The expanding neurological phenotype of DNM1L-related disorders

Brain. 2018 Apr 1;141(4):e28. doi: 10.1093/brain/awy024.

Authors

Michael F Wangler^{1

2

3}, Nurit Assia Batzir¹, Laurie A Robak^{1

3}, Mary K Koenig⁴, Carlos A Bacino^{1

3}, Fernando Scaglia^{1

3}, Hugo J Bellen^{1

2

5}

Affiliations

¹ Department of Molecular and Human Genetics, Baylor College of Medicine, Houston TX 77030, USA.
² Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston TX 77030, USA.
³ Texas Children's Hospital, Houston TX 77030, USA.
⁴ Department of Pediatric Neurology, University of Texas Medical School at Houston, Houston TX 77030, USA.
⁵ Howard Hughes Medical Institute, Baylor College of Medicine, Houston TX 77030, USA.

No abstract available

Publication types

Letter
Comment

MeSH terms

Dynamins
GTP Phosphohydrolases / genetics
Humans
Microtubule-Associated Proteins / genetics
Mitochondrial Dynamics*
Mitochondrial Proteins
Mutation
Optic Atrophy, Autosomal Dominant*
Phenotype

Substances

Microtubule-Associated Proteins
Mitochondrial Proteins
GTP Phosphohydrolases
OPA1 protein, human
DNM1L protein, human
Dynamins

Grants and funding

R01 HG011795/HG/NHGRI NIH HHS/United States