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Dr. Aparna Renigunta

Dr. Renigunta’s research focus is centered on deciphering the role of tubular transport mechanisms in kidney physiology (health) and pathophysiology (disease and infection). 

Students (Faculties: Medicine and human biology) interested in pursuing MD thesis or Master thesis are welcome to apply to aparna.renigunta@staff.uni-marburg.de

 You can find Dr. Reniguntas C.V. here(PDF).

  • Membrane proteins and ion channels

    Ion channels are integral membrane proteins complexes that allow/control the flow of ions across membranes. In the kidney, the permeability of renal tubules to different solutes and water is determined by a synchronized interplay between an array of epithelial ion channels and transporters at the expense of energy molecules (transcellular). The kidney also utilizes the organelles at cell-cell junctions to transport ions (paracellular). Impairment in these two trans-epithelial ion transport mechanisms lead to a wide range of kidney disorders. Similar mechanisms are prevalent in other epithelia of especially functionally related organs. The focus of our research is to explore the vast spectrum of ion channels in health, disease and infection. 

    A) Hereditary tubulopathies:

    Inherited tubulopatheis owing from impaired salt handling, calcium and magnesium handling and acid-base handling.

    Filtered NaCl is re-absorbed in nephron segments via well co-ordinated interplay of transportation proteins. Identification of transportation processes involving these proteins facilitated the elucidation of rare, recessively inherited salt loosing tubulopathies. Despite various advancements in clinical genetics, a large cohort of the patients with innate salt wasting disorders are genetically inexplicable. Therefore, it is tempting to speculate whether the already known transport systems in the TAL epithelia are described to their actual completeness? The major focus of my research is to understand the complex molecular machinery, dynamics and function of renal Kir channels and their role in renal tubulopathies.

    In co-operation with the University of Washington (Prof. Jianghui Hou) we attempt to understand the role of claudins (CLDN) in renal salt handling and decipher the genetic causes of the pathogenesis of Familial Hypercalciuric Hypomagnesemia with Nephrocalcinosis (FHHNC) and Hypercalciuric Nephrolithiasis (HN).

    B) Viroporins and membrane proteins:

    Functional characterization of viral proteins as viroporins and understanding viroporin-host cell interactions.

    Diverse sets of viruses encode ion channels dubbed viroporins, which play an important role in viral infection and viral pathogenicity. In co-operation with the Dept. of Virology, JLU (Prof. John Ziebuhr), we attempt to identify and characterize Corona virus encoded viroporins. The aim of this study is to perform a comprehensive functional characterization of these putative viroporins and identify their cellular and viral interaction partners, as promising novel targets for the development of anti-viral drugs. Viroporin research is a new addition to our spectrum of ion channel research. These studies gained recent importance due to the pandemic distribution of the novel Corona virus SARS-CoV2.

DFG - GEPRIS -Projekt

Identification and characterization of novel KCNJ16-interacting proteins in the pathophysiology of the new complex KCNJ16-associated hereditary renal salt-losing tubulopathy. Click here for the project description (GER).

LOEWE grantees- CoroPan

P5: Functions and interactions of coronavirus ion channel proteins. We have summarized further information on CoroPan for you in the project description.

Von Behring Röntgen Foundation- Funded project

Viroporins and ion channels: Interactions of coronavirus and host cellular ion channels: Implications for viral replication, pathogenesis and antiviral drug development. Click here for the project description(GER).

PUBLICATIONS

  • Hereditary tubulopathies

    Radi A, Nasrah S, Auer M, Renigunta A, Weber S, Seaayfan E, Kömhoff M. MAGED2 Enhances Expression and Function of NCC at the Cell Surface via cAMP Signaling Under Hypoxia. Cells. 2025 Jan 23;14(3):175. PMID: 39936967

    Schlingmann KP, Renigunta A*, Hoorn EJ, Forst AL, Renigunta V, Atanasov V, Mahendran S, Barakat TS, Gillion V, Godefroid N, Brooks AS, Lugtenberg D, Lake J, Debaix H, Rudin C, Knebelmann B, Tellier S, deBaaij JHF, Weber S, Palygin O, Staruschenko A, Kleta R, Houillier P, Bockenhauer D, Devuyst O, Vargas-Poussou R, Warth R, Zdebik AA, Konrad M. Defects in KCNJ16 cause a novel tubulopathy with hypokalemia, salt wasting, disturbed acid-base homeostasis and sensorineural deafness. J Am Soc Nephrol. 2021 Jun 1;32(6):1498-1512. PMID: 33811157 (* shared first author)

    Hou J, Renigunta V, Nie M, Sunq A, Himmerkus N, Quintanova C, Bleich M, Renigunta A, Wolf MTF. Phosphorylated claudin-16 interacts with Trpv5 and regulates transcellular calcium transport in the kidney. Proc Natl Acad Sci U S A. 2019 Sep 17;116(38):19176-19186. PMID: 31488724.

    Gong Y, Renigunta V, Zhou Y, Sunq A, Wang J, Yang J, Renigunta A, Baker LA, Hou J. Biochemical and biophysical analyses of tight junction permeability made of claudin-16 and claudin-19 dimerization. Mol Biol Cell. 2015 Dec 1;26(24):4333-46. PMID: 26446843.

    Gong Y, Renigunta V, Himmerkus N, Zhang J, Renigunta A, Bleich M, Hou J. Claudin-14 regulates renal Ca⁺⁺ transport in response to CaSR signalling via a novel microRNA pathway. EMBO J. 2012 Apr 18;31(8):1999-2012.xPMID: 22373575.

    Renigunta A*, Renigunta V, Saritas T, Decher N, Mutig K, Waldegger S. Tamm-Horsfall glycoprotein interacts with renal outer medullary potassium channel ROMK2 and regulates its function. J Biol Chem. 2011;286(3):2224-35. PMID: 21081491 (* Corresponding author)

    Renigunta A, Mutig K, Rottermann K, Schlichthörl G, Preisig-Müller R, Daut J, Waldegger S, Renigunta V. The glycolytic enzymes glyceraldehyde 3-phosphate dehydrogenase and enolase interact with the renal epithelial K+ channel ROMK2 and regulate its function. Cell Physiol Biochem. 2011;28(4):663-72. PMID: 22178878

    Hou J, Renigunta A, Yang J, Waldegger S. Claudin-4 forms paracellular chloride channel in the kidney and requires claudin-8 for tight junction localization. Proc Natl Acad Sci U S A. 2010 Oct 19;107(42):18010-5. PMID: 20921420. 

    Hou J, Renigunta A, Gomes AS, Hou M, Paul DL, Waldegger S, Goodenough DA. Claudin-16 and claudin-19 interaction is required for their assembly into tight junctions and for renal reabsorption of magnesium. Proc Natl Acad Sci U S A. 2009 Sep 8;106(36):15350-5. PMID: 19706394.

    Hou J*, Renigunta A*, Konrad M, Gomes AS, Schneeberger EE, Paul DL, Waldegger S, Goodenough DA. Claudin-16 and claudin-19 interact and form a cation-selective tight junction complex. J Clin Invest. 2008 Feb;118(2):619-28. PMID: 18188451. (*contributed equally)

    Konrad M, Hou J, Weber S, Dötsch J, Kari JA, Seeman T, Kuwertz-Bröking E, Peco-Antic A, Tasic V, Dittrich K, Alshaya HO, von Vigier RO, Gallati S, Goodenough DA, Schaller A. CLDN16 genotype predicts renal decline in familial hypomagnesemia with hypercalciuria and nephrocalcinosis. J Am Soc Nephrol. 2008; 19(1):171-81. PMID: 18003771

    Peters M, Ermert S, Jeck N, Derst C, Pechmann U, Weber S, Schlingmann KP, Seyberth HW, Waldegger S, Konrad M. Classification and rescue of ROMK mutations underlying hyperprostaglandin E syndrome/antenatal Bartter syndrome. Kidney Int. 2003 Sep;64(3):923-32. PMID: 12911542

    Weber S, Schneider L, Peters M, Misselwitz J, Rönnefarth G, Böswald M, Bonzel KE, Seeman T, Suláková T, Kuwertz-Bröking E, Gregoric A, Palcoux JB, Tasic V, Manz F, Schärer K, Seyberth HW, Konrad M. Novel paracellin-1 mutations in 25 families with familial hypomagnesemia with hypercalciuria and nephrocalcinosis. J Am Soc Nephrol. 2001; 12(9):1872-81. PMID: 11518780.

  • Viroporine und Membranaproteine

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Call for Paper für Cells-Special Issue "Kidney and Lung Disorders: The Role of Tubular and Alveolar Epithela in Health, Diesease, Infection, and Organ Crosstalk"

Further information on this Call for Paper can be found here.