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Mirajul H. Kazi, PhD

Academic Title:

Research Associate

Primary Appointment:



685 West Baltimore Street Baltimore

Phone (Primary):


Phone (Secondary):




Education and Training

I graduated from Vidyasagar University, West Bengal, India, with MS and BS from the University of Burdwan in Human Physiology. I obtained a Ph.D. degree from the Jadavpur University, Kolkata, India, by the sponsorship of the Indian Council of Medical Research, Govt. of India. I received postdoctoral training in transport Physiology with Prof. Henry Binder at Yale University School of Medicine and later at the Johns Hopkins University, USA.


I was a PI and Assistant Professor (Scientist -D and offered Scientist-E later) Of Health Research Cadre of the Govt. of India for the National Institute of Cholera & Enteric Diseases (NICED), Kolkata, India, before taking a position at the University of Maryland School of Medicine. I worked for six years (2010 – 2016) at NICED. I supervised four Ph.D. students who have completed their Ph.D. program; all of them are now in postdoctoral training programs in the USA. Because of family obligations, I had to resign from the permanent Govt. job in India. I returned to the US and resumed my investigative research career successfully with Dr. Owen M. Woodward here at Dept. of Physiology. I have held editorial positions for Physiological reports, Frontier in Physiology. I have published 27 original papers in the area of my research and review articles and book chapters. I am considered by my peers to be a standard basic science researcher in the study of epithelial transport physiology and its relevance for the epithelial linked disease. I was the first scientist to show the unequivocal physiologic evidence of the anti-diarrheal mechanism of zinc. My discovery guided other investigators to identify the basis for the introduction of Zn in diarrheal disease therapy. I am the first person to establish the role of ANO6 in intestinal Cl- secretion. 


Research/Clinical Keywords

Epithelial transport, diarrhea, gut inflammation, potassium and chloride channel targeted drug therapy for intestinal disease and disorders, barrier function, Uric acid transport mechanism in the gut, mouse model for enteric infection and mucosal immunity.

Highlighted Publications

  1. Hoque KM., Dixon E., Lewis L., Allan J., Gamble G., Phipps-Green A., Kuhns Halperin V., Honne A., Stamp L., Merriman T., Dalbeth N and Woodward WM. (2020). The ABCG2 Q141K hyperuricemia and gout associated variant illuminates the physiology of human urate excretionNature Commun 11(1):doi: 10.1038/s41467-020-16525-w.
  2. Sarkar P., Saha T., Sheikh IA., CHakraborty S., Aoun J., Chakrabarti MK., Rajendran VM., Ameen NA, Dutta S and Hoque KM*  (2019) Zinc Ameliorates Intestinal Barrier Dysfunctions in Shigellosis by Reinstating Claudin-2 and -4 on the Membranes. Am J Gastrointest Livr Physiol  316(2):G229 - 246.
  3. Aoun, J; Mikio Hayashi, Sheikh IA, Sarkar P, Tultul Saha, Tanya Chatterjee, Pinak Chakrabarti, Manoj K Chakrabarti and Hoque KM* (2016) Anoctamin 6 Contributes to Cl- Secretion in Accessory Cholera Enterotoxin (ACE) Stimulated Diarrhea: new signaling mechanismfor cholera.  J Biol Chem. 291(52):26816 – 26836.
  4. *Hoque K.M., Owen, MW., vanRossum D.B.,  Nickolas C. Zachos., Chen L., Leung GPH., Guggino WB., Guggino S.E., and Tse, C.M., (2010) Epac1 mediates Protein Kinase A independent mechanism of forskolin (FSK) stimulated Cl secretion in T84 cellsJ Gen Physiol 135(1):43-58.  PMCID: PMC2806414
  5. Hoque, K. M, Rajendran, V.M., Binder, H. J. (2005) Zinc inhibits cAMP-stimulated Cl secretion via basolateral K channel blockade in rat ileum. Am J.  Physiol-Gastrointest Liver Physiol 288: G956-G963.  PMID: 15618279

Additional Publication Citations

  1. Rehman S., Narayanan, K., Nickerson, A., Coon, S., Hoque, KM., Sandle, G., and Rajendran V., Parallel intermediate conductance K+(IK) and Cl- (CLC2) channel activity mediates electroneutral K+ exit across basolateral membranes in rat distal colon. 2020; Am J. Physiol Gastro Liver PhysiolDOI: 1152/ajpgi.00011.2020
  2. Ahsan MK, Figueora-Hall, L., Baratta, V., Garcia-Milian, R., Lam, T., Hoque, KM., Salas, P., and Ameen, N. Glucocorticoids and Serum and Glucocorticoid-inducible kinase 1 are potent regulators of CFTR in the native intestine: implications for stress-induced diarrhea. 2020 Am J Physiol Gastrointes Liver Physiol
  3. Pore D., Hoque KM., and Chakrabarti MK. Animal Biotechnology (2nd Edition) Models in Discovery and Translation. Verma, A & Singh A (Editors), Animal Biotechnology (2nd Edition). Animal models in advancement of research in enteric disease. P199 – 216. Publish by Academic Press (ELSEVIER) in June 2020 ISBN: 978-0-12-811710-1.
  4. Tanaya Chatterjee; Tanaya Chatterjee; Barun Chatterjee; Tultul Saha; Hoque KM; Pinak Chakrabarti. (2017)  Structure and function of Vibrio cholerae Accessory cholera enterotoxin in presence of gold nanoparticles: dependence on morphology.  Biochim Biophys Acta. 2017 Feb 12. pii: S0304-4165(17)30051-X. doi: 10.1016/j.bbagen.2017.02.007.  PMID: 28215703
  5. Sarwar S, Chakraborti S, Bera S, Sheikh IA, Hoque KM, Chakrabarti P. (2016)  The antimicrobial activity of ZnO nanoparticles against Vibrio cholerae: Variation in response depends on biotype. Nanomedicine 12(6):1499-50. PMID: 26970029
  6. Irshad Ali, HemantaKoley, Manoj K. Chakraborty, and Hoque KM*(2013). The Epac1 signaling pathway regulates Cl- secretion via modulation of apical KCNN4c channel in secretory diarrhea J Biol. Chem. 288(28):20404-15.
  7. Chatterjee T., Sheikh IA., Chakravarty D., Chakrabarti P., Saha T., Chakrabarti MK., and Hoque KM. (2015) Effects of small molecule calcium-activated chloride channel inhibitors on structure and function of Accessory cholera enterotoxin (Ace) of Vibrio cholera. PLoS One, 10(11):e0141283.  PMCID: PMC4634967
  8. Hoque KM, Irshad Ali, RafiquelSarker, Boyoung Cha, Nicholas C Zachos, Brain D. Harfe, Mark Donowitz and Chung Ming Tse.  (2012) Tmem16A and NHERf1 Regulates Ca2+ and cAMP Stimulated Cl- Secretion in Murine Colon. FASEB J. 26:1111.
  9. Hoque KM* and Sk, AI, New advances in the Pathophysiology of enteric infections and their impact on therapy (2012). Expert Review of Anti-infective Therapy 10(6): 687-99.
  10. Chatterjee T; Mukherjee D; Dey, S; Pal, A; Hoque KM; and Chakrabarti P (2011) Accessory cholera enterotoxin,Ace, from Vibrio cholerae: studies on structure, unforlding and virstatinbinding. Biochem; J 50(14):2962-72.
  11. Hoque KM, Linxi Chen, George PH Leung and Chung-Ming Tse. (2008) A Novel purine-selective nucleobase/nucleoside transporter in PK15NTD cells. Am J PhysiolRegulIntegr Comp Physiol. 294(6):R1988-95.
  12. R. Murtazina, O. Kovbasnjuk, N. Zachos, X. Li, Y. Chen, A. Hubbard, B. Hogema, D. Steplock,U. Seidler, Hoque, KM, M. Tse, H. De Jonge, E. Weinman, and M. Donowitz (2007). Tissue specific regulation of sodium-proton exchanger isoform 3 (NHE3) activity in NA/H exchanger regulatory factor 1 (NHERF1) null mice: cAMP inhibition is differentially dependent on NHERF1 and exchange protein directly activated by cAMP (EPAC) in ileum versus proximal tubule. J Biol Chem. 282(34):25141-51.  PMID: 17580307
  13. Ghosh A, Saha, DR, Hoque KM, Saha, DR, Asakuna, M, Yamazaki, S, Koley H, Das SS, and Chakrabarti MK. (2006) Enterotoxicity of 45kDa matured and 35-kDa processed forms of hemagglutininprotease purified from a cholera toxin negative V. choleraenon-O1.non-O139 strain. Infect. Immun. 74: 2937-2946.  PMCID: PMC1459690
  14. Chakrabarti MK, Hoque KM, Chakrabarty M, Mahalanabish D. (2005). Effect of reducing sodium or glucose concentration in a hypo-osmolar ORS (Oral Rehydration Salts) on absorption efficiency: Marker perfusion in rat jejunum. Dig. Dis. Sci. 50: 241-245.  PMID: 15745079
  15. *Hoque KM, Sarker, R, Guggino, SE, and Tse, C-M (2009). A New Insight into Patho-physiological Mechanisms of Zinc in Diarrhea. Ann N.Y. Acad. Sci. 1165:279-284.  PMID: 19538317
  16. Crane JK and Hoque KM*. (2008). Zinc for Infectious Diarrhea in Developed Countries: Should we be Sprinkling our own Lawns? J Pediatr Gastroenterol Nutr. 46(5):484-485.   PMID: 18493201
  17. Chakrabarti M. K., Hoque K.M., Chakrabarty M., Mahalanabish D. (2005). Effect of reducing sodium or glucose concentration in a hypo-osmolar ORS (Oral Rehydration Salts) on absorption efficiency: Marker perfusion in rat jejunum. Dis. Sci. 50: 241-245.
  18. Hoque, K. M., Saha, S., Chakrabarti, M. K. (2004). Role of nitric oxide induced store operated calcium influx in the mechanism of action of NAG-ST produced by Vibrio cholerae non-O1 in isolated rat enterocytes. Toxicology 201: 95-103

Research Interests

(1) My scientific research focuses on elucidating mechanisms of epithelial ion transport for developing host-directed therapy to control the epithelial linked disease that includes diarrhea, intestinal inflammation, and hyperuricemia. I am currently interested in uric acid (UA) handling by the gut to know the pathophysiologically important pathway(s) responsible for the uric acid excretion in the intestinal lumen, impacting gout and kidney disease (Nature Commun 2020). I am also inclined to investigate the set of physiological signals that stimulates excess UA-dependent immune response that include cellular components, production of AMPs, other soluble mediators (Chemokines, cytokines, complement) seek to identify the UA transport machinery that facilitates regional and global immune responses. Understanding the mechanisms that control urate homeostasis in the body is an active area of my research. It is hoped that uncovering the mechanism used by the intestinal epithelium to prevent hyperuricemia may direct therapeutic approaches to a broad range of epithelial linked diseases and relationships with other important disorders, including hypertension, chronic kidney disease, and metabolic syndrome, cardiovascular disease and inflammatory conditions.


(2) My research experiences have generated a long-term interest in the regulation of intestinal Cl- secretion and barrier function of the intestinal epithelium. Cystic Fibrosis Transmembrane Regulator (CFTR) is considered the sole luminal Cl− channel responsible for abnormal fluid loss during secretory diarrhea. This absolute role of CFTR as the only apical Cl− channel involved in massive Cl− efflux during diarrhea is hard to imagine, given that other Cl− channels such as the recently discovered anoctamins (also named TMEM16s) are reported to localize at the luminal surface of intestinal epithelia. Contribution of TMEM16A and TMEM16F to diarrhea becomes more promising with our recent finding on the mode of action of Accessory cholera enterotoxin (Ace) (J Biol Chem 2016). It is of interest to know how these channels are regulated under normal physiologic as well as in the pathologic condition. It is uncertain whether CFTR is any way involved in the regulation of TMEM16A and/or TMEM16F function. Barrier defects occur in intestinal infection and may be involved in pathogenesis. I am interested in identifying the potential mechanisms involved in the perturbation of mucosal barrier functions in intestinal infection and therapeutic to counteract these defects. Indeed, working in this direction, we have identified a new avenue for therapeutic normalization of colonic barrier properties using zinc in shigellosis (Am J Physiol 2019).

Awards and Affiliations


  1. Early career Investigator Award by the American Gastroenterological Association on June 5th 2018 at Walter E. Washington Convention Center.
  2. Grant Award from Bill & Melinda Gates Foundation and International Vaccine Institute for presentation to the 52nd US-Japan Joint Panel Meeting held on Feb 20-24, 2018 at Hat Yai, Thailand.
  3. Invited to serve as Review Editor in Gastrointestinal Sciences of the Frontiers in Physiology Journal.
  4. American Gastroenterological Association's Early Career faculty Award presented at the American Gastroenterological Association 2018 Meeting at Washington DC.
  5. American Physiological Society’s Research Recognition Award (Junior Faculty Category) presented at the APS GI & Liver Section of Experimental Biology 2014 meeting, April 26th – 30th in San Diego, CA, USA.        
  6. International Early Career Physiologist Award by American Physiological Society, presented at the Experimental Biology Meeting 2012, April 21-24th in San Diego, CA, USA.
  7. Honorable Mention Research Award for my accomplishment in the field of Gastrointestinal & Liver Physiology Section by the American Physiological Society (Sponsored by Takeda Pharmaceuticals, North America) in Experimental Biology 2010 meeting at Anaheim, CA, April 24-28, 2010.
  8. IUPS (International Union of Physiological Society) Young Scientist & Fenn Fund Award, in Kyoto, Japan, July 27th –Aug 1st, 2009
  9. Young Investigator Award by the Journal of Gastroenterology & Hepatology Foundation (JGHF) at the Asian Pacific Digestive Week in New Delhi, 13th-16th September 2008.
  10. UNESCO-ASM (American Society for Microbiology) Visiting Resource Person Programe  Award
  11. UNESCO-ASM International Award for pre-doctoral training at Signal Transduction Laboratory of National Institute of Environmental Health Sciences (NIH), North Carolina, USA.


2000-Present     Member, American Physiological Society

2003-Present     Member, American Gastroenterological Association

2006-Present     Member, Gastroenterology Research Group, USA

2008-Present     Member, The Physiological Society, UK

Grants and Contracts

  1. ICMR Visiting Scientist Scheme of Indian Council of Medical Research, Govt. of India [no. 3/1/3/ICMR/VFS/HRD-2016] for 3 years. Title of the grant: Mode of action of Accessory Cholera Enterotoxin: Potential Druggable Target of Diarrhea and Other Gastrointestinal Disorders. Amount: 100,000 US $
  2. ICMR[Indian Council of Medical Research] extramural grant: Title of the grant: Impact of calcium activated chloride channel in diarrhea: The host directed therapeutic intervention.[no. 5/8-1(50) 2013-14ECD II; Amount ~50,000 US $
  3. R & D support from the Dept. of Biotechnology, [BT/PR/6462/FNS/20/669/2012 dated 23/8/2013, Govt. of India]. Title of grant proposal: Anti-diarrheal mechanism of Zinc: Effect on epithelial ion transport and barrier function. Amount in INR 51.50 lakhs (1,00,000 US$)
  4. Ramalingaswami Grant for 5 + 1 years from the Ministry of Science & Technology, Govt. of India, Dept. of Biotechnology, D.O. NO.BT/HRD/35/02, Title of grant proposal: Epac-A New Player in Diarrheal Diseases: Role in Intestinal ion Transport and Barrier Function. Amount in INR ~ 96 lakhs (1,70,000 US $)
  5. (2009)NIH T32 Training Grant [2T32DK00763221], Dept. of Medicine, Johns Hopkins University, Baltimore, USA only for one year. Role: Trainee.
  6. Supplement to parent Core grant at the Gastroenterology Division of the Johns Hopkins University; Title of grant proposal: Role of a non-CFTR Chloride Channel in Diarrhea & Digestive Diseases. (20,000 US $); Role PI.[Priority score 1.


  1. 2009   Project submitted to NIH (K01): Mechanisms of Epac-mediated signaling in cAMP stimulated Cl secretion and barrier function (1K01DK084264-01A1). Priority score 50



In the News


Professional Activity

  • Review Editor in Gastrointestinal Sciences of Frontier in Physiology
  • Currently I am in the editorial board member of the journal ‘The Physiological Report’ – a sister journal of American Physiological Society and UK Physiological Society.
  • Invited reviewer/judge for reviewing and ranking the applications and abstracts for Young Investigator Award 2008 of Society for Experimental Biology.
  • Reviewer of: American Journal of Physiology Liv., Journal of Physiology, Journal of Experimental Physiology, World Journal of Pediatrics, Journal of Pediatrics, Physiological Reports, Scientific Report, Frontier in Physiology.