencing platforms to study DNA methylation and chromatin organization;2) provide extensive quality controls and assurance information for all high-throughput assays, generated as part of each analysis;3) provide readily available dedicated systems administrators and programmers, relational database services, high-performance computing resources and data storage/backup systems through the Computational and Statistical Epigenomics Resource and Research Informatics;4) advise investigators regarding the best experimental platforms and protocols to use for the specific biological question being asked;5) disseminate current and new technological development information and foster investigator Interactions through weekly workshops and journal clubs;and 6) provide laboratory training of students, postdoctoral fellows, investigators and technical staff in performing epigenomics methodologies and data analyses. All these services are available to investigators new to diabetes research, as well as to investigators working on diabetes-related projects that can be enriched and extended by the use of the expertise and facilities of this core.

Public Health Relevance

The Epigenomics Core provides cost effective, high quality resources that facilitate the scientific progress made by a large group of scientists committed to improve our understanding of the genetics of diabetes in order to improve the treatment of patients with diabetes.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Comprehensive Center (P60)
Project #
5P60DK020541-35
Application #
8377561
Study Section
Special Emphasis Panel (ZDK1-GRB-2)
Project Start
Project End
Budget Start
2012-04-01
Budget End
2013-03-31
Support Year
35
Fiscal Year
2012
Total Cost
$21,436
Indirect Cost
$8,523
Name
Albert Einstein College of Medicine
Department
Type
DUNS #
110521739
City
Bronx
State
NY
Country
United States
Zip Code
10461
Tang, Yan; Kwon, Hyokjoon; Neel, Brian A et al. (2018) The fructose-2,6-bisphosphatase TIGAR suppresses NF-?B signaling by directly inhibiting the linear ubiquitin assembly complex LUBAC. J Biol Chem 293:7578-7591
Chemaly, Elie R; Troncone, Luca; Lebeche, Djamel (2018) SERCA control of cell death and survival. Cell Calcium 69:46-61
Iqbal, Niloy Jafar; Lu, Zhonglei; Liu, Shun Mei et al. (2018) Cyclin-dependent kinase 4 is a preclinical target for diet-induced obesity. JCI Insight 3:
Schloss, Jennifer; Ali, Riyasat; Racine, Jeremy J et al. (2018) HLA-B*39:06 Efficiently Mediates Type 1 Diabetes in a Mouse Model Incorporating Reduced Thymic Insulin Expression. J Immunol 200:3353-3363
Racine, Jeremy J; Stewart, Isabel; Ratiu, Jeremy et al. (2018) Improved Murine MHC-Deficient HLA Transgenic NOD Mouse Models for Type 1 Diabetes Therapy Development. Diabetes 67:923-935
Shu, Jun; Santulli, Gaetano (2018) Update on peripheral artery disease: Epidemiology and evidence-based facts. Atherosclerosis 275:379-381
Zhao, Xiaoping; Zhao, Li; Yang, Hao et al. (2018) Pyruvate kinase M2 interacts with nuclear sterol regulatory element-binding protein 1a and thereby activates lipogenesis and cell proliferation in hepatocellular carcinoma. J Biol Chem 293:6623-6634
Qiu, Yunping; Moir, Robyn D; Willis, Ian M et al. (2018) Enhanced Isotopic Ratio Outlier Analysis (IROA) Peak Detection and Identification with Ultra-High Resolution GC-Orbitrap/MS: Potential Application for Investigation of Model Organism Metabolomes. Metabolites 8:
Liu, Shunmei; Marcelin, Genevieve; Blouet, Clemence et al. (2018) A gut-brain axis regulating glucose metabolism mediated by bile acids and competitive fibroblast growth factor actions at the hypothalamus. Mol Metab 8:37-50
Llewellyn, Sean R; Britton, Graham J; Contijoch, Eduardo J et al. (2018) Interactions Between Diet and the Intestinal Microbiota Alter Intestinal Permeability and Colitis Severity in Mice. Gastroenterology 154:1037-1046.e2

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