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3. Angiotensin II Directly Increases Endothelial Calcium and Nitric Oxide in Kidney and Brain Microvessels In Vivo With Reduced Efficacy in Hypertension

Author

Becerra Calderon, Alejandra, primary, Shroff, Urvi Nikhil, additional, Deepak, Sachin, additional, Izuhara, Audrey, additional, Trogen, Greta, additional, McDonough, Alicia A., additional, Gurley, Susan B., additional, Nelson, Jonathan W., additional, Peti‐Peterdi, János, additional, and Gyarmati, Georgina, additional

Published
2024
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6. Kidney Renin–Angiotensin System: Lost in a RAS Cascade.

Author

Crowley, Steven D., Navar, L. Gabriel, Prieto, Minolfa C., Gurley, Susan B., and Coffman, Thomas M.

Abstract

Renin was discovered more than a century ago. Since then, the functions of the renin–angiotensin system in the kidney have been the focus of intensive research revealing its importance in regulation of renal physiology and in the pathogenesis of heart, vascular, and kidney diseases. Inhibitors of renin–angiotensin system components are now foundational therapies for a range of kidney and cardiovascular diseases from hypertension to heart failure to diabetic nephropathy. Despite years of voluminous research, emerging studies continue to reveal new complexities of the regulation of the renin–angiotensin system within the kidney and identification of nonclassical components of the system like the prorenin receptor (PRR) and ACE2 (angiotensin-converting enzyme 2), with powerful renal effects that ultimately impact the broader cardiovascular system. With the emergence of a range of novel therapies for cardiovascular and kidney diseases, the importance of a detailed understanding of the renin–angiotensin system in the kidney will allow for the development of informed complementary approaches for combinations of treatments that will optimally promote health and longevity over the century ahead. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Severe Acute Respiratory Syndrome Coronavirus 2, COVID-19, and the Renin-Angiotensin System: Pressing Needs and Best Research Practices

Author

Sparks, Matthew A., South, Andrew M., Badley, Andrew D., Baker-Smith, Carissa M., Batlle, Daniel, Bozkurt, Biykem, Cattaneo, Roberto, Crowley, Steven D., Dell’Italia, Louis J., Ford, Andria L., Griendling, Kathy, Gurley, Susan B., Kasner, Scott E., Murray, Joseph A., Nath, Karl A., Pfeffer, Marc A., Rangaswami, Janani, Taylor, W. Robert, and Garovic, Vesna D.

Published
2020
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12. Data from Targeting eNOS in Pancreatic Cancer

Author

Lampson, Benjamin L., primary, Kendall, S. DiSean, primary, Ancrile, Brooke B., primary, Morrison, Meghan M., primary, Shealy, Michael J., primary, Barrientos, Katharine S., primary, Crowe, Matthew S., primary, Kashatus, David F., primary, White, Rebekah R., primary, Gurley, Susan B., primary, Cardona, Diana M., primary, and Counter, Christopher M., primary

Published
2023
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13. Supplementary Figure Legends 1-3 from Targeting eNOS in Pancreatic Cancer

Author

Lampson, Benjamin L., primary, Kendall, S. DiSean, primary, Ancrile, Brooke B., primary, Morrison, Meghan M., primary, Shealy, Michael J., primary, Barrientos, Katharine S., primary, Crowe, Matthew S., primary, Kashatus, David F., primary, White, Rebekah R., primary, Gurley, Susan B., primary, Cardona, Diana M., primary, and Counter, Christopher M., primary

Published
2023
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14. Supplementary Figure 3 from Targeting eNOS in Pancreatic Cancer

Author

Lampson, Benjamin L., primary, Kendall, S. DiSean, primary, Ancrile, Brooke B., primary, Morrison, Meghan M., primary, Shealy, Michael J., primary, Barrientos, Katharine S., primary, Crowe, Matthew S., primary, Kashatus, David F., primary, White, Rebekah R., primary, Gurley, Susan B., primary, Cardona, Diana M., primary, and Counter, Christopher M., primary

Published
2023
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15. Supplementary Figure 2 from Targeting eNOS in Pancreatic Cancer

Author

Lampson, Benjamin L., primary, Kendall, S. DiSean, primary, Ancrile, Brooke B., primary, Morrison, Meghan M., primary, Shealy, Michael J., primary, Barrientos, Katharine S., primary, Crowe, Matthew S., primary, Kashatus, David F., primary, White, Rebekah R., primary, Gurley, Susan B., primary, Cardona, Diana M., primary, and Counter, Christopher M., primary

Published
2023
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17. Soluble ACE2 Is Filtered into the Urine

Author

Nelson, Jonathan W., primary, Ortiz-Melo, David I., additional, Mattocks, Natalie K., additional, Emathinger, Jacqueline M., additional, Prescott, Jessica, additional, Xu, Katherine, additional, Griffiths, Robert C., additional, Wakasaki, Rumie, additional, Piehowski, Paul D., additional, Hutchens, Michael P., additional, Coffman, Thomas M., additional, and Gurley, Susan B., additional

Published
2022
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25. Combined Kelch-like 3 and Cullin 3 Degradation is a Central Mechanism in Familial Hyperkalemic Hypertension in Mice

Author

Maeoka, Yujiro, primary, Ferdaus, Mohammed Z., additional, Cornelius, Ryan J., additional, Sharma, Avika, additional, Su, Xiao-Tong, additional, Miller, Lauren N., additional, Robertson, Joshua A., additional, Gurley, Susan B., additional, Yang, Chao-Ling, additional, Ellison, David H., additional, and McCormick, James A., additional

Published
2022
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27. Chronic activation of vasopressin-2 receptors induces hypertension in Liddle mice by promoting Na+ and water retention.

Author

Stockand, James D., Mironova, Elena V., Hong Xiang, Soares, Antonio G., Contreras, Jorge, McCormick, James A., Gurley, Susan B., and Pao, Alan C.

Subjects
HYPERTENSION, BLOOD pressure, MICE, DESMOPRESSIN, AQUAPORINS, BLOOD plasma, ANGIOTENSIN-receptor blockers
Abstract

The renin-angiotensin-aldosterone and arginine vasopressin-V2 receptor-aquaporin-2 (AQP2) systems converge on the epithelial Na+ channel (ENaC) to regulate blood pressure and plasma tonicity. Although it is established that V2 receptors initiate renal water reabsorption through AQP2, whether V2 receptors can also induce renal Na+ retention through ENaC and raise blood pressure remains an open question. We hypothesized that a specific increase in V2 receptor-mediated ENaC activity can lead to high blood pressure. Our approach was to test effects of chronic activation of V2 receptors in Liddle mice, a genetic mouse model of high ENaC activity, and compare differences in ENaC activity, urine Na+ excretion, and blood pressure with control mice. We found that ENaC activity was elevated in Liddle mice and could not be stimulated further by administration of desmopressin (dDAVP), a V2 receptor-specific agonist. In contrast, Liddle mice showed higher levels of expression of AQP2 and aquaporin-3, but they could still respond to dDAVP infusion by increasing phospho-AQP2 expression. With dDAVP infusion, Liddle mice excreted smaller urine volume and less urine Na+ and developed higher blood pressure compared with control mice; this hypertension was attenuated with administration of the ENaC inhibitor benzamil. We conclude that V2 receptors contribute to hypertension in the Liddle mouse model by promoting primary Na+ and concomitant water retention. [ABSTRACT FROM AUTHOR]

Published
2022
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29. Vascular control of kidney epithelial transporters

Author

Sparks, Matthew A., primary, Dilmen, Emre, additional, Ralph, Donna L., additional, Rianto, Fitra, additional, Hoang, Thien A., additional, Hollis, Alison, additional, Diaz, Edward J., additional, Adhikari, Rishav, additional, Chew, Gabriel, additional, Petretto, Enrico G., additional, Gurley, Susan B., additional, McDonough, Alicia A., additional, and Coffman, Thomas M., additional

Published
2021
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31. Influence of genetic background on albuminuria and kidney injury in [Ins2.sup.+/C96Y] (Akita) mice

Author

Gurley, Susan B., Mach, Carrie L., Stegbauer, Johannes, Yang, Jihong, Snow, Kamie P., Hu, Ann, Meyer, Timothy W., and Coffman, Thomas M.

Subjects
Kidney diseases -- Development and progression, Kidney diseases -- Genetic aspects, Type 1 diabetes -- Development and progression, Type 1 diabetes -- Models, Albuminuria -- Development and progression, Albuminuria -- Genetic aspects, Biological sciences
Abstract

Previous studies have shown that Akita mice bearing the [Ins2.sup.+/C96Y] mutation have significant advantages as a type I diabetes platform for developing models of diabetic nephropathy (DN; Gurley SB, Clare SE, Snow KP, Hu A, Meyer TW, Coffman TM. Am J Physiol Renal Physiol 290: F214-F222, 2006). In view of the critical role for genetic factors in determining susceptibility to DN in humans, we investigated the role of genetic background on kidney injury in Akita mice. To generate a series of inbred Akita mouse lines, we back-crossed the [Ins2.sup.C96Y] mutation more than six generations onto the 129/SvEv and DBA/2 backgrounds and compared the extent of hyperglycemia and renal disease with the standard C57BL/6-[Ins2.sup.+/C96Y] fine. Male mice from all three Akita strains developed marked and equivalent hyperglycemia. However, there were significant differences in the level of albuminuria among the lines with a hierarchy of DBA/2 > 129/SvEv > C57BL/6. Renal and glomerular hypertrophy was seen in all of the lines, but significant increases in mesangial matrix compared with baseline nondiabetic controls were observed only in the 129 and C57BL/6 backgrounds. In F1(DBA/2 x C57BL/6)-[Ins2.sup.+/C96Y] mice, the extent of albuminuria was similar to the parental DBA/2-[Ins2.sup.+/C96Y] line; they also developed marked hyperfiltration. These studies identify strong effects of genetic background to modify the renal phenotype associated with the [Ins2.sup.C96Y] mutation. Identification of these naturally occurring strain differences should prove useful for nephropathy modeling and may be exploited to allow identification of novel susceptibility alleles for albuminuria in diabetes. mouse model of type I diabetes; albuminuria; strain comparison doi:10.1152/ajprenal.90515.2008

Published
2010

35. Altered blood pressure responses and normal cardiac phenotype in ACE2-null mice

Author

Gurley, Susan B., Allred, Alicia, Le, Thu H., Griffiths, Robert, Mao, Lan, Philip, Nisha, Haystead, Timothy A., Donoghue, Mary, Breitbart, Roger E., Acton, Susan L., Rockman, Howard A., and Coffman, Thomas M.

Subjects
Angiotensin converting enzyme -- Research, Blood pressure -- Research, Mice -- Research, Phenotype -- Research
Abstract

The carboxypeptidase ACE2 is a homologue of angiotensin-converting enzyme (ACE). To clarify the physiological roles of ACE2, we generated mice with targeted disruption of the Ace2 gene. ACE2-deficient mice were [...]

Published
2006

36. Impact of genetic background on nephropathy in diabetic mice

Author

Gurley, Susan B., Clare, Sharon E., Snow, Kamie P., Hu, Ann, Meyer, Timothy W., and Coffman, Thomas M.

Subjects
Albuminuria -- Research, Mice -- Research, Mice -- Health aspects, Streptozocin -- Research, Biological sciences
Abstract

With the goal of identifying optimal platforms for developing better models of diabetic nephropathy in mice, we compared renal effects of streptozotocin (STZ)-induced diabetes among five common inbred mouse strains (C57BL/6, MRL/ Mp, BALB/c, DBA/2, and 129/SvEv). We also evaluated the renal consequences of chemical and genetic diabetes on the same genetic background (C57BL/6). There was a hierarchical response of blood glucose level to the STZ regimen among the strains (DBA/2 > C57BL/6 > MRL/MP > 129/SvEv > BALB/c). In all five strains, males demonstrated much more robust hyperglycemia with STZ than females. STZ-induced diabetes was associated with modest levels of albuminuria in all of the strains but was greatest in the DBA/2 strain, which also had the most marked hyperglycemia. Renal structural changes on light microscopy were limited to the development of mesangial expansion, and, while there were some apparent differences among strains in susceptibility to renal pathological changes, there was a significant positive correlation between blood glucose and the degree of mesangial expansion, suggesting that most of the variability in renal pathological abnormalities was because of differences in hyperglycemia. Although the general character of renal involvement was similar between chemical and genetic diabetes, Akita mice developed more marked hyperglycemia, elevated blood pressures, and less variability in renal structural responses. Thus, among the strains and models tested, the DBA/2 genetic background and the Akita (Ins[2.sup.+/C96Y]) model may be the most useful platforms for model development. mouse models of type I diabetes; streptozotocin; Akita mice; albuminuria; strain comparison

Published
2006

37. Direct Actions of AT 1 (Type 1 Angiotensin) Receptors in Cardiomyocytes Do Not Contribute to Cardiac Hypertrophy

Author

Sparks, Matthew A., primary, Rianto, Fitra, additional, Diaz, Edward, additional, Revoori, Ritika, additional, Hoang, Thien, additional, Bouknight, Lucas, additional, Stegbauer, Johannes, additional, Vivekanandan-Giri, Anuradha, additional, Ruiz, Phillip, additional, Pennathur, Subramaniam, additional, Abraham, Dennis M., additional, Gurley, Susan B., additional, Crowley, Steven D., additional, and Coffman, Thomas M., additional

Published
2021
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39. List of Contributors

Author

Abrahamson, Dale R., primary, Al-Awqati, Qais, additional, Alpern, Robert J., additional, Altenberg, Guillermo A., additional, Bailey, Matthew A., additional, Baum, Michel, additional, Bichet, Daniel G., additional, Blantz, Roland C., additional, Breyer, Matthew D., additional, Breyer, Richard M., additional, Brinkkoetter, Paul T., additional, Bush, Kevin T., additional, Cantley, Lloyd, additional, Cao, Chunhua, additional, Capasso, Giovambattista, additional, Castrop, Hayo, additional, Chan, Laurence, additional, Cina, Davide, additional, Coffman, Thomas M., additional, Crowley, Steven D., additional, Dimke, Henrik, additional, Eisner, Gilbert M., additional, Eladari, Dominique, additional, Ellison, David H., additional, Endou, Hitoshi, additional, Felder, Robin A., additional, Féraille, Eric, additional, Frøkiær, Jørgen, additional, Gamba, Gerardo, additional, Gattineni, Jyothsna, additional, Giebisch, Gerhard, additional, Gmurczyk, Aleksandra, additional, Granger, Joey P., additional, Griffin, Sian V., additional, Guggino, William B., additional, Gurley, Susan B., additional, Hall, John E., additional, Hall, Michael E., additional, Hallows, Kenneth R., additional, Hanner, Fiona, additional, Harris, Raymond C., additional, Hasler, Udo, additional, Kevin Hix, J., additional, Huang, Chou-Long, additional, Johns, Edward J., additional, Jose, Pedro A., additional, Kaissling, Brigitte, additional, Kleyman, Thomas R., additional, Kopp, Ulla C., additional, Kriz, Wilhelm, additional, Kwon, Tae-Hwan, additional, Lang, Florian, additional, Layton, Harold E., additional, Le, Thu H., additional, Lifton, Richard P., additional, Loffing, Johannes, additional, Maezawa, Yoshiro, additional, Malnic, Gerhard, additional, Matlin, Karl S., additional, Charles Michel, C., additional, Miner, Jeffrey H., additional, Muto, Shigeaki, additional, Nielsen, Søren, additional, Nigam, Sanjay K., additional, Oh, Man S., additional, Oliver, Juan A., additional, Pallone, Thomas L., additional, Palmer, Biff F., additional, Palmer, Lawrence G., additional, Peti-Peterdi, János, additional, Pieczynski, Jay N., additional, Quaggin, Susan E., additional, Reuss, Luis, additional, Rivard, Christopher J., additional, Robertson, Gary L., additional, Rosa, Robert M., additional, Sackin, Henry, additional, Sahni, Vaibhav, additional, Sakurai, Hiroyuki, additional, Sands, Jeff M., additional, Satlin, Lisa M., additional, Schild, Laurent, additional, Schnermann, Jürgen B., additional, Scholl, Ute I., additional, Sekine, Takashi, additional, Seldin, Donald W., additional, Shankland, Stuart J., additional, Sheng, Shaohu, additional, Shirley, David G., additional, Silver, Stephen M., additional, Skott, Martin, additional, Staub, Olivier, additional, Sterns, Richard H., additional, Stockand, James D., additional, Tam, Frederick W.K., additional, Thomson, Scott C., additional, Trepiccione, Francesco, additional, Unwin, Robert J., additional, Vesely, David L., additional, Wang, Wei, additional, Wang, Wenhui, additional, Weinstein, Alan M., additional, Welling, Paul A., additional, Wildman, Scott S.P., additional, Woodward, Owen M., additional, Yoder, Bradley K., additional, Yu, Alan S.L., additional, and Zacchia, Miriam, additional

Published
2012
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43. Contributors

Author

ABBATE, MAURO, primary, ABRAHAMSON, DALE R., additional, ADAMCZAK, MARCIN, additional, ADROGUÉ, HORACIO J., additional, ALPER, SETH L., additional, ALPERN, ROBERT J., additional, ANDREOLI, THOMAS E., additional, APERIA, ANITA C., additional, BAILEY, MATTHEW A., additional, BATLLE, DANIEL, additional, BAUM, MICHEL, additional, BERNDT, THERESA J., additional, BEVENSEE, MARK O., additional, BIBER, JÜRG, additional, BICHET, DANIEL G., additional, BINDELS, RENÉ J.M., additional, BLANTZ, ROLAND C., additional, BORON, WALTER F., additional, BRATER, D. CRAIG, additional, BRIGGS, JOSEPHINE P., additional, BROWN, ALEX, additional, BRUNSKILL, NIGEL J., additional, BURCKHARDT, GERHARD, additional, BURNSTOCK, GEOFFREY, additional, CANTLEY, LLOYD, additional, CAO, CHUNHUA, additional, CAPASSO, GIOVAMBATTISTA, additional, CAPLAN, MICHAEL J., additional, CARROLL, HUGH J., additional, CHAN, LAURENCE, additional, CHUNG-PARK, MOONJA, additional, COE, FREDRIC L., additional, COFFMAN, THOMAS M., additional, COMPER, WAYNE D., additional, CONRAD, KIRK P., additional, CROWLEY, STEVEN D., additional, CURTHOYS, NORMAN P., additional, CUTILLAS, PEDRO R., additional, DANOFF, THEODORE M., additional, DEBNAM, EDWARD S., additional, DIMKE, HENRIK, additional, DOUCET, ALAIN, additional, DUBEY, RAGHVENDRA K., additional, DUSSO, ADRIANA, additional, ECKARDT, KAI-UWE, additional, ELLISON, DAVID H., additional, ENDOU, HITOSHI, additional, ENDRE, ZOLTÁN HUBA, additional, EPSTEIN, FRANKLIN H., additional, EVAN, ANDREW, additional, FALK, RONALD J., additional, FARBAKHSH, KAMBIZ, additional, FERRERI, NICHOLAS R., additional, FONG, PEYING, additional, FONTELES, MANASSES CLAUDINO, additional, FORSTER, IAN, additional, FORTE, LEONARD RALPH, additional, FRANCH, HAROLD A., additional, FRASSETTO, LYNDA A., additional, FRIEDMAN, PETER A., additional, FRØKLÆR, JØRGEN, additional, GEIBEL, JOHN P., additional, GEKLE, MICHAEL, additional, GIEBISCH, GERHARD, additional, GINÈS, PERE, additional, GOLDSTEIN, STEVE A.N., additional, GORAL, SIMIN, additional, GRIFFIN, SIAN V., additional, GUGGINO, WILLIAM B., additional, GUISE, THERESA A., additional, GURLEY, SUSAN B., additional, HALL, STEPHEN D., additional, HALPERIN, MITCHELL L., additional, HAMM, L. LEE, additional, HEBERT, STEVEN C., additional, HEDIGER, MATTHIAS A., additional, HELDERMAN, J. HAROLD, additional, HENRICH, WILLIAM L., additional, HERAS-HERZIG, AILLEEN, additional, HERNANDO, NATI, additional, HOENDEROP, JOOST G.J., additional, HOLTBÄCK, ULLA, additional, HORISBERGER, JEAN-DANIEL, additional, HUMMLER, EDITH, additional, HUNLEY, TRACY E., additional, JACKSON, EDWIN K., additional, JENNETTE, J. CHARLES, additional, JOHNS, EDWARD J., additional, JOHNSON, JOHN P., additional, KAISSLING, BRIGITTE, additional, KAMEL, KAMEL S., additional, KARUMANCHI, S. ANANTH, additional, KASHTAN, CLIFFORD E., additional, KASISKE, BERTRAM L., additional, KATZ, ADRIAN I., additional, KING, BRIAN F., additional, KLAHR, SAULO, additional, KLEYMAN, THOMAS R., additional, KOEPSELL, HERMANN, additional, KON, VALENTINA, additional, KONRAD, MARTIN, additional, KOPP, ULLA C., additional, KRAPF, RETO, additional, KRIZ, WILHELM, additional, KUMAR, RAJIV, additional, KURSCHAT, CHRISTINE E., additional, KURTZ, ARMIN, additional, KWON, TAE-HWAN, additional, LANDOWSKI, CHRISTOPHER P., additional, LANGONE, ANTHONY J., additional, LANG, FLORIAN, additional, LAYTON, HAROLD E., additional, LE, THU H., additional, LEVY, DANIEL I., additional, LIN, SHIH-HUA, additional, LINDHEIMER, MARSHALL D., additional, LU, CHRISTOPHER Y., additional, MADAIO, MICHAEL P., additional, MADIAS, NICOLAOS E., additional, MALNIC, GERHARD, additional, MATLIN, KARL S., additional, McCLELLAN, WILLIAM C., additional, MCGIFF, JOHN C., additional, MICHEL, C. CHARLES, additional, MINER, JEFFREY H., additional, MITCH, WILLIAM E., additional, MIYAZAKI, HIROKI, additional, MOE, ORSON W., additional, MOLITORIS, BRUCE A., additional, MORRIS, R. CURTIS, additional, MUJAIS, SALIM K., additional, MURER, HEINI, additional, MUTO, SHIGEAKI, additional, NATTIE, EUGENE, additional, NEILSON, ERIC G., additional, NIELSEN, SØREN, additional, NIGAM, SANJAY K., additional, NOGUEIRA, JOSEPH M., additional, OH, MAN S., additional, OKUSA, MARK D., additional, OSICKA, TANYA M., additional, PALLONE, THOMAS L., additional, PALMER, BIFF F., additional, PALMER, LAWRENCE G., additional, PARKER, MARK D., additional, PARKS, JOAN H., additional, PREISIG, PATRICIA A., additional, QUAMME, GARY A., additional, QUARLES, L. DARRYL, additional, QUIGLEY, RAYMOND, additional, REEVES, W. BRIAN, additional, REMUZZI, GIUSEPPE, additional, REUSS, LUIS, additional, RICCARDI, DANIELA, additional, RINGHOFER, BRIAN, additional, RITZ, EBERHARD, additional, RIVARD, CHRISTOPHER J., additional, ROBERTSON, GARY L., additional, ROSA, ROBERT M., additional, ROSSIER, BERNARD C., additional, RUSSO, LEILEATA M., additional, SACKIN, HENRY, additional, SAKURAI, HIROYUKI, additional, SANDS, JEFF M., additional, SATLIN, LISA M., additional, SCHAEFER, HEIDI, additional, SCHELLING, JEFFREY R., additional, SCHILD, LAURENT, additional, SCHLINGMANN, KARL P., additional, SCHNERMANN, JÜRGEN B., additional, SCHRIER, ROBERT W., additional, SEBASTIAN, ANTHONY, additional, SEDOR, JOHN R., additional, SEGAL, YOAV, additional, SEKINE, TAKASHI, additional, SELDIN, DONALD W., additional, SENITKO, MARTIN, additional, SHAH, MALATHI, additional, SHAH, SUDHIR V., additional, SHANKLAND, STUART J., additional, SHARFUDDIN, ASIF A., additional, SHARMA, KUMAR, additional, SHENG, SHAOHU, additional, SHIRLEY, DAVID G., additional, SILBERNAGL, STEFAN, additional, SILVER, STEPHEN M., additional, SILVERMAN, MEL, additional, SLATOPOLSKY, EDUARDO, additional, SOMLO, STEFAN, additional, STERNS, RICHARD H., additional, STEWART, ANDREW K., additional, SUZUKI, YOSHIRO, additional, TEBBEN, PETER J., additional, THOMSON, SCOTT C., additional, TORRES, VICENTE E., additional, UNWIN, ROBERT J., additional, VERREY, FRANÇOIS, additional, VESELY, DAVID L., additional, WAGNER, CARSTEN A., additional, WALDMAN, MERYL, additional, WALKER, ROBERT JAMES, additional, WANG, WEI, additional, WANG, WEN-HUI, additional, WANG, YINGHONG, additional, WEINSTEIN, ALAN M., additional, WELLING, PAUL A., additional, WOLF, GUNTER, additional, WORCESTER, ELAINE, additional, ZIYADEH, FUAD N., additional, and ZOJA, CARLA, additional

Published
2008
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47. Advancing Nephrology

Author

Braden, Gregory L., primary, Chapman, Arlene, additional, Ellison, David H., additional, Gadegbeku, Crystal A., additional, Gurley, Susan B., additional, Igarashi, Peter, additional, Kelepouris, Ellie, additional, Moxey-Mims, Marva M., additional, Okusa, Mark D., additional, Plumb, Troy J., additional, Quaggin, Susan E., additional, Salant, David J., additional, Segal, Mark S., additional, Shankland, Stuart J., additional, and Somlo, Stefan, additional

Published
2020
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48. Phosphorylation of ACTN4 Leads to Podocyte Vulnerability and Proteinuric Glomerulosclerosis

Author

Feng, Di, primary, Kumar, Mukesh, additional, Muntel, Jan, additional, Gurley, Susan B., additional, Birrane, Gabriel, additional, Stillman, Isaac E., additional, Ding, Lai, additional, Wang, Minxian, additional, Ahmed, Saima, additional, Schlondorff, Johannes, additional, Alper, Seth L., additional, Ferrante, Tom, additional, Marquez, Susan L., additional, Ng, Carlos F., additional, Novak, Richard, additional, Ingber, Donald E., additional, Steen, Hanno, additional, and Pollak, Martin R., additional

Published
2020
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49. Increased phosphorylation of ACTN4 leads to podocyte vulnerability and proteinuric kidney disease and is stimulated by high glucose and TGF‐b

Author

Feng, Di, primary, Kumar, Mukesh, additional, Muntel, Jan, additional, Gurley, Susan B., additional, Birrane, Gabriel, additional, Stillman, Isaac E., additional, Ding, Lai, additional, Wang, Minxian B., additional, Ahmed, Saima, additional, Schlondorff, Johannes, additional, Alper, Seth L., additional, Novak, Richard, additional, Ingber, Donald E., additional, Steen, Hanno, additional, and Pollak, Martin R., additional

Published
2020
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50. DNAJB9 Is Not Transcriptionally Upregulated in the Glomerulus in Fibrillary Glomerulonephritis

Author

Avasare, Rupali S., primary, Robinson, Bridget A., additional, Nelson, Jonathan, additional, Woltjer, Randy, additional, Krajbich, Victoria, additional, Nguyen, Vy, additional, Garcia, Daphne, additional, Setthavongsack, Naly, additional, Kizzar, Chris, additional, Raess, Phillip W., additional, Gurley, Susan B., additional, Smith, Kelly D., additional, and Andeen, Nicole K., additional

Published
2020
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