ArticlePlant signaling & behavior2012
The Arabidopsis voltage-dependent anion channel 2 is required for plant growth.
Article in Plant signaling & behavior, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- Solute Transport through Mitochondrial Porins In Vitro and In Vivo.Biomolecules · 2024Review
- VDAC1 Negatively Regulates Floral Transition inInternational journal of molecular sciences · 2021Article
- A Novel Insight Into the Fate of Cardiomyocytes in Ischemia-Reperfusion Injury: From Iron Metabolism to Ferroptosis.Frontiers in cell and developmental biology · 2021Review
- Historical Perspective of Pore-Forming Activity Studies of Voltage-Dependent Anion Channel (Eukaryotic or Mitochondrial Porin) Since Its Discovery in the 70th of the Last Century.Frontiers in physiology · 2021Review
- Novel insights into ferroptosis: Implications for age-related diseases.Theranostics · 2020Review
- On GxxxG in N-terminal stretches of type-1 VDAC/porin: critical in vertebrate apoptosis, missing in plants.Plant molecular biology · 2012Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The voltage-dependent anion channels (VDACs) known as a major group of outer mitochondrial membrane proteins are present in all eukaryotic species. In mammalian cells, they have been established as a key player in mitochondrial metabolism and apoptosis regulation. By contrast, little is known about the function of plant VDACs. Recently, we performed functional analysis of all VDAC gene members in Arabidopsis thaliana, and revealed that each AtVDAC member has a specialized function. Especially, in spite of similar subcellular localization and expression profiling of AtVDAC2 and AtVDAC4, both the T-DNA insertion knockout mutants of them, vdac2-2 and vdac4-2, showed severe growth retardation. These results suggest that AtVDAC2 and AtVDAC4 proteins clearly have distinct functions. Here, we introduced the AtVDAC2 gene into the vdac2-2 mutant, and demonstrated that the miniature phenotype of vdac2-2 plant is abolished by AtVDAC2 expression.
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Registered trials
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