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Faculty Detail Faculty Entry   
Name JI-BIN PENG  
Campus Address ZRB 634 Zip 0007
Phone 205-975-6130
E-mail jpeng@uab.edu" id="FacultyDetail1EmailAddress"><a href="mailto:jpeng@uab.edu">jpeng@uab.edu</a>
URL
 
 

Department Affiliations(s)
Appointment Type Department Division Rank
Center  Center for Metabolic Bone Disease  Center for Metabolic Bone Disease Associate Professor
Center  Medicine  Comprehensive Diabetes Ctr Associate Professor
Center  Medicine  Med - Nephrology Associate Professor
Primary  Medicine  Med - Nephrology Associate Professor
Secondary  Cell, Developmntl, & Integrative Biology  Cell, Developmntl, & Integrative Biology Associate Professor

Biographical Sketch 
Dr. Peng received his Ph.D. degree from Shanghai Institute of Cell Biology of the Chinese Academy of Sciences. Dr. Peng had his postdoctoral training at Brigham & Women’s Hospital and Harvard Medical School during 1997 to 2000 (Mentored by Drs. Matthias Hediger and Edward Brown). He became an Instructor in Medicine at Harvard Medical School in 2000. Dr. Peng Joined the University of Alabama at Birmingham (UAB) as an Assistant Professor in 2003. He is currently an Associate Professor of Medicine at UAB.

Society Memberships
Organization Name Position Held Org Link
American Heart Association  Member   
American Physiological Society  Member   
American Society for Biochemistry and Molecular Biology  Member   
American Society of Nephrology  Member   
 

Research/Clinical Interest
Title
Calcium transport proteins and their roles in health and disease
Description
Research in Dr. Peng’s laboratory is centered on the mechanism and regulation of calcium transport pathways. Calcium is a major inorganic component of the skeleton and serves as a key extracellular and intracellular messenger. Intestinal absorption and renal reabsorption of calcium play crucial roles in maintaining calcium balance of the body. Defects in calcium transport may result in disorders such as kidney stone disease and osteoporosis.

Towards a better understanding of calcium transport and its relation to hypercalciuria and hypertension, Dr. Peng’s laboratory is investigating molecular mechanisms of calcium absorption and reabsorption. Two calcium channels, TRPV5 and TRPV6, are the focus of current investigation. Dr. Peng’s group is also working on the mechanisms of WNK4 kinase activation by calcium ions. WNK4 is a protein kinase linked to pseudohypoaldosteronism type II, a genetic form of hypertension. It is expected that those studies will lead to novel therapeutic strategies for hypercalciuria and hypertension.

Postdoc Positions Available
Date Posted Position Title
02/26/2007  Molecular and physiological studies of epithelial calcium channels 
A highly motivated Postdoctoral Research Fellow is sought for molecular and physiological studies of epithelial calcium channels in Dr. Ji-Bin Peng’s lab. The research program focuses on the regulation of epithelial calcium channels by protein kinases and interactions between the epithelial calcium channels and relevant proteins.

The successful candidate should have a Ph.D. degree with experience in molecular and cellular biology or physiology. Experience in one of the following two areas is particularly important for the studies to be performed: 1) molecular and cellular biology techniques, including epithelial cell culture, DNA, RNA and protein isolation, molecular cloning and mutagenesis, Western blot analysis, immunohistochemical staining, immunoprecipitation, pull-down assay; 2) Electrophysiological techniques, such as voltage-clamp, patch clamp, and calcium imaging. The successful candidate should show ability to work independently and to write manuscripts.

Please submit curriculum vitae, summary of research experience, and three references to: Dr. Ji-Bin Peng (jpeng@uab.edu).
   
 

Selected Publications 
Publication PUBMEDID
Zhang Y, Zhang Y, Bone RN, Cui W, Peng JB, Gene P. Siegal GP, Wang H, Wu H. Regeneration of Pancreatic non-&#946; Endocrine Cells in Adult Mice Following a Single Diabetes-Inducing Dose of Streptozotocin. PLoS ONE, 7(5):e36675.2012.  22586489 
Wu G, Zhang W, Na T, Jing H, Wu H, Peng JB. Suppression of intestinal calcium entry channel TRPV6 by OCRL, a lipid phosphatase associated with Lowe syndrome and Dent disease. Am J Physiol Cell Physiol. 302:C1479-91, 2012.  22378746 
Na T, Wu G, Peng JB. Disease-causing mutations in the acidic motif of WNK4 impair the sensitivity of WNK4 kinase to calcium ions. Biochem Biophys Res Commun. 419: 293-298. 2012.   22342722 
Jing H, Na T, Zhang W, Wu G, Liu C, Peng JB. Concerted actions of NHERF2 and WNK4 in regulating TRPV5. Biochem Biophys Res Commun. 404:979-84, 2011.  21187068 
Peng JB. TRPV5 and TRPV6 in transcellular Ca2+ transport: regulation, gene duplication, and polymorphisms in African populations. Adv Exp Med Biol. 704:239-75, 2011.  21290300 
Zhang W, Na T, Wu, G, Jing H, Peng JB. Downregulation of intestinal apical calcium entry channel TRPV6 by ubiquitin E3 ligase Nedd4-2. J Biol Chem. 285:36586-96.2010.  20843805  
Lieben L, Benn BS, Ajibade D, Stockmans I, Moermans K, Hediger MA, Peng JB, Christakos S, Bouillon R, Carmeliet G. Trpv6 mediates intestinal calcium absorption during calcium restriction and contributes to bone homeostasis. Bone. 47(2):301-8. 2010.   20399919 
Na T, Zhang W, Jiang Y, Liang YY, Ma HP, Warnock DG, Peng JB. The A563T variation of the renal epithelial channel TRPV5 among African Americans enhances calcium influx. Am J Physiol Renal Physiol. 2009 Mar 4. [Epub ahead of print]  19261737 
Ji HL, Song W, Gao Z, Su XF, Nie HG, Jiang Y, Peng JB, He YX, Liao Y, Zhou YJ, Tousson A, Matalon S. SARS-CoV proteins decrease levels and activity of human ENaC via activation of distinct PKC isoforms. Am J Physiol Lung Cell Mol Physiol. 296:L372-83. 2009.   19112100 
Nie HG, Tucker T, Su XF, Na T, Peng JB, Smith PR, Idell S, Ji HL. Expression and Regulation of Epithelial Na+ Channels by Nucleotides in Pleural Mesothelial Cells. Am J Respir Cell Mol Biol. 2008 Oct 16. [Epub ahead of print]  18927349 
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Keywords
Calcium transport, absorption, reabsorption, hyercalciuria, hypertension, TRPV6, TRPV5, WNK4

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