scholarly journals Molecular and genetic characterization of the gene family encoding the voltage-dependent anion channel in Arabidopsis

2011 ◽  
Vol 62 (14) ◽  
pp. 4773-4785 ◽  
Author(s):  
Chika Tateda ◽  
Kanako Watanabe ◽  
Tomonobu Kusano ◽  
Yoshihiro Takahashi
Keyword(s):  
Gene Family ◽  
Genetic Characterization ◽  
Anion Channel ◽  
Voltage Dependent Anion Channel ◽  
Voltage Dependent

scholarly journals Purification and Characterization of Two Voltage-Dependent Anion Channel Isoforms from Plant Seeds

2000 ◽  
Vol 124 (3) ◽  
pp. 1181-1190 ◽  
Author(s):  
Helge Abrecht ◽  
Ruddy Wattiez ◽  
Jean-Marie Ruysschaert ◽  
Fabrice Homblé
Keyword(s):  
Anion Channel ◽  
Voltage Dependent Anion Channel ◽  
Purification And Characterization ◽  
Plant Seeds ◽  
Voltage Dependent

scholarly journals The Murine Voltage-dependent Anion Channel Gene Family

1997 ◽  
Vol 272 (30) ◽  
pp. 18966-18973 ◽  
Author(s):  
Margaret J. Sampson ◽  
Rhonda S. Lovell ◽  
William J. Craigen
Keyword(s):  
Gene Family ◽  
Anion Channel ◽  
Voltage Dependent Anion Channel ◽  
Channel Gene ◽  
Voltage Dependent

scholarly journals Characterization of Oyster Voltage-Dependent Anion Channel 2 (VDAC2) Suggests Its Involvement in Apoptosis and Host Defense

PLoS ONE ◽  
2016 ◽  
Vol 11 (1) ◽  
pp. e0146049 ◽  
Author(s):  
Yingxiang Li ◽  
Linlin Zhang ◽  
Tao Qu ◽  
Li Li ◽  
Guofan Zhang
Keyword(s):  
Host Defense ◽  
Anion Channel ◽  
Voltage Dependent Anion Channel ◽  
Voltage Dependent

scholarly journals VDAC1 in the diseased myocardium and the effect of VDAC1-interacting compound on atrial fibrosis induced by hyperaldosteronism

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Hadar Klapper-Goldstein ◽  
Ankit Verma ◽  
Sigal Elyagon ◽  
Roni Gillis ◽  
Michael Murninkas ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Apoptotic Cell ◽  
Anion Channel ◽  
Immunohistochemical Analysis ◽  
Voltage Dependent Anion Channel ◽  
Cardiac Tissues ◽  
Therapeutic Implications ◽  
Voltage Dependent ◽  
Models Of Lupus

AbstractThe voltage-dependent anion channel 1 (VDAC1) is a key player in mitochondrial function. VDAC1 serves as a gatekeeper mediating the fluxes of ions, nucleotides, and other metabolites across the outer mitochondrial membrane, as well as the release of apoptogenic proteins initiating apoptotic cell death. VBIT-4, a VDAC1 oligomerization inhibitor, was recently shown to prevent mitochondrial dysfunction and apoptosis, as validated in mouse models of lupus and type-2 diabetes. In the present study, we explored the expression of VDAC1 in the diseased myocardium of humans and rats. In addition, we evaluated the effect of VBIT-4 treatment on the atrial structural and electrical remodeling of rats exposed to excessive aldosterone levels. Immunohistochemical analysis of commercially available human cardiac tissues revealed marked overexpression of VDAC1 in post-myocardial infarction patients, as well as in patients with chronic ventricular dilatation\dysfunction. In agreement, rats exposed to myocardial infarction or to excessive aldosterone had a marked increase of VDAC1 in both ventricular and atrial tissues. Immunofluorescence staining indicated a punctuated appearance typical for mitochondrial-localized VDAC1. Finally, VBIT-4 treatment attenuated the atrial fibrotic load of rats exposed to excessive aldosterone without a notable effect on the susceptibility to atrial fibrillation episodes induced by burst pacing. Our results indicate that VDAC1 overexpression is associated with myocardial abnormalities in common pathological settings. Our data also indicate that inhibition of the VDAC1 can reduce excessive fibrosis in the atrial myocardium, a finding which may have important therapeutic implications. The exact mechanism\s of this beneficial effect need further studies.

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