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Cell
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December 31, 1993
Mutations in the human Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism
M R Pollak, E M Brown, Y H Chou, et al.
Proceedings of the National Academy of Sciences of the United States of America
|
January 31, 2018
Disease-causing mutation in α-actinin-4 promotes podocyte detachment through maladaptation to periodic stretch
Di Feng, Jacob Notbohm, Ava Benjamin, et al.
Journal of the American Society of Nephrology : JASN
|
March 29, 2014
Mutations in PAX2 associate with adult-onset FSGS
Moumita Barua, Emilia Stellacci, Lorenzo Stella, et al.
Kidney International Reports
|
July 19, 2019
APOL1-Associated Kidney Disease in Brazil
Cristian Riella, Tobias A Siemens, Minxian Wang, et al.
Nature Genetics
|
December 1, 1995
A mouse model of human familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism
C Ho, D A Conner, M R Pollak, et al.
Kidney International
|
August 24, 2024
Differing sensitivities to angiotensin converting enzyme inhibition of kidney disease mediated by APOL1 high-risk variants G1 and G2
Esilida Sula Karreci, Sonako Jacas, Olivia Donovan, et al.
Biorxiv : the Preprint Server for Biology
|
June 25, 2024
Missense Mutant Gain-of-Function Causes Inverted Formin 2 (INF2)-Related Focal Segmental Glomerulosclerosis (FSGS)
Balajikarthick Subramanian, Sarah Williams, Sophie Karp, et al.
The Journal of Biological Chemistry
|
November 4, 2006
Alpha-actinin-4 is required for normal podocyte adhesion
Savita V Dandapani, Hikaru Sugimoto, Benjamin D Matthews, et al.
Journal of the American Society of Nephrology : JASN
|
August 7, 2010
The apolipoprotein L1 (APOL1) gene and nondiabetic nephropathy in African Americans
Barry I Freedman, Jeffrey B Kopp, Carl D Langefeld, et al.
American Journal of Physiology. Cell Physiology
|
June 26, 2015
BH3 domain-independent apolipoprotein L1 toxicity rescued by BCL2 prosurvival proteins
J F Heneghan, D H Vandorpe, B E Shmukler, et al.
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of 33
Search research articles
Search
Showing results (251-260 of 326) with videos related to
Sort By:
Page
of 33
Cell
|
December 31, 1993
Mutations in the human Ca(2+)-sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism
M R Pollak, E M Brown, Y H Chou, et al.
Proceedings of the National Academy of Sciences of the United States of America
|
January 31, 2018
Disease-causing mutation in α-actinin-4 promotes podocyte detachment through maladaptation to periodic stretch
Di Feng, Jacob Notbohm, Ava Benjamin, et al.
Journal of the American Society of Nephrology : JASN
|
March 29, 2014
Mutations in PAX2 associate with adult-onset FSGS
Moumita Barua, Emilia Stellacci, Lorenzo Stella, et al.
Kidney International Reports
|
July 19, 2019
APOL1-Associated Kidney Disease in Brazil
Cristian Riella, Tobias A Siemens, Minxian Wang, et al.
Nature Genetics
|
December 1, 1995
A mouse model of human familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism
C Ho, D A Conner, M R Pollak, et al.
Kidney International
|
August 24, 2024
Differing sensitivities to angiotensin converting enzyme inhibition of kidney disease mediated by APOL1 high-risk variants G1 and G2
Esilida Sula Karreci, Sonako Jacas, Olivia Donovan, et al.
Biorxiv : the Preprint Server for Biology
|
June 25, 2024
Missense Mutant Gain-of-Function Causes Inverted Formin 2 (INF2)-Related Focal Segmental Glomerulosclerosis (FSGS)
Balajikarthick Subramanian, Sarah Williams, Sophie Karp, et al.
The Journal of Biological Chemistry
|
November 4, 2006
Alpha-actinin-4 is required for normal podocyte adhesion
Savita V Dandapani, Hikaru Sugimoto, Benjamin D Matthews, et al.
Journal of the American Society of Nephrology : JASN
|
August 7, 2010
The apolipoprotein L1 (APOL1) gene and nondiabetic nephropathy in African Americans
Barry I Freedman, Jeffrey B Kopp, Carl D Langefeld, et al.
American Journal of Physiology. Cell Physiology
|
June 26, 2015
BH3 domain-independent apolipoprotein L1 toxicity rescued by BCL2 prosurvival proteins
J F Heneghan, D H Vandorpe, B E Shmukler, et al.
Page
of 33