Two populations of node monocilia initiate left-right asymmetry in the mouse (Q29617071)

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author name string

McGrath J

1

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Somlo S

2

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Makova S

3

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Tian X

4

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Brueckner M

5

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publication date

11 July 2003

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30 April 2017

language of work or name

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volume

114

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issue

1

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page(s)

61-73

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A Human Syndrome Caused by Immotile Cilia

30 April 2017

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The Caenorhabditis elegans autosomal dominant polycystic kidney disease gene homologs lov-1 and pkd-2 act in the same pathway

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Mutations in the DNAH11 (axonemal heavy chain dynein type 11) gene cause one form of situs inversus totalis and most likely primary ciliary dyskinesia

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Identification and characterization of polycystin-2, the PKD2 gene product

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Mechanisms of left-right determination in vertebrates

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Chlamydomonas Kinesin-II–dependent Intraflagellar Transport (IFT): IFT Particles Contain Proteins Required for Ciliary Assembly in Caenorhabditis elegans Sensory Neurons

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Relationship between asymmetric nodal expression and the direction of embryonic turning

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Conserved function for embryonic nodal cilia.

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

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Axonemal dynein intermediate-chain gene (DNAI1) mutations result in situs inversus and primary ciliary dyskinesia (Kartagener syndrome)

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Co-assembly of polycystin-1 and -2 produces unique cation-permeable currents

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Polycystin-2 is an intracellular calcium release channel

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PKCgamma regulates syndecan-2 inside-out signaling during xenopus left-right development

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Random determination of a developmental process: Reversal of normal visceral asymmetry in the mouse

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Gap junctions are involved in the early generation of left-right asymmetry

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A molecular pathway determining left-right asymmetry in chick embryogenesis

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Asymmetries in H+/K+-ATPase and cell membrane potentials comprise a very early step in left-right patterning

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Conserved left-right asymmetry of nodal expression and alterations in murine situs inversus.

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Situs inversus and embryonic ciliary morphogenesis defects in mouse mutants lacking the KIF3A subunit of kinesin-II

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PKD2, a gene for polycystic kidney disease that encodes an integral membrane protein

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Cloning of inv, a gene that controls left/right asymmetry and kidney development.

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

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7 January 2021

Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells

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7 January 2021

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

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7 January 2021

Determination of left–right patterning of the mouse embryo by artificial nodal flow

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7 January 2021

Abnormal nodal flow precedes situs inversus in iv and inv mice

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Mutations in DNAH5 cause primary ciliary dyskinesia and randomization of left-right asymmetry

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Loss-of-function mutations in a human gene related to Chlamydomonas reinhardtii dynein IC78 result in primary ciliary dyskinesia.

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The ion channel polycystin-2 is required for left-right axis determination in mice

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Bending the MDCK Cell Primary Cilium Increases Intracellular Calcium

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Identifiers

DOI

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&retmode=json&id=12859898

PubMed publication ID

2 references

30 April 2017

Consolidated OpenCitations Corpus – April 2017