Dr. Cardinale is a Research Scientist at CAG, having joined us in July, 2010. He began his career in research as an undergraduate at Harvard University, where he earned an A.B. cum laude in Biochemical Sciences and completed a senior thesis in 1999. The next stage of his career took him to the NYU School of Medicine as an MD/PhD student. He received a Ph.D. in molecular and cellular biology for research on RNA polymerase and transcription in E. coli. He finished his M.D. in 2010 and then began a postdoctoral fellowship under Dr. Hakonarson at CAG.
His main research interest concerns the molecular genetic basis of pediatric-onset inflammatory bowel disease, that is, Crohn’s disease and ulcerative colitis. He makes use of next-generation sequencing, exome analysis, gene expression profiling, and molecular biology techniques to discover and characterize variants that confer risk for IBD and other diseases. His skills are a combination of bioinformatics and wet-lab biology.
His work on IBD is funded by the Crohn’s and Colitis Foundation of America and the National Institute of Diabetes, Digestive, and Kidney Disease.
CAG PublicationsAn updated list of publications is available at My NCBI Collections.
Relevant papers include:
A novel BHLHE41 variant is associated with short sleep and resistance to sleep deprivation in humans.
Pellegrino R, Kavakli IH, Goel N, Cardinale CJ, Dinges DF, et al.
Sleep. 2014; 37(8):1327-36.
Transcriptome profiling of human ulcerative colitis mucosa reveals altered expression of pathways enriched in genetic susceptibility loci.
Cardinale CJ, Wei Z, Li J, Zhu J, Gu M, et al.
PloS one. 2014; 9(5):e96153.
Impact of exome sequencing in inflammatory bowel disease.
Cardinale CJ, Kelsen JR, Baldassano RN, Hakonarson H.
World journal of gastroenterology : WJG. 2013; 19(40):6721-9.
Targeted resequencing identifies defective variants of decoy receptor 3 in pediatric-onset inflammatory bowel disease.
Cardinale CJ, Wei Z, Panossian S, Wang F, Kim CE, et al.
Genes and immunity. 2013; 14(7):447-52.
Extended haplotype association study in Crohn's disease identifies a novel, Ashkenazi Jewish-specific missense mutation in the NF-κB pathway gene, HEATR3.
Zhang W, Hui KY, Gusev A, Warner N, Ng SM, et al.
Genes and immunity. 2013; 14(5):310-6.
Large sample size, wide variant spectrum, and advanced machine-learning technique boost risk prediction for inflammatory bowel disease.
Wei Z, Wang W, Bradfield J, Li J, Cardinale C, et al.
American journal of human genetics. 2013; 92(6):1008-12.
Whole-genome DNA/RNA sequencing identifies truncating mutations in RBCK1 in a novel Mendelian disease with neuromuscular and cardiac involvement.
Wang K, Kim C, Bradfield J, Guo Y, Toskala E, et al.
Genome medicine. 2013; 5(7):67.
Termination factor Rho and its cofactors NusA and NusG silence foreign DNA in E. coli.
Cardinale CJ, Washburn RS, Tadigotla VR, Brown LM, Gottesman ME, et al.
Science (New York, N.Y.). 2008; 320(5878):935-8.
An allosteric path to transcription termination.
Epshtein V, Cardinale CJ, Ruckenstein AE, Borukhov S, Nudler E.
Molecular cell. 2007; 28(6):991-1001.
The B cell SH2/PH domain-containing adaptor Bam32/DAPP1 is required for T cell-independent II antigen responses.
Fournier E, Isakoff SJ, Ko K, Cardinale CJ, Inghirami GG, et al.
Current biology : CB. 2003; 13(21):1858-66