- Gomez Zubieta DM*, Hamood MA, Beydoun R*, Pall AE* and Kondapalli KC. MicroRNA-135a regulates NHE9 to inhibit proliferation and migration of glioblastoma cells. Cell Communication and Signaling. 2017; 15(1):55.
- Beydoun R*, Hamood MA*, Gomez Zubieta DM* and Kondapalli KC. Na+/H+ Exchanger 9 Regulates Iron Mobilization at the Blood Brain Barrier in Response to Iron Starvation. Journal of Biological Chemistry. 2017; 292(10):4293-4301.
- Kondapalli KC, Todd Alexander R, Pluznick JL and Rao R. NHA2 is expressed in distal nephron and regulated by dietary sodium. Journal of Physiology and Biochemistry. 2016; 73(2):199-205.
- Kondapalli KC, Llongueras JP, Capilla-González V, Prasad H, Hack A, Smith C, Guerrero-Cázares H, Quiñones-Hinojosa A and Rao R. A leak pathway for luminal protons in endosomes drives oncogenic signalling in glioblastoma. Nature Communications. 2015; 6:6289.
- Kondapalli KC, Prasad H and Rao R. An inside job: how endosomal Na(+)/H(+) exchangers link to autism and neurological disease. Frontiers in Cellular Neuroscience. 2014; 8:172.
- Kondapalli KC, Hack A, Schushan M, Landau M, Ben-Tal N and Rao R. Functional evaluation of autism-associated mutations in NHE9. Nature Communications. 2013;4:2510.
Biography and Education
Kalyan C. Kondapalli joined the Department of Natural Sciences in Fall 2014. Prior to joining the faculty at the University of Michigan-Dearborn, he was a postdoctoral fellow at the Johns Hopkins University’s School of Medicine. Dr. Kondapalli has a unique cross-disciplinary background. While his graduate training was in protein biochemistry and investigative approaches were mainly biophysical, his postdoctoral work complemented this with specific training in cell biology and cellular physiology. He used the opportunities to gain expertise in a number of diverse techniques, while working towards a common goal: rigorous mechanistic characterization of cellular and molecular ion regulation that underlies health and disease. During all those years he mentored several undergraduate and graduate students, and also published with them as co-authors. As member and leader of Johns Hopkins Postdoctoral Association, one of the largest postdoctoral associations in the country, he co-developed an undergraduate training program that utilized the “teacher scholar model”. He found this combination of a rigorous laboratory research experience with a mentored teaching experience very lively, refreshing and intellectually stimulating. When ready to transition to an independent position, he found the strong focus on teacher-scholar model within the Department of Natural Sciences at UM-Dearborn as the main attractor. The proximity and accessibility to major research one institutes (Wayne State and UM-Ann Arbor) was a bonus.
Johns Hopkins University, School of Medicine, Baltimore, Maryland
Postdoctoral training, Cellular and Molecular Physiology
Wayne State University, School of Medicine, Detroit, Michigan
Ph.D., Biochemistry and Molecular Biology
Wayne State University, College of Science, Detroit, Michigan
M.S., Molecular Biotechnology
Teaching and Research
Kondapalli laboratory focuses on the characterization of cellular and molecular cation regulatory mechanisms that underlie health and disease. Under this broad theme, the laboratory pursues two specific lines of research:
1. Glioblastoma multiforme (GBM) is the most common and lethal form of adult brain cancer, with a median patient survival of ~12-14 months post-diagnosis. A critical factor for this poor prognosis has been a “one size fits all” approach to treatment, and it is becoming increasingly clear that a more individually tailored approach is required. This “Precision medicine” (PM) involves comprehensive, in-depth profiling of tumor tissue in individual patients to identify specific molecules or pathways to be targeted. Its potential to improve patient survival rates led to the compilation of large databases of molecular level (e.g. DNA and proteins) changes in GBM patients. Mining of GBM patient databases led to an unexpected discovery that in a subset of GBM patients, the autism-associated gene SLC9A9 drives cancer genesis and progression. These GBM patients express unusually high levels of a protein known as NHE9, coded by the gene SLC9A9. GBM patients with high NHE9 have a 3-fold lower survival rate relative to GBM patients with normal levels of NHE9. Moreover, these patients do not respond to chemotherapy and radiation. This discovery implies a possible strategy to combat GBM within a PM approach, as it strongly suggests NHE9 levels influence GBM progression in a patient-dependent manner. Before such development is possible, however, the precise mechanisms connecting NHE9 levels to tumor formation and progression have to be elucidated; this has become the main focus of the laboratory at UM-Dearborn. The long-term goal is to develop treatment strategies tailored for GBM patients with abnormally high levels of NHE9.
2. Diabetes is a major risk factor for heart disease. Long-term goal of the laboratory is to utilize the unique opportunity offered by disease states such as Friedreich’s Ataxia (patients have both diabetes and cardiomyopathy) and pre-diabetes (undiagnosed pathological condition where injury to the heart is initiated) to define cellular mechanisms connecting diabetes and cardiac disease.
For a full publication list see: Kalyan C. Kondapalli's Bibliography
* Indicates UM-Dearborn undergraduate students
Bencze KZ, Kondapalli KC, and Stemmler T L. X-Ray Absorption Spectroscopy in Applications of Physical Methods in Inorganic and Bioinorganic Chemistry, pp.513-528. 2007John Wiley & Sons, Ltd, Chichester, UK
Kondapalli KC, Dancis A and Stemmler TL. Molecular Interaction between Frataxin and Ferrochelatase during Heme Assembly, Biochemistry: Synthetic Models and Cellular Systems. 2008. Vol. 1, ACS Publishing, Michael Baldwin and Eric Long, Eds, 17-30
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