Podocyte-specific loss of Cdc42 leads to congenital nephropathy

scientific article

Podocyte-specific loss of Cdc42 leads to congenital nephropathy is …
instance of (P31):
scholarly articleQ13442814

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P356DOI10.1681/ASN.2011121206
P932PMC publication ID3380653
P698PubMed publication ID22518006

P50authorCord BrakebuschQ30093323
P2093author name stringJulie Ruston
Tony Pawson
Nina Jones
Steve P Hawley
Jianmei Du
Rizaldy P Scott
P2860cites workAn ultrastructural study of the glomerular slit diaphragm in New Zealand black/white miceQ40009914
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Rac1 deletion in mouse neutrophils has selective effects on neutrophil functions.Q40646102
Cytoskeletal changes in podocytes associated with foot process effacement in Masugi nephritis.Q42049689
Insulin signaling to the glomerular podocyte is critical for normal kidney functionQ42110064
Filament arrangements in negatively stained cultured cells: the organization of actinQ42830885
Loss of podocyte aPKClambda/iota causes polarity defects and nephrotic syndromeQ43152476
Fluvastatin ameliorates podocyte injury in proteinuric rats via modulation of excessive Rho signalingQ46923382
Cdc42 controls the polarity of the actin and microtubule cytoskeletons through two distinct signal transduction pathways.Q53673562
Progressive impairment of kidneys and reproductive organs in mice lacking Rho GDIalphaQ73023855
Nck adaptor proteins link nephrin to the actin cytoskeleton of kidney podocytesQ24307359
Rho, rac, and cdc42 GTPases regulate the assembly of multimolecular focal complexes associated with actin stress fibers, lamellipodia, and filopodiaQ27861126
Arhgap24 inactivates Rac1 in mouse podocytes, and a mutant form is associated with familial focal segmental glomerulosclerosisQ28504659
The Rho-kinase inhibitor, fasudil, attenuates diabetic nephropathy in streptozotocin-induced diabetic ratsQ28580779
Cdc42 controls progenitor cell differentiation and beta-catenin turnover in skinQ28587207
Mammalian Rho GTPases: new insights into their functions from in vivo studiesQ29615191
An essential role of the universal polarity protein, aPKClambda, on the maintenance of podocyte slit diaphragmsQ33399707
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Actin-depolymerizing factor cofilin-1 is necessary in maintaining mature podocyte architectureQ33991246
INF2 mutations in Charcot-Marie-Tooth disease with glomerulopathyQ34242050
RhoA is dispensable for skin development, but crucial for contraction and directed migration of keratinocytesQ34611649
Glomerular-specific alterations of VEGF-A expression lead to distinct congenital and acquired renal diseasesQ34835409
Gene targeting of Cdc42 and Cdc42GAP affirms the critical involvement of Cdc42 in filopodia induction, directed migration, and proliferation in primary mouse embryonic fibroblastsQ35128385
Rac1 GTPase in rodent kidneys is essential for salt-sensitive hypertension via a mineralocorticoid receptor-dependent pathwayQ35142803
Activation of RhoA in podocytes induces focal segmental glomerulosclerosisQ35210190
Synaptopodin protects against proteinuria by disrupting Cdc42:IRSp53:Mena signaling complexes in kidney podocytesQ35916016
Hereditary proteinuria syndromes and mechanisms of proteinuriaQ36435101
Molecular make-up of the glomerular filtration barrierQ37759816
Modification of mineralocorticoid receptor function by Rac1 GTPase: implication in proteinuric kidney diseaseQ39912709
P433issue7
P921main subjectcongenital disorderQ727096
kidney diseaseQ1054718
P304page(s)1149-1154
P577publication date2012-04-19
P1433published inJournal of the American Society of NephrologyQ17123893
P1476titlePodocyte-specific loss of Cdc42 leads to congenital nephropathy
P478volume23

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cites work (P2860)
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