(Q38756528)

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Quantification of the Relative Contributions of Loss-of-function and Gain-of-function Mechanisms in TAR DNA-binding Protein 43 (TDP-43) Proteinopathies

scientific article published on 21 July 2016

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Europe PubMed Central

PMC publication ID

26 September 2017

Quantification of the Relative Contributions of Loss-of-function and Gain-of-function Mechanisms in TAR DNA-binding Protein 43 (TDP-43) Proteinopathies (English)

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Europe PubMed Central

PMC publication ID

26 September 2017

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Christopher M Dobson

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Europe PubMed Central

PMC publication ID

26 September 2017

author name string

Roberta Cascella

1

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Europe PubMed Central

PMC publication ID

26 September 2017

Claudia Capitini

2

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Europe PubMed Central

PMC publication ID

26 September 2017

Giulia Fani

3

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Europe PubMed Central

PMC publication ID

26 September 2017

Cristina Cecchi

5

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Europe PubMed Central

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26 September 2017

Fabrizio Chiti

6

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26 September 2017

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21 July 2016

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Europe PubMed Central

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26 September 2017

Journal of Biological Chemistry

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Europe PubMed Central

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26 September 2017

291

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Europe PubMed Central

PMC publication ID

26 September 2017

37

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Europe PubMed Central

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26 September 2017

19437-19448

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Europe PubMed Central

PMC publication ID

26 September 2017

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Europe PubMed Central

11 June 2022

https://www.ebi.ac.uk/europepmc/webservices/rest/PMC5016682/fullTextXML

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Physiological functions and pathobiology of TDP-43 and FUS/TLS proteins

1 reference

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Effect of molecular chaperones on aberrant protein oligomers in vitro: super-versus sub-stoichiometric chaperone concentrations

1 reference

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27 September 2017

Activation of AMP-activated protein kinase α1 mediates mislocalization of TDP-43 in amyotrophic lateral sclerosis.

1 reference

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Imaging frontotemporal lobar degeneration

1 reference

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TDP-43 inclusion bodies formed in bacteria are structurally amorphous, non-amyloid and inherently toxic to neuroblastoma cells

1 reference

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Similar dose-dependence of motor neuron cell death caused by wild type human TDP-43 and mutants with ALS-associated amino acid substitutions

1 reference

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Mutations in prion-like domains in hnRNPA2B1 and hnRNPA1 cause multisystem proteinopathy and ALS

1 reference

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The C9orf72 GGGGCC repeat is translated into aggregating dipeptide-repeat proteins in FTLD/ALS.

1 reference

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1 reference

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Mechanisms of disease in frontotemporal lobar degeneration: gain of function versus loss of function effects

1 reference

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27 September 2017

Does a loss of TDP-43 function cause neurodegeneration?

1 reference

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Neuronal sensitivity to TDP-43 overexpression is dependent on timing of induction

1 reference

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27 September 2017

TDP-43 aggregation in neurodegeneration: are stress granules the key?

1 reference

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27 September 2017

Gains or losses: molecular mechanisms of TDP43-mediated neurodegeneration

1 reference

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27 September 2017

Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia

1 reference

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TDP-43: the relationship between protein aggregation and neurodegeneration in amyotrophic lateral sclerosis and frontotemporal lobar degeneration

1 reference

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27 September 2017

TDP-43 potentiates alpha-synuclein toxicity to dopaminergic neurons in transgenic mice

1 reference

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TDP-43-induced death is associated with altered regulation of BIM and Bcl-xL and attenuated by caspase-mediated TDP-43 cleavage

1 reference

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27 September 2017

Dysregulation of the ALS-associated gene TDP-43 leads to neuronal death and degeneration in mice

1 reference

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Exome sequencing reveals VCP mutations as a cause of familial ALS

1 reference

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27 September 2017

TDP-43 regulates its mRNA levels through a negative feedback loop

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5016682

27 September 2017

Altered distributions of Gemini of coiled bodies and mitochondria in motor neurons of TDP-43 transgenic mice.

1 reference

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27 September 2017

Wild-type human TDP-43 expression causes TDP-43 phosphorylation, mitochondrial aggregation, motor deficits, and early mortality in transgenic mice

1 reference

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27 September 2017

Elevated expression of TDP-43 in the forebrain of mice is sufficient to cause neurological and pathological phenotypes mimicking FTLD-U.

1 reference

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27 September 2017

Mutations of optineurin in amyotrophic lateral sclerosis

1 reference

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27 September 2017

Loss of murine TDP-43 disrupts motor function and plays an essential role in embryogenesis

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5016682

27 September 2017

TDP-43 transgenic mice develop spastic paralysis and neuronal inclusions characteristic of ALS and frontotemporal lobar degeneration

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5016682

27 September 2017

TDP-43 is a developmentally regulated protein essential for early embryonic development

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5016682

27 September 2017

Gain and loss of function of ALS-related mutations of TARDBP (TDP-43) cause motor deficits in vivo

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5016682

27 September 2017

TDP-43 mutant transgenic mice develop features of ALS and frontotemporal lobar degeneration

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5016682

27 September 2017

TDP-43 depletion induces neuronal cell damage through dysregulation of Rho family GTPases

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=5016682

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Truncation and pathogenic mutations facilitate the formation of intracellular aggregates of TDP-43.

1 reference

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27 September 2017

Aberrant cleavage of TDP-43 enhances aggregation and cellular toxicity

1 reference

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Mutations in FUS, an RNA processing protein, cause familial amyotrophic lateral sclerosis type 6

1 reference

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Expression of TDP-43 C-terminal Fragments in Vitro Recapitulates Pathological Features of TDP-43 Proteinopathies

1 reference

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27 September 2017

Structural determinants of the cellular localization and shuttling of TDP-43.

1 reference

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TDP-43 mutations in familial and sporadic amyotrophic lateral sclerosis

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Disturbance of nuclear and cytoplasmic TAR DNA-binding protein (TDP-43) induces disease-like redistribution, sequestration, and aggregate formation

1 reference

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Angiogenin loss-of-function mutations in amyotrophic lateral sclerosis

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Ubiquitinated TDP-43 in frontotemporal lobar degeneration and amyotrophic lateral sclerosis

1 reference

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ALS phenotypes with mutations in CHMP2B (charged multivesicular body protein 2B)

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DNA/RNA helicase gene mutations in a form of juvenile amyotrophic lateral sclerosis (ALS4)

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New consensus research on neuropathological aspects of familial amyotrophic lateral sclerosis with superoxide dismutase 1 (SOD1) gene mutations: inclusions containing SOD1 in neurons and astrocytes.

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Amyotrophic lateral sclerosis

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Neuroblastoma x spinal cord (NSC) hybrid cell lines resemble developing motor neurons

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TDP-43, a neuro-pathosignature factor, is essential for early mouse embryogenesis

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Pathological TDP-43 distinguishes sporadic amyotrophic lateral sclerosis from amyotrophic lateral sclerosis with SOD1 mutations.

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Amyotrophic lateral sclerosis

1 reference

https://pubmed.ncbi.nlm.nih.gov/27445339

12 December 2020

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Identifiers

10.1074/JBC.M116.737726

1 reference

Europe PubMed Central

PMC publication ID

26 September 2017

PMC publication ID

1 reference

Europe PubMed Central

PMC publication ID

26 September 2017

PubMed publication ID

1 reference

Europe PubMed Central

PMC publication ID

26 September 2017

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