Tingting Mills
Regular Member
Assistant Professor
The University of Texas Health Science Center at Houston
Department of Biochemistry and Molecular Biology
My research is primarily centered on elucidating the molecular mechanisms regulating various human diseases, including idiopathic pulmonary fibrosis (IPF), systemic sclerosis (SSc), and acute respiratory distress syndrome (ARDS). My major research projects are highlighted below:
- Alternative Polyadenylation in human diseases: A major part of my research has focused on studying the complex and multifaceted role of alternative polyadenylation in human diseases. Alternative polyadenylation is an RNA processing mechanism that regulates the 3'UTR length of mRNA. Our lab has studied the roles of Cleavage factor Im 25 (CFIm25 or NUDT21) mediated alternative polyadenylation in SSc, IPF, and ARDS, and its contribution to enhanced protein translation of target genes involved in the development and progression of these diseases. In addition to NUDT21, we also seek to investigate other factors that could modulate the alternative polyadenylation.
- Adenosine signaling in acute lung injury: Previous studies have shown that adenosine signaling can function to dampen pulmonary edema and inflammation during ARDS. We are interested in studying the role of adenosine and deoxyadenosine signaling in ARDS and lung fibrosis. Our lab has discovered a novel role of HIF1A inducible deoxycytidine kinase (DCK) as a regulator of abnormal cell apoptosis in both acute and chronic lung diseases. Moreover, we have also demonstrated novel roles of equilibrative nucleoside transporters (ENTs) - particularly ENT2 in lung protection by enhancing extracellular adenosine levels.
- Circadian rhythms and emphysema. Accumulating evidence has suggested a potential link between circadian rhythms and the pathogenesis of chronic obstructive pulmonary disease (COPD); however, the molecular link is not fully understood. Through working with experts in circadian rhythms, we are interested in investigating novel roles of circadian transcription factors in emphysema by promoting inflammation and attenuating lung epithelial cell proliferation.
Education & Training
PhD, Oklahoma State University, 2010