The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes - Wikidata - wikimedia - TriplyDB

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

http://www.wikidata.org/entity/Q27342580

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The Exocyst Complex in Health and Disease A polycystin-centric view of cyst formation and disease: the polycystins revisited Molecular complexes that direct rhodopsin transport to primary cilia Intraciliary calcium oscillations initiate vertebrate left-right asymmetry New frontiers: discovering cilia-independent functions of cilia proteins Dissecting a hidden gene duplication: the Arabidopsis thaliana SEC10 locus Phosphodiesterase 1A modulates cystogenesis in zebrafish.The exocyst and regulatory GTPases in urinary exosomes.Ciliopathies: the trafficking connection.Ciliary membrane proteins traffic through the Golgi via a Rabep1/GGA1/Arl3-dependent mechanism Exocyst Sec10 protects renal tubule cells from injury by EGFR/MAPK activation and effects on endocytosis.Medical school hotline: The Institute for Biogenesis Research: a flower in the Pacific.The small GTPase Cdc42 is necessary for primary ciliogenesis in renal tubular epithelial cells.Cilia and Diseases Urothelial Defects from Targeted Inactivation of Exocyst Sec10 in Mice Cause Ureteropelvic Junction Obstructions.Cdc42 and sec10 Are Required for Normal Retinal Development in Zebrafish.VIP17/MAL expression modulates epithelial cyst formation and ciliogenesis Arl13b and the exocyst interact synergistically in ciliogenesis Unilateral nephrectomy elongates primary cilia in the remaining kidney via reactive oxygen species.Lethal giant larvae 2 regulates development of the ciliated organ Kupffer's vesicle.Dynamin Binding Protein (Tuba) Deficiency Inhibits Ciliogenesis and Nephrogenesis in Vitro and in Vivo Cdc42 deficiency causes ciliary abnormalities and cystic kidneys.Organization and execution of the epithelial polarity programme.Cilia and polycystic kidney disease, kith and kin.Diverse Functions and Signal Transduction of the Exocyst Complex in Tumor Cells.Role of Polarity Proteins in the Generation and Organization of Apical Surface Protrusions.Primary Cilia in Cystic Kidney Disease.The serologically defined colon cancer antigen-3 (SDCCAG3) is involved in the regulation of ciliogenesis.Laterality defects are influenced by timing of treatments and animal model.Routes and machinery of primary cilium biogenesis.Phosphoinositide 3-Kinase-C2α Regulates Polycystin-2 Ciliary Entry and Protects against Kidney Cyst Formation.The exocyst gene Sec10 regulates renal epithelial monolayer homeostasis and apoptotic sensitivity.The Golgi matrix protein giantin is required for normal cilia function in zebrafish.Identification and Expression Analysis of the Complete Family of Zebrafish pkd Genes.Neurodevelopmental disease mechanisms, primary cilia, and endosomes converge on the BLOC-1 and BORC complexes.The exocyst is required for photoreceptor ciliogenesis and retinal development.Loss-of-function of the ciliopathy protein Cc2d2a disorganizes the vesicle fusion machinery at the periciliary membrane and indirectly affects Rab8-trafficking in zebrafish photoreceptors.BLOC-1 is required for selective membrane protein trafficking from endosomes to primary cilia.

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The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

http://www.wikidata.org/entity/Q27342580

description

2011 nî lūn-bûn

@nan

2011 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի ապրիլին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@ast

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@en

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@nl

type

label

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@ast

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@en

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@nl

prefLabel

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@ast

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@en

The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@nl

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JOURNAL.PGEN.1001361

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The exocyst protein Sec10 interacts with Polycystin-2 and knockdown causes PKD-phenotypes

@en

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Ben Fogelgren

http://www.w3.org/2001/XMLSchema#string

Joshua H Lipschutz

http://www.w3.org/2001/XMLSchema#string

Kimberly M Jaffe

http://www.w3.org/2001/XMLSchema#string

Kwon Moo Park

http://www.w3.org/2001/XMLSchema#string

P Darwin Bell

http://www.w3.org/2001/XMLSchema#string

Ryan J Reichert

http://www.w3.org/2001/XMLSchema#string

Shin-Yi Lin

http://www.w3.org/2001/XMLSchema#string

Xiaofeng Zuo

http://www.w3.org/2001/XMLSchema#string

P2860

Polycystin-2, the protein mutated in autosomal dominant polycystic kidney disease (ADPKD), is a Ca2+-permeable nonselective cation channel

The intraflagellar transport protein IFT20 is associated with the Golgi complex and is required for cilia assembly

Pericentrin forms a complex with intraflagellar transport proteins and polycystin-2 and is required for primary cilia assembly

Polaris, a protein involved in left-right axis patterning, localizes to basal bodies and cilia

The exocyst localizes to the primary cilium in MDCK cells.

Identification of 23 complementation groups required for post-translational events in the yeast secretory pathway.

Exo84p is an exocyst protein essential for secretion.

The exocyst is an effector for Sec4p, targeting secretory vesicles to sites of exocytosis.

Intraflagellar transport (IFT) role in ciliary assembly, resorption and signalling.

The exocyst protein Sec10 is necessary for primary ciliogenesis and cystogenesis in vitro.

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e1001361

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scholarly article

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2353953

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10.1371/JOURNAL.PGEN.1001361

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4

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7

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Rebecca D. Burdine

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2011-04-07T00:00:00Z

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51049318

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21490950

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3072367

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