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Kansas State University

Faculty

 

Philine Wangemann

 

 

 

 

 

Philine Wangemann

PhD, Biology, Albert-Ludwig-University, Freiburg, Germany, 1987

University Distinguished Professor 

Phone (785) 532-4863 
e-mail wange@vet.k-state.edu

Dr. Wangemann's laboratory webpage

 

 

 



Research Interests

More than 28 million people in the United States are deaf or hard of hearing and about two million are impaired by dizziness or have difficulties with balance. Research in Dr. Wangemann’s laboratory centers on epithelial physiology and vascular biology of the inner ear with the goal to prevent deafness and vestibular disorders in humans and animals.

Selected publications:

Singh, R., Wangemann, P. (2008) Free radical stress mediated loss of Kcnj10 protein expression in stria vascularis contributes to deafness in Pendred syndrome mouse model. Am. J. Physiol. Renal Physiol. 294: F139-148.

Lang, F., Vallon, V., Knipper, M., Wangemann, P. (2007) Invited Review: Functional significance of channels and transporters expressed in the inner ear and the kidney. Am. J. Physiol. Cell Physiol. 293: C1187-C1208.

Nakaya, K., Harbidge, D.G., Wangemann, P., Schultz, B.D., Green, E.D., Wall, S.M. Marcus, D.C. (2007) Lack of pendrin HCO3- transport elevates vestibular endolymphatic [Ca2+] by inhibition of acid-sensitive TRPV5 and TRPV6 channels. Am. J. Physiol. Renal Physiol. 292: F1314-F1321.

Wangemann, P., Nakaya, K., Wu, T., Maganti, R., Itza, E.M., Sannemann, J., Harbidge, D., Billings, S., Marcus, D.C. (2007) Loss of cochlear HCO3- secretion causes deafness via endolymphatic acidification and inhibition of Ca2+ reabsorption in a Pendred syndrome mouse model. Am. J. Physiol. Renal Physiol. 292: F1345-F1345.

 

Selected reviews and Most cited publications