Mice deficient in α-actinin-4 have severe glomerular disease-Reference-Cited by-同舟云学术

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Mice deficient in α-actinin-4 have severe glomerular disease

Published:2003-06-01 Issue:11 Volume:111 Page:1683-1690
ISSN:0021-9738
Container-title:Journal of Clinical Investigation
language:en
Short-container-title:J. Clin. Invest.

Author:

Kos Claudine H.,Le Tu Cam,Sinha Sumita,Henderson Joel M.,Kim Sung Han,Sugimoto Hikaru,Kalluri Raghu,Gerszten Robert E.,Pollak Martin R.

Publisher

American Society for Clinical Investigation

Subject

General Medicine

Reference17 articles.

1. Focal segmental glomerulosclerosis

2. Mutations in ACTN4, encoding α-actinin-4, cause familial focal segmental glomerulosclerosis

3. Positionally Cloned Gene for a Novel Glomerular Protein—Nephrin—Is Mutated in Congenital Nephrotic Syndrome

4. NPHS2, encoding the glomerular protein podocin, is mutated in autosomal recessive steroid-resistant nephrotic syndrome

5. Congenital Nephrotic Syndrome in Mice Lacking CD2-Associated Protein

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1. The Immunosuppressive Drug LF15-0195 Acts Also on Glomerular Lesions, by a Change in Cytoskeleton Distribution in Podocyte;American Journal of Nephrology;2024-07-29

2. Protein tyrosine phosphatase 1B is a regulator of alpha-actinin4 in the glomerular podocyte;Biochimica et Biophysica Acta (BBA) - Molecular Cell Research;2024-01

3. MAGI2 ameliorates podocyte apoptosis of diabetic kidney disease through communication with TGF‐β‐Smad3/nephrin pathway;The FASEB Journal;2023-11-11

4. Current understanding of the molecular mechanisms of circulating permeability factor in focal segmental glomerulosclerosis;Frontiers in Immunology;2023-09-19

5. Analysis of the association of NPHS2 and ACTN4 genes polymorphism with nephrotic syndrome in Egyptian children;Molecular Biology Reports;2023-04-04

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