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.
Disease-causing mutation in α-actinin-4 promotes podocyte detachment through maladaptation to periodic stretch.
Focal segmental glomerulosclerosis; why does it occur segmentally?
The sclerosing glomerulus in mice and man: novel insights.
A kidney-specific genome-scale metabolic network model for analyzing focal segmental glomerulosclerosis.
The FERM protein EPB41L5 regulates actomyosin contractility and focal adhesion formation to maintain the kidney filtration barrier.
AT<sub>2</sub> R deficiency mediated podocyte loss via activation of ectopic hedgehog interacting protein (Hhip) gene expression.
Ubiquitin C-terminal hydrolase L1 deletion ameliorates glomerular injury in mice with ACTN4-associated focal segmental glomerulosclerosis.
The Hippo pathway regulator KIBRA promotes podocyte injury by inhibiting YAP signaling and disrupting actin cytoskeletal dynamics.
TRPC6 channel as an emerging determinant of the podocyte injury susceptibility in kidney diseases.