Ciliogenesis and cell cycle alterations contribute to KIF2A-related malformations of cortical development. (Q47595186)

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:29077851%20AND%20SRC:MED&resulttype=core&format=json

8 April 2020

title

Ciliogenesis and cell cycle alterations contribute to KIF2A-related malformations of cortical development (English)

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8 April 2020

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13

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8 April 2020

Juliette D Godin

18

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8 April 2020

Johan G Gilet

6

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Alexandre Benmerah

14

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Nadia Bahi-Buisson

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Laurent Nguyen

17

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8 April 2020

author name string

Loïc Broix

1

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8 April 2020

Laure Asselin

2

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8 April 2020

Carla G Silva

3

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8 April 2020

Ekaterina L Ivanova

4

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8 April 2020

Peggy Tilly

5

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8 April 2020

Nicolas Lebrun

7

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8 April 2020

Hélène Jagline

8

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8 April 2020

Giuseppe Muraca

9

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8 April 2020

Yoann Saillour

10

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8 April 2020

Nathalie Drouot

11

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8 April 2020

Madeline Louise Reilly

12

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8 April 2020

Richard Belvindrah

16

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8 April 2020

Jamel Chelly

19

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8 April 2020

Maria-Victoria Hinckelmann

20

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publication date

1 January 2018

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8 April 2020

published in

Human Molecular Genetics

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8 April 2020

volume

27

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8 April 2020

issue

2

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8 April 2020

page(s)

224-238

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doublecortin is the major gene causing X-linked subcortical laminar heterotopia (SCLH)

8 April 2020

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Doublecortin, a brain-specific gene mutated in human X-linked lissencephaly and double cortex syndrome, encodes a putative signaling protein

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Mutations in the neuronal ß-tubulin subunit TUBB3 result in malformation of cortical development and neuronal migration defects

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Mutations in TUBG1, DYNC1H1, KIF5C and KIF2A cause malformations of cortical development and microcephaly

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Mutations in the murine homologue of TUBB5 cause microcephaly by perturbing cell cycle progression and inducing p53-associated apoptosis

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Beta tubulin isoforms are not interchangeable for rescuing impaired radial migration due to Tubb3 knockdown

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Recurrent KIF2A mutations are responsible for classic lissencephaly

21 January 2018

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A patient with lissencephaly, developmental delay, and infantile spasms, due to de novo heterozygous mutation of KIF2A.

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Kin I kinesins are microtubule-destabilizing enzymes

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DDA3 recruits microtubule depolymerase Kif2a to spindle poles and controls spindle dynamics and mitotic chromosome movement

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Efficient mitosis in human cells lacking poleward microtubule flux

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Aurora B and Kif2A control microtubule length for assembly of a functional central spindle during anaphase

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DDA3 and Mdp3 modulate Kif2a recruitment onto the mitotic spindle to control minus-end spindle dynamics.

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The kinesin-13 proteins Kif2a, Kif2b, and Kif2c/MCAK have distinct roles during mitosis in human cells.

21 January 2018

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21 January 2018

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KIF2 is a new microtubule-based anterograde motor that transports membranous organelles distinct from those carried by kinesin heavy chain or KIF3A/B.

21 January 2018

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The Microtubule-Depolymerizing Activity of a Mitotic Kinesin Protein KIF2A Drives Primary Cilia Disassembly Coupled with Cell Proliferation.

21 January 2018

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Whole-exome sequencing identifies recessive WDR62 mutations in severe brain malformations

21 January 2018

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Radial glial cells: key organisers in CNS development

21 January 2018

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21 January 2018

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The KinI kinesin Kif2a is required for bipolar spindle assembly through a functional relationship with MCAK

21 January 2018

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21 January 2018

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21 January 2018

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Identifiers

DOI

10.1093/HMG/DDX384

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:29077851%20AND%20SRC:MED&resulttype=core&format=json

8 April 2020

1 reference