Identification of the electrogenic 2Cl-/H+ exchanger, ClC5, as a chloride secreting transporter candidate in kidney cyst epithelium in tuberous sclerosis.

[1]  E. Henske,et al.  Kidney intercalated cells and the transcription factor FOXi1 drive cystogenesis in tuberous sclerosis complex , 2021, Proceedings of the National Academy of Sciences.

[2]  Ming-Zhi Zhang,et al.  Notch signaling is essential in collecting duct epithelial cell fate determination during development and maintenance of cell type homeostasis in adult. , 2019, Annals of translational medicine.

[3]  B. Siroky,et al.  Tuberous sclerosis complex exhibits a new renal cystogenic mechanism , 2019, Physiological reports.

[4]  Marie E. Edwards,et al.  Long-Term Administration of Tolvaptan in Autosomal Dominant Polycystic Kidney Disease. , 2018, Clinical journal of the American Society of Nephrology : CJASN.

[5]  M. Soleimani,et al.  Probenecid Pre-treatment Downregulates the Kidney Cl-/HCO3- Exchanger (Pendrin) and Potentiates Hydrochlorothiazide-Induced Diuresis , 2018, Front. Physiol..

[6]  A. McDonough,et al.  Downregulation of the Cl-/HCO3-Exchanger Pendrin in Kidneys of Mice with Cystic Fibrosis: Role in the Pathogenesis of Metabolic Alkalosis , 2018, Cellular Physiology and Biochemistry.

[7]  F. Reis,et al.  Recent Advances and Challenges of mTOR Inhibitors Use in the Treatment of Patients with Tuberous Sclerosis Complex , 2017, Oxidative medicine and cellular longevity.

[8]  P. Ashton-Prolla,et al.  TSC1 and TSC2 gene mutations and their implications for treatment in Tuberous Sclerosis Complex: a review , 2017, Genetics and molecular biology.

[9]  G. Seki,et al.  Functional coupling of V-ATPase and CLC-5 , 2017, World journal of nephrology.

[10]  E. Henske,et al.  New developments in the genetics and pathogenesis of tumours in tuberous sclerosis complex , 2017, The Journal of pathology.

[11]  A. Sangoi,et al.  Tuberous sclerosis complex: Hamartin and tuberin expression in renal cysts and its discordant expression in renal neoplasms. , 2016, Pathology, research and practice.

[12]  J. Bissler,et al.  Optimal treatment of tuberous sclerosis complex associated renal angiomyolipomata: a systematic review , 2016, Therapeutic advances in urology.

[13]  E. Thiele,et al.  Tuberous Sclerosis Complex , 2019, Harper's Textbook of Pediatric Dermatology.

[14]  L. Lagae,et al.  Tuberous sclerosis complex: the past and the future , 2015, Pediatric Nephrology.

[15]  R. Rasooly,et al.  Tuberous sclerosis complex, mTOR, and the kidney: report of an NIDDK-sponsored workshop. , 2014, American journal of physiology. Renal physiology.

[16]  M. Soleimani,et al.  Slc26a11, a chloride transporter, localizes with the vacuolar H(+)-ATPase of A-intercalated cells of the kidney. , 2011, Kidney international.

[17]  Roberto Zoncu,et al.  mTORC1 Senses Lysosomal Amino Acids Through an Inside-Out Mechanism That Requires the Vacuolar H+-ATPase , 2011, Science.

[18]  D. Corey,et al.  Regulation of TFEB and V-ATPases by mTORC1 , 2011, The EMBO journal.

[19]  J. Bissler,et al.  Tuberous Sclerosis Complex Renal Disease , 2010, Nephron Experimental Nephrology.

[20]  B. Rutkowski,et al.  Rapamycin as a therapy of choice after renal transplantation in a patient with tuberous sclerosis complex. , 2009, Transplantation proceedings.

[21]  T. Schüpbach,et al.  The vacuolar proton pump, V-ATPase, is required for notch signaling and endosomal trafficking in Drosophila. , 2009, Developmental cell.

[22]  Sylvie Breton,et al.  The Forkhead Transcription Factor Foxi1 Is a Master Regulator of Vacuolar H+-ATPase Proton Pump Subunits in the Inner Ear, Kidney and Epididymis , 2009, PloS one.

[23]  S. Glenn,et al.  In vivo analysis of key elements within the renin regulatory region. , 2008, Physiological genomics.

[24]  L. Cantley,et al.  Cyst formation and activation of the extracellular regulated kinase pathway after kidney specific inactivation of Pkd1. , 2008, Human molecular genetics.

[25]  Vincent J Schmithorst,et al.  Sirolimus for angiomyolipoma in tuberous sclerosis complex or lymphangioleiomyomatosis. , 2008, The New England journal of medicine.

[26]  K. Guan,et al.  Expanding mTOR signaling , 2007, Cell Research.

[27]  M. Gambello,et al.  Generation of a conditional disruption of the Tsc2 gene , 2007, Genesis.

[28]  P. Crino,et al.  The tuberous sclerosis complex. , 2006, The New England journal of medicine.

[29]  S. Petrovic,et al.  Chloride/bicarbonate exchanger SLC26A7 is localized in endosomes in medullary collecting duct cells and is targeted to the basolateral membrane in hypertonicity and potassium depletion. , 2006, Journal of the American Society of Nephrology : JASN.

[30]  J. Avruch,et al.  Rheb Binding to Mammalian Target of Rapamycin (mTOR) Is Regulated by Amino Acid Sufficiency* , 2005, Journal of Biological Chemistry.

[31]  D. Kwiatkowski,et al.  A mouse model of cardiac rhabdomyoma generated by loss of Tsc1 in ventricular myocytes. , 2005, Human molecular genetics.

[32]  E. Hafen,et al.  Regulation of mTOR function in response to hypoxia by REDD1 and the TSC1/TSC2 tumor suppressor complex. , 2004, Genes & development.

[33]  G. Bergström,et al.  Distal renal tubular acidosis in mice that lack the forkhead transcription factor Foxi1. , 2004, The Journal of clinical investigation.

[34]  K. Inoki,et al.  Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling. , 2003, Genes & development.

[35]  J. Blenis,et al.  Mammalian cell size is controlled by mTOR and its downstream targets S6K1 and 4EBP1/eIF4E. , 2002, Genes & development.

[36]  Hongbing Zhang,et al.  A mouse model of TSC1 reveals sex-dependent lethality from liver hemangiomas, and up-regulation of p70S6 kinase activity in Tsc1 null cells. , 2002, Human molecular genetics.

[37]  Thomas J. Jentsch,et al.  ClC-5 Cl--channel disruption impairs endocytosis in a mouse model for Dent's disease , 2000, Nature.

[38]  L. A. Haddad,et al.  Similarities and differences in the subcellular localization of hamartin and tuberin in the kidney. , 2000, American journal of physiology. Renal physiology.

[39]  H. Onda,et al.  Tsc2(+/-) mice develop tumors in multiple sites that express gelsolin and are influenced by genetic background. , 1999, The Journal of clinical investigation.

[40]  P. Courtoy,et al.  Intra-renal and subcellular distribution of the human chloride channel, CLC-5, reveals a pathophysiological basis for Dent's disease. , 1999, Human molecular genetics.

[41]  P. Stricklett,et al.  Targeting Collecting Tubules Using the Aquaporin-2 Promoter , 1999, Nephron Experimental Nephrology.

[42]  T. Jentsch,et al.  ClC-5, the chloride channel mutated in Dent's disease, colocalizes with the proton pump in endocytotically active kidney cells. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[43]  D. Ausiello,et al.  Expression of an AQP2 Cre recombinase transgene in kidney and male reproductive system of transgenic mice. , 1998, American journal of physiology. Cell physiology.

[44]  P. Harris,et al.  The molecular genetics of tuberous sclerosis. , 1994, Human molecular genetics.

[45]  J. Rapola,et al.  Polycystic disease of the kidney. Evaluation and classification based on nephron segment and cell-type specific markers. , 1990, Laboratory investigation; a journal of technical methods and pathology.