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Division Chief, Division of Pulmonary, Allergy and Critical Care Medicine UPMC Endowed Professor and Director, Acute Lung Injury Center of Excellence
UPMC Division of Pulmonary, Allergy, and Critical Care Medicine
UPMC Montefiore Hospital - NW628
3459 Fifth Avenue
Pittsburgh, PA 15213
Dr. Mallampalli received his MD from the University of Wisconsin. He completed an internship and residency in Internal Medicine at Hennepin County Medical Center in Minneapolis, MN where he also served as chief medical resident. Dr. Mallampalli completed a Pulmonary and Critical Care fellowship at the University of Iowa, where he obtained his research training under the mentorship of Dr. Gary Hunninghake. At Iowa, Dr. Mallampalli was appointed Professor of Medicine and Biochemistry and served as Associate Chair. Dr. Mallampalli serves as Editor for the Journal of Biological Chemistry and the American Journal of Physiology. He serves on multiple peer review panels including the LIRR Study Section for NIH grant reviews. He is an elected member of the American Society of Clinical Investigation, an Established Investigator of the American Heart Association, and a Career Investigator of the American Lung Association. In September of 2009, Dr. Mallampalli was recruited as Chief of the Pulmonary Division of the VA Pittsburgh Healthcare System and as the Director of the Acute Lung Injury Center at the University of Pittsburgh.
Chen BB, Glasser JR, Coon TA, and Mallampalli RK. F box protein FBXL2 exerts human lung tumor suppressor-like activity by ubiquitin-mediated degradation of cyclin D3 resulting in cell cycle arrest. Oncogene, 31: 2566-2579, 2012.
Agassandian M, Chen BB, Pulijala R, and Mallampalli RK. Calcium-calmodulin kinase I cooperatively regulates nucleocytoplasmic shuttling of CCT? by accessing a nuclear export signal. Mol. Biol. Cell (In Press), 2012.
Chen BB, Glasser JR, Coon TA, Zou C, Miller HL, Fenton, M, McDyer JF, Boyiadzis M, and Mallampalli RK. F box protein FBXL2 targets cyclin D2 for ubiquitination and degradation to inhibit leukemic cell proliferation. Blood 119 (13): 3132-3141, 2012, 2012.
Zhao J, Wei J, Mialki RK, Chen BB, Coon C, Zou C, *Mallampalli RK, Zhao Y. F-box protein FBXL19-mediated ubiquitination and degradation of the IL-33 receptor limits pulmonary inflammation. Nat. Immunol. (In Press), 2012. *co-senior author.
Chen BB, Coon TA, Glasser JR, and Mallampalli RK. Calmodulin antagonizes a calcium-activated SCF ubiquitin E3 ligase subunit, FBXL2, to regulate surfactant homeostasis. Mol. Cell. Biol. 31: 1905-1920, 2011.
Ray NB, Durairaj L, Chen BB, McVerry BJ, Ryan AJ, Donahoe M, Waltenbaugh AK, O'Donnell CP, Henderson FC, Etscheidt C, McCoy D, Agassandian M, Hayes-Rowan E, Coon TA, Butler TL, Gakhar L, Mathur SN, Sieren JC, Tyurina YY, Kagan VE, McLennan G, and Mallampalli RK. Dynamic regulation of cardiolipin by the lipid pump, ATP8b1, determines the severity of lung injury in experimental pneumonia. Nat. Med. 16:1120-27, 2010.
Dr. Mallampalli’s research in the area pulmonary epithelial molecular and cell biology as it relates to acute lung injury and the mechanisms of sepsis. He is a nationally recognized investigator in the area of pulmonary lipid metabolism.
The primary goal of his research is to investigate the molecular mechanisms for control of the major phospholipid of animal membranes and of lung surfactant, phosphatidylcholine (PC). PC levels are tightly controlled, in part, by the rate-regulatory phosphoenzyme cytidylyltransferase (CCT). His work investigates the molecular physiology of how CCT is controlled by reversible phosphorylation events within its carboxyl-terminus and its regulation by enzyme turnover. In models of inflammatory lung injury, surfactant PC biosynthesis is impaired because CCT activity decreases as a result of post-translational enzyme modification and gene transcriptional repression. Specifically, he has discovered that CCT is coordinately degraded by calpains and the ubiquitin system in models of pulmonary sepsis. These adverse effects are opposed by the calcium- sensor, calmodulin, that binds and stabilizes CCT during infection. CCT is also inactivated by stress kinases stimulated during lung inflammation that target novel docking motifs and phosphorylation sites within the enzyme resulting in greatly decreased PC production.