Evidence map›Paper›PMID 35957687›Full record

ArticleFrontiers in genetics2022

Re-Expression of Tafazzin Isoforms in TAZ-Deficient C6 Glioma Cells Restores Cardiolipin Composition but Not Proliferation Rate and Alterations in Gene Expression.

Gayatri Jagirdar, Matthias Elsner, Christian Scharf, Stefan Simm, Katrin Borucki, Daniela Peter, Michael Lalk, Karen Methling, Michael Linnebacher, Mathias Krohn and 2 more

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Article in Frontiers in genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Gayatri JagirdarInstitute of Medical Biochemistry and Molecular Biology, University Medicine Greifswald, University of Greifswald, Greifswald, Germany.
Matthias ElsnerInstitute of Clinical Biochemistry, Hannover Medical School, Hannover, Germany.
Christian ScharfDepartment of Otorhinolaryngology, Head, and Neck Surgery, University Medicine Greifswald, Greifswald, Germany.
Stefan SimmInstitute of Bioinformatics, University Medicine Greifswald, Greifswald, Germany.
Katrin BoruckiInstitute of Clinical Chemistry, Department of Pathobiochemistry, Medical Faculty, Otto-von-Guericke University Magdeburg, Magdeburg, Germany.
Daniela PeterInstitute of Clinical Chemistry, Department of Pathobiochemistry, Medical Faculty, Otto-von-Guericke University Magdeburg, Magdeburg, Germany.
Michael LalkInstitute of Biochemistry, University of Greifswald, Greifswald, Germany.
Karen MethlingInstitute of Biochemistry, University of Greifswald, Greifswald, Germany.
Michael LinnebacherDepartment of General Surgery, Molecular Oncology, and Immunotherapy, Rostock University Medical Center, Rostock, Germany.
Mathias KrohnDepartment of General Surgery, Molecular Oncology, and Immunotherapy, Rostock University Medical Center, Rostock, Germany.
Carmen WolkeInstitute of Medical Biochemistry and Molecular Biology, University Medicine Greifswald, University of Greifswald, Greifswald, Germany.
Uwe LendeckelInstitute of Medical Biochemistry and Molecular Biology, University Medicine Greifswald, University of Greifswald, Greifswald, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tafazzin-an acyltransferase-is involved in cardiolipin (CL) remodeling. CL is associated with mitochondrial function, structure and more recently with cell proliferation. Various tafazzin isoforms exist in humans. The role of these isoforms in cardiolipin remodeling is unknown. Aim of this study was to investigate if specific isoforms like Δ5 can restore the wild type phenotype with respect to CL composition, cellular proliferation and gene expression profile. In addition, we aimed to determine the molecular mechanism by which tafazzin can modulate gene expression by applying promoter analysis and (Ingenuity Pathway Analyis) IPA to genes regulated by TAZ-deficiency. Expression of Δ5 and rat full length TAZ in C6-TAZ- cells could fully restore CL composition and-as proven for Δ5-this is naturally associated with restoration of mitochondrial respiration. A similar restoration of CL-composition could not be observed after re-expression of an enzymatically dead full-length rat TAZ (H69L; TAZMut). Re-expression of only rat full length TAZ could restore proliferation rate. Surprisingly, the Δ5 variant failed to restore wild-type proliferation. Further, as expected, re-expression of the TAZMut variant completely failed to reverse the gene expression changes, whereas re-expression of the TAZ-FL variant largely did so and the Δ5 variant to somewhat less extent. Very likely TAZ-deficiency provokes substantial long-lasting changes in cellular lipid metabolism which contribute to changes in proliferation and gene expression, and are not or only very slowly reversible.

Indexed as

Barth syndromeBarth syndrome (BTHS)cardiolipincellular proliferationgene expressiontafazzin

Identifiers

PMID35957687
PMCPMC9358009

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.