Publication:
The ciliopathy protein CC2D2A Associates with NINL and functions in RAB8-MICAL3-regulated vesicle trafficking

Date

Date

Date
2015
Journal Article
Published version

Abstract

Abstract

Abstract
Ciliopathies are a group of human disorders caused by dysfunction of primary cilia, ubiquitous microtubule-based organelles involved in transduction of extra-cellular signals to the cell. This function requires the concentration of receptors and channels in the ciliary membrane, which is achieved by complex trafficking mechanisms, in part controlled by the small GTPase RAB8, and by sorting at the transition zone located at the entrance of the ciliary compartment. Mutations in the transition zone gene CC2D2A cause the related Joubert a

Additional indexing

Creators (Authors)

  • Dona, Margo
    affiliation.icon.alt
  • Hetterschijt, Lisette
    affiliation.icon.alt
  • Tonnaer, Edith
    affiliation.icon.alt
  • Peters, Theo
    affiliation.icon.alt
  • de Vrieze, Erik
    affiliation.icon.alt
  • Mans, Dorus A
    affiliation.icon.alt
  • van Beersum, Sylvia E C
    affiliation.icon.alt
  • Phelps, Ian G
    affiliation.icon.alt
  • Arts, Heleen H
    affiliation.icon.alt
  • Keunen, Jan E
    affiliation.icon.alt
  • Ueffing, Marius
    affiliation.icon.alt
  • Roepman, Ronald
    affiliation.icon.alt
  • Boldt, Karsten
    affiliation.icon.alt
  • Doherty, Dan
    affiliation.icon.alt
  • Moens, Cecilia B
    affiliation.icon.alt
  • Kremer, Hannie
    affiliation.icon.alt
  • van Wijk, Erwin
    affiliation.icon.alt

Journal/Series Title

Journal/Series Title

Journal/Series Title

Volume

Volume

Volume
11

Number

Number

Number
10

Page range/Item number

Page range/Item number

Page range/Item number
e1005575

Item Type

Item Type

Item Type
Journal Article

Dewey Decimal Classifikation

Dewey Decimal Classifikation

Dewey Decimal Classifikation

Language

Language

Language
English

Publication date

Publication date

Publication date
2015-10

Date available

Date available

Date available
2015-12-10

Publisher

Publisher

Publisher

ISSN or e-ISSN

ISSN or e-ISSN

ISSN or e-ISSN
1553-7390

OA Status

OA Status

OA Status
Gold

Free Access at

Free Access at

Free Access at
Pubmed ID

PubMed ID

PubMed ID

PubMed ID
Gold Open Access
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Files

Files

Files
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Files

Files

Files
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