Reviews & Correspondences

Reviews & Comments

Jentsch T.J., Pusch M. (2018)
CLC chloride channels and transporters - structure, function, physiology, and disease.
Physiol. Reviews 98: 1493-1590.
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Jentsch T.J. (2016)
VRACs and other ion channels and transporters in the regulation of cell volume and beyond.
Nature Rev. Mol. Cell. Biol. 17: 293-307.
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Jentsch T.J, Lutter D., Planells-Cases R., Ullrich F., Voss F.K. (2016)
VRAC: Molecular identification as LRRC8 heteromers with differential functions.
Pflügers Archiv 468: 385-393.
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Jentsch T.J., Hoegg-Beiler M.B., Vogt J. (2015)
Departure gate of acidic Ca2+ confirmed.
EMBO J.  34: 1737-1739
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Jentsch T.J. (2015)
Discovery of CLC transport proteins: Cloning, structure, function, and pathophysiology.
J. Physiol.  593: 4091-4109.
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Jentsch T.J. (2013)
From mice to man: chloride transport in leukoencephalopathy.
Lancet Neurology 12: 626-628.
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Stauber T., Jentsch T.J. (2013)
Chloride in vesicular trafficking and function.
Annu. Rev. Physiol. 75: 453-477.
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Stauber T., Weinert S., Jentsch T.J. (2012)
Cell biology and physiology of CLC chloride channels and transporters.
Comprehensive Physiol. 2 (8),1701-1744.
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Zdebik A.A., Wangemann P., Jentsch T.J. (2009)
Potassium ion movement in the inner ear: Insights from genetic disease and mouse models.
Physiology 24, 307-316.
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Planells-Cases R., Jentsch T.J. (2009)
Chloride channelopathies.
Biochim. Biophys. Acta (Molec Basis of Disease) 1792, 173-189. 
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Plans V., Rickheit G., Jentsch T.J. (2009)
Physiological roles of CLC Cl-/H+ exchangers in renal proximal tubules.
Pflügers Arch. Eur. J. Physiol. 458, 23-37.
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Jentsch T.J. (2008)
CLC chloride channels and transporters: From genes to protein structure, pathology, and physiology.
Crit. Rev. Biochem. Molec. Biol. 43, 3-36.
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Jentsch T.J. (2007)
Chloride and the endosomal-lysosomal pathway - emerging roles of CLC chloride transporters.
J. Physiol. 578.3, 633-640.
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Jentsch T.J., Maritzen T., Zdebik A.A. (2005)
Chloride channel diseases resulting from impaired transepithelial transport or vesicular function.
J. Clin. Invest. 115, 2039-2046.
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Jentsch T.J., Neagoe I., Scheel O. (2005)
CLC chloride  channels and transporters.
Curr. Opin. Neurobiol. 15, 319-325
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Jentsch T.J. (2005)
Chloride transport in the kidney: lessons from human disease and knock-out mice.
J. Am. Soc. Nephrol. 16, 1549-1561.
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Jentsch T.J., Poët M., Fuhrmann J.C., Zdebik A.A. (2005)
Physiological functions of CLC Cl- channels gleaned from human genetic disease and mouse models.
Annu. Rev. Physiol. 67, 779-807.
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Jentsch T.J., Hübner C.A., Fuhrmann J. (2004)
Ion channels: function unravelled by  dysfunction.
Nature Cell Biol. 6, 1039-1047.
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Günther W., Piwon N., Jentsch T.J. (2003)
The ClC-5 chloride channel knock-out mouse - an animal model for Dent's disease.
Pflügers Arch. Eur. J. Physiol. 445, 456-462.
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Hübner C.A., Jentsch T.J. (2002)
Ion channel disaeses.
Hum. Mol. Genet. 11, 2435-2445.
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Estévez R., Jentsch T.J. (2002)
CLC chloride channels: Correlating structure with function.
Curr.Opin. Struct. Biol. 12, 531-539.
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Jentsch T.J., Stein V.,  Weinreich F.,  Zdebik A.A. (2002)
Molecular structure and physiological function of chloride channels.
Physiol. Rev. 82,  503-568.
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Jentsch T.J. (2002)
Chloride channels are different.
Nature 415, 276-277.
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Jentsch T.J. (2000)
Neuronal KCNQ potassium channels: Physiology and role in disease.
Nature Reviews Neuroscience 1, 21-30.
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Weinreich F.  Jentsch T.J. (2000)
Neurological diseases caused by ion-channel mutations.
Curr. Opin. Neurobiol. 10, 409-415.
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Jentsch T.J., Friedrich T., Schriever A., Yamada H. (1999)
The CLC chloride channel family.
Pflügers Arch. Eur. J. Physiol. 437,783-795.
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Jentsch T.J. (1994).
Trinity of cation channels.
Nature 367, 412-413.
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Correspondence

Jentsch T.J., Maritzen T., Keating D.J., Zdebik A.A., Thévenod F. (2010)
ClC-3 - a granular anion transporter involved in insulin secretion?
Cell Metabolism 12, 307-308.
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Niemeyer M.I., Cid L.P., Sepúlveda F.V., Blanz J., Auberson M., Jentsch T.J. (2010)
No evidence for a role of CLCN2 variants in idiopathic generalized epilepsy. 
Nature Genet.. 42, 3.
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