faculty

Rong Tian

rongtian@uw.edu

University of Washington, 

Cell Signaling & Cell/Environment Interactions

Developmental Biology, Stem Cells & Aging

Mitochondrial and Metabolic mechanisms of human diseases

Faculty Contact Information

Building: SLU North Building Room: N130 Phone: 206-543-8982 Alt Phone: 206-616-5672 http://depts.washington.edu/mmcslu/faculty/rong-tian-md-phd/

Lab Information

Accepting Students For:

Rotation, Autumn
Rotation, Spring
Rotation, Summer
Rotation, Winter
Permanent

Publications

Increased sensitivity with automated validation of XL-MS cleavable peptide crosslinks.

Keller A, Chavez JD, Bruce JE.

Bioinformatics (Oxford, England). 2019; 35(5):895-897.

PubMed [journal]
PMID:
30137231
PMCID:
PMC6394394

Extending the Scope of 1H NMR Spectroscopy for the Analysis of Cellular Coenzyme A and Acetyl Coenzyme A.

Nagana Gowda GA, Abell L, Tian R.

Analytical chemistry. 2019; 91(3):2464-2471.

PubMed [journal]
PMID:
30608643

Tools for 3D Interactome Visualization.

Keller A, Chavez JD, Eng JK, Thornton Z, Bruce JE.

Journal of proteome research. 2019; 18(2):753-758. NIHMSID: NIHMS1025326

PubMed [journal]
PMID:
30520642
PMCID:
PMC6519740

Heart specific knockout of Ndufs4 ameliorates ischemia reperfusion injury.

Zhang H, Gong G, Wang P, Zhang Z, Kolwicz SC, Rabinovitch PS, Tian R, Wang W.

Journal of molecular and cellular cardiology. 2018; 123:38-45. NIHMSID: NIHMS990623

PubMed [journal]
PMID:
30165037
PMCID:
PMC6192835

Mitochondrial dysfunction in pathophysiology of heart failure.

Zhou B, Tian R.

The Journal of clinical investigation. 2018; 128(9):3716-3726.

PubMed [journal]
PMID:
30124471
PMCID:
PMC6118589

Research Summary

The Tian Laboratory focuses on the roles of cell metabolism and mitochondrial function in the pathogenesis of human diseases. Our research combines the high resolution NMR techniques and metabolomics with the ability to target molecular regulatory mechanisms via genetic manipulation in animal models. Current research topics include:
Mitochondrial mechanisms in stress response;
Metabolic reprogramming during the development and disease;
Regulation of pathological cardiac hypertrophy by substrate metabolism.