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1. Full Text Thick ascending limb of the loop of henle
by Mount, David B
Clinical Journal of the American Society of Nephrology, ISSN 1555-9041, 2014, Volume 9, Issue 11, pp. 1974 - 1986
The thick ascending limb occupies a central anatomic and functional position in human renal physiology, with critical roles in the defense of the extracellular... 
NACL TRANSPORT | ALANINE-RICH KINASE | CALCIUM-SENSING RECEPTOR | UROLOGY & NEPHROLOGY | TAMM-HORSFALL PROTEIN | NA-K-2CL COTRANSPORTER | FUNCTIONAL-CHARACTERIZATION | K+ CHANNEL | BARTTERS-SYNDROME | BASOLATERAL MEMBRANE | MACULA DENSA | Potassium - metabolism | Loop of Henle - anatomy & histology | Calcium - metabolism | Humans | Homeostasis | Loop of Henle - metabolism | Uromodulin - metabolism | Magnesium - metabolism | Sodium - metabolism | Ammonium Compounds - metabolism | Chlorides - metabolism | Bicarbonates - metabolism | Ion Transport - physiology | Renal Physiology | Na transport | water transport | calcium receptor | acidosis
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2. Full Text Mosaic expression of claudins in thick ascending limbs of Henle results in spatial separation of paracellular Na+ and Mg2+ transport
by Milatz, S and Himmerkus, N and Wulfmeyer, VC and Drewell, H and Mutig, K and Hou, JH and Breiderhoff, T and Muller, D and Fromm, M and Bleich, M and Gunzel, D
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, ISSN 0027-8424, 01/2017, Volume 114, Issue 2, pp. E219 - E227
The thick ascending limb (TAL) of Henle's loop drives paracellular Na+, Ca2+, and Mg2+ reabsorption via the tight junction (TJ). The TJ is composed of claudins... 
LOCALIZATION | paracellular ion transport | DIFFERENTIAL EXPRESSION | NEPHRON SEGMENTS | MULTIDISCIPLINARY SCIENCES | LOOP | microperfusion | claudin interaction | MAGNESIUM | MOUSE NEPHRON | FRET | TIGHT JUNCTION PROTEINS | KIDNEY | SELECTIVITY | REABSORPTION | tight junction | Tight Junctions - metabolism | Claudins - genetics | Humans | Mice, Inbred C57BL | Loop of Henle - metabolism | Magnesium - metabolism | Loop of Henle - physiology | Sodium - metabolism | Rats, Sprague-Dawley | Mice, Knockout | Animals | Claudins - metabolism | HEK293 Cells | Biological Sciences | PNAS Plus
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3. Full Text Randall's plaque of patients with nephrolithiasis begins in basement membranes of thin loops of Henle
by Evan, Andrew P and Lingeman, James E and Coe, Fredric L and Parks, Joan H and Bledsoe, Sharon B and Shao, Youzhi and Sommer, Andre J and Paterson, Ryan F and Kuo, Ramsay L and Grynpas, Marc
Journal of Clinical Investigation, ISSN 0021-9738, 2003, Volume 111, Issue 5, pp. 607 - 616
Our purpose here is to test the hypothesis that Randall's plaques, calcium phosphate deposits in kidneys of patients with calcium renal stones, arise in unique... 
Kidney Calculi - etiology | Postoperative Complications - etiology | Humans | Intestines - surgery | Middle Aged | Loop of Henle - metabolism | Loop of Henle - pathology | Kidney Calculi - metabolism | Kidney Calculi - pathology | Spectroscopy, Fourier Transform Infrared | Basement Membrane - metabolism | Basement Membrane - pathology | Calcium Oxalate - metabolism | X-Ray Diffraction | Adult | Aged
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4. Full Text A sall1-NuRD interaction regulates multipotent nephron progenitors and is required for loop of henle formation
by Basta, Jeannine M and Robbins, Lynn and Denner, Darcy R and Kolar, Grant R and Rauchman, Michael
Development (Cambridge), ISSN 0950-1991, 09/2017, Volume 144, Issue 17, pp. 3080 - 3094
The formation of the proper number of nephrons requires a tightly regulated balance between renal progenitor cell self-renewal and differentiation. The... 
Lgr5 | Loop of henle | NuRD | Sall1 | Nephron progenitor | ZINC-FINGER | SELF-RENEWAL | DEVELOPMENTAL BIOLOGY | IDENTIFICATION | CAUSATIVE GENE | TOWNES-BROCKS-SYNDROME | Loop of Henle | MUTATIONS | DEACETYLASE COMPLEX | KIDNEY | EXPRESSION | Biomarkers - metabolism | Amino Acid Sequence | Cell Proliferation - genetics | Protein Binding - genetics | Transcription Factors - chemistry | Multipotent Stem Cells - metabolism | Loop of Henle - metabolism | Mi-2 Nucleosome Remodeling and Deacetylase Complex - metabolism | Mutation - genetics | Transcription Factors - metabolism | Cell Differentiation - genetics | Homozygote | Ureter - embryology | Animals | Gene Expression Regulation, Developmental | Multipotent Stem Cells - cytology | Organogenesis - genetics | Loop of Henle - embryology | Mice | Kidney Tubules - metabolism | Ureter - metabolism | Loop of Henle - abnormalities | Cell Lineage - genetics | Gene Ontology | Hypoplasia | Kidneys | Transcription | Syngeneic grafts | Gene expression | Progenitor cells | Nephrons | Cadmium selenide | Rodents | Stem cells | Aquaporin 1 | Clear cell-type renal cell carcinoma | 203 | Stem Cells and Regeneration
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5. Full Text Corticomedullary difference in the effects of dietary Ca2+ on tight junction properties in thick ascending limbs of Henle's loop
by Plain, A and Wulfmeyer, VC and Milatz, S and Klietz, A and Hou, JH and Bleich, M and Himmerkus, N
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, ISSN 0031-6768, 02/2016, Volume 468, Issue 2, pp. 293 - 303
The thick ascending limb of Henle's loop (TAL) drives an important part of the reabsorption of divalent cations. This reabsorption occurs via the paracellular... 
PHYSIOLOGY | Calcium | PERMEABILITY | Microperfusion | Ion transport | Paracellular permeability | MAGNESIUM | TRANSPORT | CALCIUM-SENSING RECEPTOR | FEMALE RATS | Claudin | Nephron | MOUSE NEPHRON | NEPHROCALCINOSIS | KIDNEY | CLAUDIN-16 | EXPRESSION | Tight Junctions - metabolism | Claudins - genetics | Kidney Cortex - drug effects | Up-Regulation | Calcium - metabolism | Kidney Cortex - metabolism | Kidney Medulla - drug effects | Mice, Inbred C57BL | Loop of Henle - metabolism | Magnesium - metabolism | Action Potentials | Renal Reabsorption | Animals | Claudins - metabolism | Kidney Medulla - metabolism | Female | Mice | Loop of Henle - drug effects | Calcium, Dietary - pharmacology | Sodium Chloride - metabolism | Tight Junctions - drug effects
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6. Full Text Internalization of NKCC2 is impaired in thick ascending limb of Henle in moesin knockout mice
by Kawaguchi, Kotoku and Hatano, Ryo and Matsubara, Mitsunobu and Asano, Shinji
Pflügers Archiv - European Journal of Physiology, ISSN 0031-6768, 7/2018, Volume 470, Issue 7, pp. 1055 - 1068
Moesin is expressed in several types of cells including epithelial and endothelial cells. Several groups reported that moesin plays important roles in the... 
Neurosciences | Receptors | Endocytosis | Biomedicine | Human Physiology | Cytoskeleton | Molecular Medicine | Renal physiology | Cell Biology | Mineral metabolism | HOMEOSTASIS | PHYSIOLOGY | RADIXIN | EZRIN | RATS | PROTEINS | CELL | Solute Carrier Family 12, Member 1 - metabolism | Animals | Endothelial Cells - metabolism | Membrane Microdomains - metabolism | Kidney Medulla - metabolism | Loop of Henle - metabolism | Male | Mice | Microfilament Proteins - metabolism | Extremities - physiology | Endocytosis - physiology | Mice, Knockout | Physiological aspects | Membrane proteins | Kidneys | Internalization | Hyperchloremia | Rodents | moesin | Physiology | Sodium chloride | Localization | Endothelial cells | Glomerular filtration rate
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7. Full Text A Wnt7b-dependent pathway regulates the orientation of epithelial cell division and establishes the cortico-medullary axis of the mammalian kidney
by Jing Yu and Thomas J. Carroll and Jay Rajagopal and Akio Kobayashi and Qun Ren and Andrew P. McMahon
Development, ISSN 0950-1991, 01/2009, Volume 136, Issue 1, pp. 161 - 171
The mammalian kidney is organized into a cortex where primary filtration occurs, and a medullary region composed of elongated tubular epithelia where urine is... 
Loop of Henle elongation | Mouse | Wnt7b | Renal cortico-medullary axis | Renal medulla | Collecting duct elongation | Oriented cell division | TRANSFORMATION | METANEPHRIC MESENCHYME | PERISTALTIC MACHINERY | PROLIFERATION | DEVELOPMENTAL BIOLOGY | PATHOGENESIS | LUNG ORGANOGENESIS | DISEASE | DIFFERENTIATION | WNT | EXPRESSION | Cyclin-Dependent Kinase Inhibitor p57 - metabolism | Kidney Medulla - cytology | Epithelial Cells - metabolism | Loop of Henle - metabolism | Kidney Tubules, Collecting - cytology | Wnt Proteins - metabolism | Ureter - cytology | Nephrons - cytology | Cell Division | Body Patterning | Mammals - embryology | Female | Loop of Henle - embryology | Epithelial Cells - cytology | Ureter - metabolism | Proto-Oncogene Proteins - metabolism | Kidney Tubules, Collecting - embryology | Nephrons - embryology | Signal Transduction | Kidney Medulla - embryology | Mutation - genetics | Kidney Cortex - embryology | Kidney Tubules, Collecting - metabolism | Ureter - embryology | Animals | Kidney Medulla - metabolism | Loop of Henle - cytology | Mice | Nephrons - metabolism
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8. Full Text The absence of intrarenal ACE protects against hypertension
by Gonzalez-Villalobos, Romer A and Janjoulia, Tea and Fletcher, Nicholas K and Giani, Jorge F and Nguyen, Mien T.X and Riquier-Brison, Anne D and Seth, Dale M and Fuchs, Sebastien and Eladari, Dominique and Picard, Nicolas and Bachmann, Sebastian and Delpire, Eric and Peti-Peterdi, Janos and Navar, L. Gabriel and Bernstein, Kenneth E and McDonough, Alicia A
Journal of Clinical Investigation, ISSN 0021-9738, 05/2013, Volume 123, Issue 5, pp. 2011 - 2023
Activation of the intrarenal renin-angiotensin system (RAS) can elicit hypertension independently from the systemic RAS. However, the precise mechanisms by... 
RENAL PROXIMAL TUBULE | MEDICINE, RESEARCH & EXPERIMENTAL | NA-CL COTRANSPORTER | II-INDUCED HYPERTENSION | INFUSED MICE | CORTICAL COLLECTING DUCT | INCREASES ACTIVITY | KNOCKOUT MICE | ANGIOTENSIN-CONVERTING ENZYME | NA+-K+-2CL(-) COTRANSPORTER | BLOOD-PRESSURE | NG-Nitroarginine Methyl Ester - pharmacology | Angiotensin II - metabolism | Kidney - embryology | Liver - metabolism | Water - metabolism | Loop of Henle - metabolism | Male | Sodium - metabolism | Sodium-Potassium-Chloride Symporters - metabolism | Receptors, Drug - metabolism | Symporters - metabolism | Hypertension - metabolism | Transcription Factors - metabolism | Kidney - metabolism | Solute Carrier Family 12, Member 1 | Animals | Renin-Angiotensin System | Solute Carrier Family 12, Member 3 | Peptidyl-Dipeptidase A - metabolism | Mice | Protein-Serine-Threonine Kinases - metabolism | Usage | Care and treatment | Angiotensin converting enzyme | Renal hypertension | Health aspects | Infusion therapy | Methods | Hypertension | Studies | Plasma | Hypotheses | Kidneys | Rodents | Experiments
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9. Full Text Deletion of claudin-10 rescues claudin-16–deficient mice from hypomagnesemia and hypercalciuria
by Breiderhoff, Tilman and Himmerkus, Nina and Drewell, Hoora and Plain, Allein and Günzel, Dorothee and Mutig, Kerim and Willnow, Thomas E and Müller, Dominik and Bleich, Markus
Kidney International, ISSN 0085-2538, 03/2018, Volume 93, Issue 3, pp. 580 - 588
The tight junction proteins claudin-10 and -16 are crucial for the paracellular reabsorption of cations along the thick ascending limb of Henle’s loop in the... 
paracellular pathway | magnesium | calcium | thick ascending limb | claudin | tight junction | PERMEABILITY | MG2+ TRANSPORT | PARACELLULAR NA+ | UROLOGY & NEPHROLOGY | NEPHROCALCINOSIS | MUTATIONS | HENLES LOOP | EXPRESSION | REABSORPTION | CATION | Kidney Tubules, Distal - pathology | Magnesium Deficiency - physiopathology | Calcium - metabolism | Claudins - deficiency | Loop of Henle - metabolism | Loop of Henle - pathology | Sodium - metabolism | Nephrocalcinosis - physiopathology | Magnesium Deficiency - genetics | Nephrocalcinosis - metabolism | Gene Deletion | Hypercalciuria - prevention & control | Nephrocalcinosis - prevention & control | Hypercalciuria - genetics | Magnesium Deficiency - prevention & control | Disease Models, Animal | Claudins - genetics | Genetic Predisposition to Disease | Hypercalciuria - physiopathology | Mice, Inbred C57BL | Loop of Henle - physiopathology | Magnesium - metabolism | Magnesium Deficiency - metabolism | Mice, Knockout | Phenotype | Animals | Nephrocalcinosis - genetics | Hypercalciuria - metabolism | Kidney Tubules, Distal - physiopathology | Kidney Tubules, Distal - metabolism | Urine | Phosphorylation | Excretion | Renal function | Kidneys | Calcium | Tubules | Reabsorption | Permeability | Gene expression | Hypercalciuria | Clonal deletion | Sodium | Calcinosis | Rodents | Hypermagnesemia | Mutation | Magnesium | Kidney diseases | Polyuria | Potassium | Hypomagnesemia
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10. Full Text A SPAK Isoform Switch Modulates Renal Salt Transport and Blood Pressure
by McCormick, James A and Mutig, Kerim and Nelson, Joshua H and Saritas, Turgay and Hoorn, Ewout J and Yang, Chao-Ling and Rogers, Shaunessy and Curry, Joshua and Delpire, Eric and Bachmann, Sebastian and Ellison, David H
Cell Metabolism, ISSN 1550-4131, 09/2011, Volume 14, Issue 3, pp. 352 - 364
The renal thick ascending limb (TAL) and distal convoluted tubule (DCT) play central roles in salt homeostasis and blood pressure regulation. An emerging model... 
NA+-CL-COTRANSPORTER | DISTAL CONVOLUTED TUBULE | PSEUDOHYPOALDOSTERONISM TYPE-II | MOUSE MODEL | ENDOCRINOLOGY & METABOLISM | KNOCKOUT MICE | HYPERTENSION | WNK1 KINASE | EXPRESSION | PROVOKES ACUTE TRAFFICKING | GITELMANS-SYNDROME | CELL BIOLOGY | Phosphorylation - physiology | Protein-Serine-Threonine Kinases - deficiency | Receptors, Drug - genetics | Homeostasis | Loop of Henle - metabolism | Sodium-Potassium-Chloride Symporters - metabolism | Kidney Tubules, Distal - cytology | Blood Pressure - physiology | Phosphorylation - drug effects | Sodium Chloride - metabolism | Protein-Serine-Threonine Kinases - metabolism | Protein Structure, Tertiary | Water-Electrolyte Balance - physiology | Signal Transduction | Isoenzymes - genetics | Gene Expression Regulation | Protein-Serine-Threonine Kinases - genetics | Sodium-Potassium-Chloride Symporters - genetics | Isoenzymes - deficiency | Reverse Transcriptase Polymerase Chain Reaction | Receptors, Drug - metabolism | Symporters - metabolism | Mice, Knockout | Extracellular Fluid - metabolism | Solute Carrier Family 12, Member 1 | Animals | Solute Carrier Family 12, Member 3 | Symporters - genetics | Loop of Henle - cytology | Isoenzymes - pharmacology | Mice | Salts - metabolism | Protein-Serine-Threonine Kinases - pharmacology | Kidney Tubules, Distal - metabolism | Hypertension | Blood pressure | Universities and colleges | Phosphotransferases | Analysis
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11. Full Text The ugly duckling of urinary acidification: What is the contribution of the thick ascending limb of the loop of henle to urinary acidification?
by Wagner, Carsten A and Mohebbi, Nilufar and Bourgeois, Soline
American Journal of Physiology - Renal Physiology, ISSN 0363-6127, 09/2015, Volume 309, Issue 5, pp. F431 - F433
LOCALIZATION | BICARBONATE ABSORPTION | TRANSPORT | PHYSIOLOGY | FUROSEMIDE | HYPEROSMOLALITY | UROLOGY & NEPHROLOGY | NA+ | TUBULE | KIDNEY | VACUOLAR H+-ATPASE | Bicarbonates - metabolism | Loop of Henle - metabolism | Male | Animals | Macrolides
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12. Full Text PTH-independent regulation of blood calcium concentration by the calcium-sensing receptor
by Loupy, Alexandre and Ramakrishnan, Suresh Krishna and Wootla, Bharath and Chambrey, Régine and De La Faille, Renaud and Bourgeois, Soline and Bruneval, Patrick and Mandet, Chantal and Christensen, Erik Ilso and Faure, Hélène and Cheval, Lydie and Laghmani, Kamel and Collet, Corinne and Eladari, Dominique and Dodd, Robert H and Ruat, Martial and Houillier, Pascal
Journal of Clinical Investigation, ISSN 0021-9738, 09/2012, Volume 122, Issue 9, pp. 3355 - 3367
Tight regulation of calcium levels is required for many critical biological functions. The Ca2+-sensing receptor (CaSR) expressed by parathyroid cells controls... 
MEDICINE, RESEARCH & EXPERIMENTAL | EXTRACELLULAR CA2+-SENSING RECEPTOR | PRIMARY HYPERPARATHYROIDISM | LUMINAL MEMBRANE | COLLECTING DUCT | RAT-KIDNEY | PARATHYROID-HORMONE SECRETION | FAMILIAL HYPOCALCIURIC HYPERCALCEMIA | HENLES LOOP | CALCEMIC RESPONSE | THICK ASCENDING LIMB | Calcium - metabolism | Loop of Henle - metabolism | Male | Parathyroidectomy | Receptors, Calcium-Sensing - metabolism | Sodium-Potassium-Chloride Symporters - metabolism | Calcium - blood | Osteocalcin - blood | Parathyroid Hormone - metabolism | Diphosphonates - therapeutic use | Receptors, Calcium-Sensing - antagonists & inhibitors | Hypoparathyroidism - drug therapy | Parathyroid Hormone - secretion | Permeability - drug effects | Receptors, Calcium-Sensing - physiology | Amino Acids - urine | Bone Density Conservation Agents - therapeutic use | Rats | Calcium - urine | Creatinine - urine | Rats, Sprague-Dawley | Bone Density Conservation Agents - pharmacology | Naphthalenes - pharmacology | Sodium-Potassium-Exchanging ATPase - metabolism | Solute Carrier Family 12, Member 1 | Animals | Hypoparathyroidism - blood | Diphosphonates - pharmacology | Naphthalenes - therapeutic use | Measurement | Calcium, Dietary | Analysis and chemistry | Parathyroid hormone | Research | Gene expression | Health aspects | Blood | Methods | Organic chemistry | Chemical Sciences
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13. Full Text Urinary neutrophil gelatinase-associated lipocalin levels reflect damage to glomeruli, proximal tubules, and distal nephrons
by Kuwabara, Takashige and Mori, Kiyoshi and Mukoyama, Masashi and Kasahara, Masato and Yokoi, Hideki and Saito, Yoko and Yoshioka, Tetsuro and Ogawa, Yoshihisa and Imamaki, Hirotaka and Kusakabe, Toru and Ebihara, Ken and Omata, Mitsugu and Satoh, Noriko and Sugawara, Akira and Barasch, Jonathan and Nakao, Kazuwa
Kidney International, ISSN 0085-2538, 02/2009, Volume 75, Issue 3, pp. 285 - 294
Urinary neutrophil gelatinase-associated lipocalin (Ngal or lipocalin 2) is a very early and sensitive biomarker of kidney injury. Here we determined the... 
albuminuria | acute renal failure | obstructive nephropathy | diabetic nephropathy | nephrotic syndrome | Diabetic nephropathy | Obstructive nephropathy | Nephrotic syndrome | Albuminuria | Acute renal failure | NGAL | ACUTE KIDNEY INJURY | MOUSE | DIABETIC-NEPHROPATHY | IRON | TISSUE GROWTH-FACTOR | CARDIAC-SURGERY | INSULIN-RESISTANCE | UROLOGY & NEPHROLOGY | ALBUMIN | RENAL INJURY | Acute-Phase Proteins - urine | Biomarkers - urine | Nephrotic Syndrome - urine | Nephritis, Interstitial - urine | Angiotensin II Type 1 Receptor Blockers - therapeutic use | Humans | Proto-Oncogene Proteins - urine | Nephrotic Syndrome - metabolism | Lipocalins - urine | Loop of Henle - metabolism | Ureteral Obstruction - metabolism | RNA, Messenger - metabolism | Nephritis, Interstitial - metabolism | Time Factors | Sensitivity and Specificity | Kidney Glomerulus - metabolism | Diabetes Mellitus, Experimental - metabolism | Benzimidazoles - therapeutic use | Disease Models, Animal | Diabetic Nephropathies - urine | Lipocalins - metabolism | Proto-Oncogene Proteins - metabolism | Kidney Tubules, Proximal - cytology | Acute-Phase Proteins - metabolism | Albumins - metabolism | Diabetic Nephropathies - metabolism | Mice, Inbred C57BL | Mice, Transgenic | Animals | Lipocalin-2 | Kidney Tubules, Proximal - metabolism | Tetrazoles - therapeutic use | Mice | Acute Kidney Injury - metabolism | Nephrons - metabolism
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14. Full Text Increased Proliferative Cells in the Medullary Thick Ascending Limb of the Loop of Henle in the Dahl Salt-Sensitive Rat
by Yang, Chun and Stingo, Francesco C and Ahn, Kwang Woo and Liu, Pengyuan and Vannucci, Marina and Laud, Purushottam W and Skelton, Meredith and O’Connor, Paul and Kurth, Terry and Ryan, Robert P and Moreno, Carol and Tsaih, Shirng-Wern and Patone, Giannino and Hummel, Oliver and Jacob, Howard J and Liang, Mingyu and Cowley, Allen W
Hypertension, ISSN 0194-911X, 01/2013, Volume 61, Issue 1, pp. 208 - 215
Studies of transcriptome profiles have provided new insights into mechanisms underlying the development of hypertension. Cell type heterogeneity in tissue... 
kidney | cell cycle | gene expression | OXIDATIVE STRESS | PROTECTION | ENHANCED SUPEROXIDE-PRODUCTION | TRANSPORT | CHLORIDE REABSORPTION | GENE-EXPRESSION | PERIPHERAL VASCULAR DISEASE | HYPERTENSION | CONTRIBUTES | CYCLE | Cell Proliferation | Gene Expression Regulation | Loop of Henle - physiopathology | Loop of Henle - metabolism | Rats | Male | Gene Expression Profiling | Hypertension - physiopathology | Hypertension - metabolism | Animals | Cell Cycle - physiology | Rats, Inbred Dahl | Hypertension - genetics | Sodium Chloride - metabolism | salt intake | physiological genomics | Kidney
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15. Full Text Missense mutation of POU domain class 3 transcription factor 3 in Pou3f3L423P mice causes reduced nephron number and impaired development of the thick ascending limb of the loop of Henle
by Rieger, Alexandra and Kemter, Elisabeth and Kumar, Sudhir and Popper, Bastian and Aigner, Bernhard and Wolf, Eckhard and Wanke, Rüdiger and Blutke, Andreas
PLoS ONE, ISSN 1932-6203, 07/2016, Volume 11, Issue 7, pp. e0158977 - e0158977
During nephrogenesis, POU domain class 3 transcription factor 3 (POU3F3 aka BRN1) is critically involved in development of distinct nephron segments, including... 
Blood Pressure | Body Weight | RNA, Messenger - genetics | Kidney - growth & development | Loop of Henle - metabolism | Organ Size | Male | Mutation, Missense | Nephrons - abnormalities | Nerve Tissue Proteins - genetics | Kidney - metabolism | Animals | POU Domain Factors - genetics | Kidney - abnormalities | Loop of Henle - growth & development | Nephrons - growth & development | Female | Mice | Loop of Henle - abnormalities | Nephrons - metabolism | Biotechnology | Transcription factors | Laboratories | Genomes | Veterinary medicine | Homeobox | Missense mutation | Rodents | Loop of Henle | Qualitative analysis | Lesions | Urine | Hypertension | Phenotypes | Kidneys | Breeding of animals | Mutants | Urea | Pathology | Ethyl nitrosourea | Mutagenesis | Point mutation | Renal failure | Mutation | Kidney diseases | Index Medicus
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