Loss of the ciliary kinase Nek8 causes left-right asymmetry defects. - Wikidata - awgldk - TriplyDB

Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

http://www.wikidata.org/entity/Q36509302

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Congenital heart disease: emerging themes linking genetics and development A NIMA-related kinase, CNK4, regulates ciliary stability and length.A protein interaction map for cell-cell adhesion regulators identifies DUSP23 as a novel phosphatase for β-catenin.Protein arginine methyltransferases interact with intraflagellar transport particles and change location during flagellar growth and resorption.The determination factors of left-right asymmetry disorders- a short review.Mutations in ANKS6 cause a nephronophthisis-like phenotype with ESRD.Ciliopathies: the trafficking connection.The tumor suppressor pVHL down-regulates never-in-mitosis A-related kinase 8 via hypoxia-inducible factors to maintain cilia in human renal cancer cells ANKS6 is the critical activator of NEK8 kinase in embryonic situs determination and organ patterning.Novel NEK8 Mutations Cause Severe Syndromic Renal Cystic Dysplasia through YAP Dysregulation.NEK8 regulates DNA damage-induced RAD51 foci formation and replication fork protection Mechanobiology of Ciliogenesis.High-resolution genetic localization of a modifying locus affecting disease severity in the juvenile cystic kidneys (jck) mouse model of polycystic kidney disease Distinct mechanisms determine organ left-right asymmetry patterning in an uncoupled way.Developmental signaling: does it bridge the gap between cilia dysfunction and renal cystogenesis?Genetic basis of human left-right asymmetry disorders.Ciliary subcompartments and cysto-proteins.Primary Cilia in Cystic Kidney Disease.Reduction of ciliary length through pharmacologic or genetic inhibition of CDK5 attenuates polycystic kidney disease in a model of nephronophthisis.NEK8 links the ATR-regulated replication stress response and S phase CDK activity to renal ciliopathies Conserved Ankyrin Repeat Proteins and Their NIMA Kinase Partners Regulate Extracellular Matrix Remodeling and Intracellular Trafficking in Caenorhabditis elegans.Inhibition of cell-cell adhesion impairs directional epithelial migration on micropatterned surfaces.Actin organization and endocytic trafficking are controlled by a network linking NIMA-related kinases to the CDC-42-SID-3/ACK1 pathway.Homozygous loss-of-function mutations in MNS1 cause laterality defects and likely male infertility The nucleoside-diphosphate kinase NME3 associates with nephronophthisis proteins and is required for ciliary function during renal development

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P2860

Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

http://www.wikidata.org/entity/Q36509302

description

2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年論文

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2013年论文

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2013年论文

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2013年论文

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name

Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

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Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

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type

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Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

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Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

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Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

@ast

Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

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P1433

Journal of the American Society of Nephrology

P1476

Loss of the ciliary kinase Nek8 causes left-right asymmetry defects.

@en

P2093

Danielle K Manning

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

David R Beier

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

Iain Drummond

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

Jagesh V Shah

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

Jin-Hee Oh

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

Michael D Wong

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

Mikhail Sergeev

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R Mark Henkelman

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

Roy G van Heesbeen

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

Yan Liu

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

P2860

Randomization of left-right asymmetry due to loss of nodal cilia generating leftward flow of extraembryonic fluid in mice lacking KIF3B motor protein

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

Polycystin-2 is an intracellular calcium release channel

NEK8 mutations affect ciliary and centrosomal localization and may cause nephronophthisis

Mutations in a novel gene, NPHP3, cause adolescent nephronophthisis, tapeto-retinal degeneration and hepatic fibrosis

Catalysis of guanine nucleotide exchange on Ran by the mitotic regulator RCC1

Loss of nephrocystin-3 function can cause embryonic lethality, Meckel-Gruber-like syndrome, situs inversus, and renal-hepatic-pancreatic dysplasia

Mutations in INVS encoding inversin cause nephronophthisis type 2, linking renal cystic disease to the function of primary cilia and left-right axis determination

Pitx2, a bicoid-type homeobox gene, is involved in a lefty-signaling pathway in determination of left-right asymmetry

Inversin, a novel gene in the vertebrate left-right axis pathway, is partially deleted in the inv mouse

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100-112

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scholarly article

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10.1681/ASN.2012050490

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1

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24

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3537214

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