Impairment of Drosophila orthologs of the human orphan protein C19orf12 induces bang sensitivity and neurodegeneration (Q27320817)

GOA release 2020-03-11

Nazo Dmel_CG11671

1 reference

GOA release 2020-03-11

1 reference

6

0 references

Holger Prokisch

7

0 references

Arcangela Iuso

1

object named as

Arcangela Iuso

0 references

Matteo Gorza

3

object named as

Matteo Gorza

0 references

Katharina Heim

4

object named as

Katharina Heim

0 references

author name string

Ody C M Sibon

2

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Cristina Organisti

Creative Commons Attribution 4.0 International

5

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language of work or name

English

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publication date

2014

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published in

PLOS One

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volume

9

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issue

2

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page(s)

e89439

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copyright license

start time

21 February 2014

1 reference

April 2022 Public Data File from Crossref

copyright status

copyrighted

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Loss of Swiss cheese/neuropathy target esterase activity causes disruption of phosphatidylcholine homeostasis and neuronal and glial death in adult Drosophila

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Probing mechanisms that underlie human neurodegenerative diseases in Drosophila

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C19orf12 mutations in neurodegeneration with brain iron accumulation mimicking juvenile amyotrophic lateral sclerosis

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Absence of an orphan mitochondrial protein, c19orf12, causes a distinct clinical subtype of neurodegeneration with brain iron accumulation

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PANK2 and C19orf12 mutations are common causes of neurodegeneration with brain iron accumulation.

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Clinical features of neurodegeneration with brain iron accumulation due to a C19orf12 gene mutation

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Mitochondrial membrane protein associated neurodegenration: a novel variant of neurodegeneration with brain iron accumulation

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De novo CoA biosynthesis is required to maintain DNA integrity during development of the Drosophila nervous system.

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Pantothenate kinase-associated neurodegeneration: insights from a Drosophila model.

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Tauopathy in Drosophila: neurodegeneration without neurofibrillary tangles

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Polyglutamine-expanded human huntingtin transgenes induce degeneration of Drosophila photoreceptor neurons.

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A novel frameshift mutation of C19ORF12 causes NBIA4 with cerebellar atrophy and manifests with severe peripheral motor axonal neuropathy

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