Results 31 to 40 of about 22,193 (229)

VDAC, The early days

open access: yesBiochimica et Biophysica Acta (BBA) - Biomembranes, 2012
VDAC is now universally accepted as the channel in the mitochondrial outer membrane responsible for metabolite flux in and out of mitochondria. Its discovery occurred over two independent lines of investigation in the 1970s and 80s. This retrospective article describes the history of VDAC's discovery and how these lines merged in a collaboration by the
Colombini, Marco, Mannella, Carmen A.
openaire   +2 more sources

Regulation of hexokinase binding to VDAC [PDF]

open access: yesJournal of Bioenergetics and Biomembranes, 2008
Hexokinase isoforms I and II bind to mitochondrial outer membranes in large part by interacting with the outer membrane voltage-dependent anion channel (VDAC). This interaction results in a shift in the susceptibility of mitochondria to pro-apoptotic signals that are mediated through Bcl2-family proteins. The upregulation of hexokinase II expression in
John G, Pastorino, Jan B, Hoek
openaire   +2 more sources

Voltage-dependent anion channels mediated apoptosis in refractory epilepsy

open access: yesOpen Medicine, 2020
The purpose of this study was to investigate the role of voltage-dependent anion channel (VDAC) in mitochondria-mediated apoptosis of neurons in refractory epilepsy. Western blot analyses were carried out to detect the changes in cytochrome C, caspase 9,
Zhao Yan   +4 more
doaj   +1 more source

VDAC proteomics: Post-translation modifications

open access: yesBiochimica et Biophysica Acta (BBA) - Biomembranes, 2012
Voltage-dependent anion channels are abundant mitochondrial outer membrane proteins expressed in three isoforms, VDAC1-3, and are considered as "mitochondrial gatekeepers". Most tissues express all three isoforms. The functions of VDACs are several-fold, ranging from metabolite and energy exchange to apoptosis.
Kerner, Janos   +3 more
openaire   +2 more sources

Phosphorothioate Oligonucleotides Block the VDAC Channel [PDF]

open access: yesBiophysical Journal, 2007
Proapoptotic phosphorothioate oligonucleotides such as G3139 (an 18-mer) induce Bcl-2-independent apoptosis, perhaps partly via direct interaction with VDAC and reduction of metabolite flow across the mitochondrial outer membrane. Here, we analyzed the interactions at the molecular level.
Tan, Wenzhi   +4 more
openaire   +2 more sources

TSPO interacts with VDAC1 and triggers a ROS-mediated inhibition of mitochondrial quality control [PDF]

open access: yes, 2014
The 18-kDa TSPO (translocator protein) localizes on the outer mitochondrial membrane (OMM) and participates in cholesterol transport. Here, we report that TSPO inhibits mitochondrial autophagy downstream of the PINK1-PARK2 pathway, preventing essential ...
Anholt R   +22 more
core   +3 more sources

Cardiac-specific Conditional Knockout of the 18-kDa Mitochondrial Translocator Protein Protects from Pressure Overload Induced Heart Failure. [PDF]

open access: yes, 2018
Heart failure (HF) is characterized by abnormal mitochondrial calcium (Ca2+) handling, energy failure and impaired mitophagy resulting in contractile dysfunction and myocyte death.
Bers, Donald M   +7 more
core   +2 more sources

Single‐Injection Multi‐Omics Analysis by Direct Infusion Mass Spectrometry

open access: yesAngewandte Chemie, EarlyView.
A high‐throughput direct infusion mass spectrometry platform, enabled by gas‐phase ion mobility separation, supports single‐injection analysis of peptides, polar metabolites, and lipids. Coupled with custom software, it identified ∽1,300 proteins and ∽600 metabolites in ∽4.3 minutes per sample, and demonstrated broad utility in macrophage polarization ...
Yuming Jiang   +6 more
wiley   +2 more sources

Severe hepatopathy and neurological deterioration after start of valproate treatment in a 6-year-old child with mitochondrial tryptophanyl-tRNA synthetase deficiency [PDF]

open access: yes, 2018
Background: The first subjects with deficiency of mitochondrial tryptophanyl-tRNA synthetase (WARS2) were reported in 2017. Their clinical characteristics can be subdivided into three phenotypes (neonatal phenotype, severe infantile onset phenotype ...
De Bruyne, Ruth   +9 more
core   +1 more source

Apoptosis: it's BAK to VDAC [PDF]

open access: yesEMBO reports, 2009
VDAC's role in Bak‐dependent mitochondrial outer membrane permeabilization (MOMP) is controversial. Gordon Shore makes sense of it all in light of an EMBO reports paper that shows that VDAC mediates mitochondrial recruitment of Bak, thereby controlling tBid‐induced MOMP.
openaire   +2 more sources

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