Monolysocardiolipins accumulate in Barth syndrome but do not lead to enhanced apoptosis (Q28243113)

Paul G Ekert

6

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David Thorburn

David R Thorburn

7

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Jeffrey A Towbin

4

Jeffrey A Towbin

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Ronald J A Wanders

9

Ronald J A Wanders

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author name string

Fredoen Valianpour

1

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Voula Mitsakos

2

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Dimitri Schlemmer

3

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Juliet M Taylor

5

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Peter G Barth

10

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Frédéric M Vaz

Journal of Lipid Research

11

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language of work or name

English

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publication date

June 2005

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published in

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volume

46

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issue

6

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page(s)

1182-95

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cites work

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A novel X-linked gene, G4.5. is responsible for Barth syndrome

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Defective remodeling of cardiolipin and phosphatidylglycerol in Barth syndrome

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Deficiency of tetralinoleoyl-cardiolipin in Barth syndrome

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Aberrant cardiolipin metabolism in the yeast taz1 mutant: a model for Barth syndrome.

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Only one splice variant of the human TAZ gene encodes a functional protein with a role in cardiolipin metabolism

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Caspase-8 levels affect necessity for mitochondrial amplification in death ligand-induced glioma cell apoptosis

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Unlike Diablo/smac, Grim promotes global ubiquitination and specific degradation of X chromosome-linked inhibitor of apoptosis (XIAP) and neither cause apoptosis

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Ubiquitin-mediated degradation of the proapoptotic active form of bid. A functional consequence on apoptosis induction

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Neutrophils in Barth syndrome (BTHS) avidly bind annexin-V in the absence of apoptosis

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10.1194/JLR.M500056-JLR200

21 January 2018

Identifiers

DOI

1 reference

Consolidated OpenCitations Corpus – April 2017

1 reference

Consolidated OpenCitations Corpus – April 2017

PubMed publication ID

15805542

1 reference

Consolidated OpenCitations Corpus – April 2017