MAGI-1 Interacts with Nephrin to Maintain Slit Diaphragm Structure through Enhanced Rap1 Activation in Podocytes.
Ni, Jie; Bao, Sujin; Johnson, Ruth I; Zhu, Bingbing; Li, Jianhua; Vadaparampil, Justin; Smith, Christopher M; Campbell, Kirk N; Grahammer, Florian; Huber, Tobias B; He, John C; D'Agati, Vivette D; Chan, Andrew; Kaufman, Lewis.
J Biol Chem
; 291(47): 24406-24417, 2016 Nov 18.
Artigo em Inglês | MEDLINE | ID: mdl-27707879
<i>UBD</i> modifies <i>APOL1</i>-induced kidney disease risk.
[Role of cofilin in kidney disease].
Induction of steady-state glomeruloid sphere by self-assembly from human embryonic kidney cells.
APOL1-Associated Collapsing Focal Segmental Glomerulosclerosis in a Patient With Stimulator of Interferon Genes (STING)-Associated Vasculopathy With Onset in Infancy (SAVI).
Disease-causing mutation in α-actinin-4 promotes podocyte detachment through maladaptation to periodic stretch.
Focal segmental glomerulosclerosis; why does it occur segmentally?
Podocyte-Specific Sialylation-Deficient Mice Serve as a Model for Human FSGS.
Co-Deposition of IgM and C3 May Indicate Unfavorable Renal Outcomes in Adult Patients with Primary Focal Segmental Glomerulosclerosis.
Focal segmental glomerulosclerosis lesion associated with inhibition of tyrosine kinases by lenvatinib: a case report.
A kidney-specific genome-scale metabolic network model for analyzing focal segmental glomerulosclerosis.