Voltage-Dependent Anion Channel 1: Voltage-dependent anion channel 1 is the major pore-forming protein of the mitochondrial outer membrane. It also functions as a ferricyanide reductase in the PLASMA MEMBRANE.Voltage-Dependent Anion Channels: A family of voltage-gated eukaryotic porins that form aqueous channels. They play an essential role in mitochondrial CELL MEMBRANE PERMEABILITY, are often regulated by BCL-2 PROTO-ONCOGENE PROTEINS, and have been implicated in APOPTOSIS.Anions: Negatively charged atoms, radicals or groups of atoms which travel to the anode or positive pole during electrolysis.Ion Channels: Gated, ion-selective glycoproteins that traverse membranes. The stimulus for ION CHANNEL GATING can be due to a variety of stimuli such as LIGANDS, a TRANSMEMBRANE POTENTIAL DIFFERENCE, mechanical deformation or through INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS.Ion Channel Gating: The opening and closing of ion channels due to a stimulus. The stimulus can be a change in membrane potential (voltage-gated), drugs or chemical transmitters (ligand-gated), or a mechanical deformation. Gating is thought to involve conformational changes of the ion channel which alters selective permeability.Calcium Channels: Voltage-dependent cell membrane glycoproteins selectively permeable to calcium ions. They are categorized as L-, T-, N-, P-, Q-, and R-types based on the activation and inactivation kinetics, ion specificity, and sensitivity to drugs and toxins. The L- and T-types are present throughout the cardiovascular and central nervous systems and the N-, P-, Q-, & R-types are located in neuronal tissue.Membrane Potentials: The voltage differences across a membrane. For cellular membranes they are computed by subtracting the voltage measured outside the membrane from the voltage measured inside the membrane. They result from differences of inside versus outside concentration of potassium, sodium, chloride, and other ions across cells' or ORGANELLES membranes. For excitable cells, the resting membrane potentials range between -30 and -100 millivolts. Physical, chemical, or electrical stimuli can make a membrane potential more negative (hyperpolarization), or less negative (depolarization).Chloride Channels: Cell membrane glycoproteins that form channels to selectively pass chloride ions. Nonselective blockers include FENAMATES; ETHACRYNIC ACID; and TAMOXIFEN.Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization: A mass spectrometric technique that is used for the analysis of large biomolecules. Analyte molecules are embedded in an excess matrix of small organic molecules that show a high resonant absorption at the laser wavelength used. The matrix absorbs the laser energy, thus inducing a soft disintegration of the sample-matrix mixture into free (gas phase) matrix and analyte molecules and molecular ions. In general, only molecular ions of the analyte molecules are produced, and almost no fragmentation occurs. This makes the method well suited for molecular weight determinations and mixture analysis.Animal Welfare: The protection of animals in laboratories or other specific environments by promoting their health through better nutrition, housing, and care.Abattoirs: Places where animals are slaughtered and dressed for market.Chickens: Common name for the species Gallus gallus, the domestic fowl, in the family Phasianidae, order GALLIFORMES. It is descended from the red jungle fowl of SOUTHEAST ASIA.Proteomics: The systematic study of the complete complement of proteins (PROTEOME) of organisms.Voltage-Dependent Anion Channel 2: Voltage-dependent anion channel 2 is a low abundance mammalian isoform of VDAC that interacts with the inactive form of BAK PROTEIN.Ryanodine Receptor Calcium Release Channel: A tetrameric calcium release channel in the SARCOPLASMIC RETICULUM membrane of SMOOTH MUSCLE CELLS, acting oppositely to SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES. It is important in skeletal and cardiac excitation-contraction coupling and studied by using RYANODINE. Abnormalities are implicated in CARDIAC ARRHYTHMIAS and MUSCULAR DISEASES.Ryanodine: A methylpyrrole-carboxylate from RYANIA that disrupts the RYANODINE RECEPTOR CALCIUM RELEASE CHANNEL to modify CALCIUM release from SARCOPLASMIC RETICULUM resulting in alteration of MUSCLE CONTRACTION. It was previously used in INSECTICIDES. It is used experimentally in conjunction with THAPSIGARGIN and other inhibitors of CALCIUM ATPASE uptake of calcium into SARCOPLASMIC RETICULUM.Porins: Porins are protein molecules that were originally found in the outer membrane of GRAM-NEGATIVE BACTERIA and that form multi-meric channels for the passive DIFFUSION of WATER; IONS; or other small molecules. Porins are present in bacterial CELL WALLS, as well as in plant, fungal, mammalian and other vertebrate CELL MEMBRANES and MITOCHONDRIAL MEMBRANES.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Mitochondrial Membranes: The two lipoprotein layers in the MITOCHONDRION. The outer membrane encloses the entire mitochondrion and contains channels with TRANSPORT PROTEINS to move molecules and ions in and out of the organelle. The inner membrane folds into cristae and contains many ENZYMES important to cell METABOLISM and energy production (MITOCHONDRIAL ATP SYNTHASE).Cell Membrane Permeability: A quality of cell membranes which permits the passage of solvents and solutes into and out of cells.Bacterial Outer Membrane Proteins: Proteins isolated from the outer membrane of Gram-negative bacteria.Bivalvia: A class in the phylum MOLLUSCA comprised of mussels; clams; OYSTERS; COCKLES; and SCALLOPS. They are characterized by a bilaterally symmetrical hinged shell and a muscular foot used for burrowing and anchoring.Gills: Paired respiratory organs of fishes and some amphibians that are analogous to lungs. They are richly supplied with blood vessels by which oxygen and carbon dioxide are exchanged directly with the environment.Mytilidae: A family of marine MUSSELS in the class BIVALVIA.Proteome: The protein complement of an organism coded for by its genome.Corticotrophs: Anterior pituitary cells that produce ADRENOCORTICOTROPHIC HORMONE.Electrophoresis, Gel, Two-Dimensional: Electrophoresis in which a second perpendicular electrophoretic transport is performed on the separate components resulting from the first electrophoresis. This technique is usually performed on polyacrylamide gels.Research: Critical and exhaustive investigation or experimentation, having for its aim the discovery of new facts and their correct interpretation, the revision of accepted conclusions, theories, or laws in the light of newly discovered facts, or the practical application of such new or revised conclusions, theories, or laws. (Webster, 3d ed)Research Personnel: Those individuals engaged in research.Research Support as Topic: Financial support of research activities.Biomedical Research: Research that involves the application of the natural sciences, especially biology and physiology, to medicine.Social Behavior: Any behavior caused by or affecting another individual, usually of the same species.Research Design: A plan for collecting and utilizing data so that desired information can be obtained with sufficient precision or so that an hypothesis can be tested properly.Ulmus: A plant genus of the family ULMACEAE that is susceptible to Dutch elm disease which is caused by the ASCOMYCOTA fungus, Ophiostoma.Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.Haplotypes: The genetic constitution of individuals with respect to one member of a pair of allelic genes, or sets of genes that are closely linked and tend to be inherited together such as those of the MAJOR HISTOCOMPATIBILITY COMPLEX.Genome-Wide Association Study: An analysis comparing the allele frequencies of all available (or a whole GENOME representative set of) polymorphic markers in unrelated patients with a specific symptom or disease condition, and those of healthy controls to identify markers associated with a specific disease or condition.Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Polymorphism, Genetic: The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Linkage Disequilibrium: Nonrandom association of linked genes. This is the tendency of the alleles of two separate but already linked loci to be found together more frequently than would be expected by chance alone.Polymerase Chain Reaction: In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.Microfluidics: The study of fluid channels and chambers of tiny dimensions of tens to hundreds of micrometers and volumes of nanoliters or picoliters. This is of interest in biological MICROCIRCULATION and used in MICROCHEMISTRY and INVESTIGATIVE TECHNIQUES.DNA Primers: Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.Microfluidic Analytical Techniques: Methods utilizing the principles of MICROFLUIDICS for sample handling, reagent mixing, and separation and detection of specific components in fluids.Prenatal Diagnosis: Determination of the nature of a pathological condition or disease in the postimplantation EMBRYO; FETUS; or pregnant female before birth.Algorithms: A procedure consisting of a sequence of algebraic formulas and/or logical steps to calculate or determine a given task.Carbon Monoxide: Carbon monoxide (CO). A poisonous colorless, odorless, tasteless gas. It combines with hemoglobin to form carboxyhemoglobin, which has no oxygen carrying capacity. The resultant oxygen deprivation causes headache, dizziness, decreased pulse and respiratory rates, unconsciousness, and death. (From Merck Index, 11th ed)Internal Medicine: A medical specialty concerned with the diagnosis and treatment of diseases of the internal organ systems of adults.Carbon Monoxide Poisoning: Toxic asphyxiation due to the displacement of oxygen from oxyhemoglobin by carbon monoxide.Periodicals as Topic: A publication issued at stated, more or less regular, intervals.Arrhythmias, Cardiac: Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.Angina Pectoris: The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.Physicians: Individuals licensed to practice medicine.

Each mammalian mitochondrial outer membrane porin protein is dispensable: effects on cellular respiration. (1/42)

Voltage-dependent anion channels (VDACs, also known as mitochondrial porins) are small pore-forming proteins of the mitochondrial outer membrane found in all eukaryotes. Mammals harbor three distinct VDAC isoforms, with each protein sharing 65-70% sequence identity. Deletion of the yeast VDAC1 gene leads to conditional lethality that can be partially or completely complemented by the mammalian VDAC genes. In vitro, VDACs conduct a variety of small metabolites and in vivo they serve as a binding site for several cytosolic kinases involved in intermediary metabolism, yet the specific physiologic role of each isoform is unknown. Here we show that mouse embryonic stem cells lacking each isoform are viable but exhibit a 30% reduction in oxygen consumption. VDAC1 and VDAC2 deficient cells exhibit reduced cytochrome c oxidase activity, whereas VDAC3 deficient cells have normal activity. These results indicate that VDACs are not essential for cell viability and we speculate that reduced respiration in part reflects decreased outer membrane permeability for small metabolites necessary for oxidative phosphorylation.  (+info)

Characterization of porin isoforms expressed in tumor cells. (2/42)

Mitochondria from malignant tumor cell lines show a higher capability for hexokinase binding than those from normal liver. To explore possible differences in hexokinase binding sites of mitochondria between tumor cells and normal liver, we characterized porin isoforms expressed in tumor cells. Cloning experiments on the three porin isoforms, VDAC1, VDAC2 and VDAC3 from malignant tumor cell line AH130 clearly showed that their primary structures were completely identical to those of the corresponding VDACs of normal liver cells. Possible expression of the fourth porin isoform in AH130 cells was excluded by degenerate primer-based RT-PCR. However, the transcript levels of the three VDAC isoforms in AH130 cells were significantly higher than those in normal liver. These results suggest that the high hexokinase-binding capability of malignant tumor cell mitochondria was not due to any structural difference, but due to a quantitative difference in binding sites.  (+info)

VDAC2 (porin-2) expression pattern and localization in the bovine testis. (3/42)

In this study, sequencing of voltage-dependent anion channel 2 (VDAC2, porin-2) cDNA from bovine testis is reported. High identity to the murine, rabbit, and human subtypes at both the nucleotide and amino acid levels is demonstrated. mRNA analysis revealed expression of VDAC2 in bovine testis, whereas high levels of VDAC2 proteins were found in late spermatocytes, spermatids, and spermatozoa. In contrast, VDAC1 (porin-1) is exclusively localized in Sertoli cells. The possible role of testicular VDAC2 in providing energy metabolites and in germ cell apoptosis is discussed.  (+info)

Retinal voltage-dependent anion channel: characterization and cellular localization. (4/42)

PURPOSE: To characterize and localize retinal voltage-dependent anion channel (VDAC) and to understand its possible contribution to mitochondrial function and dysfunction. METHODS: VDAC was characterized by a method involving purification from isolated mitochondria and reconstitution into a planar lipid bilayer (PLB). The permeability transition pore (PTP) was monitored by Ca(2+) accumulation in isolated mitochondria and swelling of mitochondria. Localization was studied by immunocytochemistry and in situ hybridization. RESULTS: Retinal VDACs exhibited the electrophysiological fingerprint of the VDAC superfamily. It had a maximal chord conductance of 3.7 +/- 0.1 nanosiemens (nS) in 1 M NaCl, and a voltage-dependent conductance that was highest at transmembrane potential close to zero. It was modulated by glutamate, which decreased the channel's open probability, and by La(3+) and ruthenium amine binuclear complex (Ru360), which closed the channel. Energized and freshly prepared retinal mitochondria accumulated Ca(2+) that is inhibited by La(3+) ruthenium red and Ru360. Subsequent to Ca(2+) accumulation, mitochondria released the accumulated Ca(2+), probably through activation of the PTP. Ru360 inhibited Ca(2+) release and mitochondrial swelling. VDAC was present in mitochondria of all retinal cell types: photoreceptor, bipolar, horizontal, amacrine, and ganglion cells. Most cells primarily expressed VDAC-1, but they also expressed VDAC-2 and -3. CONCLUSIONS: These results suggest that VDAC is involved in PTP activity and/or regulation and thus is an important player in retinal degeneration associated with PTP-mediated mitochondrial dysfunction.  (+info)

VDAC2 inhibits BAK activation and mitochondrial apoptosis. (5/42)

The multidomain proapoptotic molecules BAK or BAX are required to initiate the mitochondrial pathway of apoptosis. How cells maintain the potentially lethal proapoptotic effector BAK in a monomeric inactive conformation at mitochondria is unknown. In viable cells, we found BAK complexed with mitochondrial outer-membrane protein VDAC2, a VDAC isoform present in low abundance that interacts specifically with the inactive conformer of BAK. Cells deficient in VDAC2, but not cells lacking the more abundant VDAC1, exhibited enhanced BAK oligomerization and were more susceptible to apoptotic death. Conversely, overexpression of VDAC2 selectively prevented BAK activation and inhibited the mitochondrial apoptotic pathway. Death signals activate "BH3-only" molecules such as tBID, BIM, or BAD, which displace VDAC2 from BAK, enabling homo-oligomerization of BAK and apoptosis. Thus, VDAC2, an isoform restricted to mammals, regulates the activity of BAK and provides a connection between mitochondrial physiology and the core apoptotic pathway.  (+info)

Neuroactive steroid interactions with voltage-dependent anion channels: lack of relationship to GABA(A) receptor modulation and anesthesia. (6/42)

Neuroactive steroids modulate the function of gamma-aminobutyric acid type A (GABA(A)) receptors in brain; this is the presumed basis of their action as anesthetics. In a previous study using the neuroactive steroid analog, (3alpha,5beta)-6-azi-3-hydroxypregnan-20-one (6-AziP), as a photoaffinity-labeling reagent, we showed that voltage-dependent anion channel-1 (VDAC-1) was the predominant protein labeled in brain. Antisera to VDAC-1 were shown to coimmunoprecipitate GABA(A) receptors, suggesting a functional relationship between steroid binding to VDAC-1 and modulation of GABA(A) receptor function. This study examines the contribution of steroid binding to VDAC proteins to modulation of GABA(A) receptor function and anesthesia. Photolabeling of 35-kDa protein with [(3)H]6-AziP was reduced 85% in brain membranes prepared from VDAC-1-deficient mice but was unaffected by deficiency of VDAC-3. The photolabeled 35-kDa protein in membranes from VDAC-1-deficient mice was identified by two-dimensional electrophoresis and electrospray ionization-tandem mass spectrometry as VDAC-2. The absence of VDAC-1 or VDAC-3 had no effect on the ability of neuroactive steroids to modulate GABA(A) receptor function as evidenced by radioligand ([(35)S] t-butylbicyclophosphorothionate) binding or by electrophysiological studies. Electrophysiological studies also showed that neuroactive steroids modulate GABA(A) receptor function normally in VDAC-2-deficient fibroblasts transfected with alpha(1)beta(2)gamma(2) GABA(A) receptor subunits. Finally, the neuroactive steroid pregnanolone [(3alpha,5beta)-3-hydroxypregnan-20-one] produced anesthesia (loss of righting reflex) in VDAC-1- and VDAC-3-deficient mice, and there was no difference in the recovery time between the VDAC-deficient mice and wild-type controls. These data indicate that neuroactive steroid binding to VDAC-1, -2, or -3 is unlikely to mediate GABA(A) receptor modulation or anesthesia.  (+info)

Voltage-dependent anion-selective channels VDAC2 and VDAC3 are abundant proteins in bovine outer dense fibers, a cytoskeletal component of the sperm flagellum. (7/42)

Outer dense fibers (ODF) are specific subcellular components of the sperm flagellum. The functions of ODF have not yet been clearly elucidated. We have investigated the protein composition of purified ODF from bovine spermatozoa and found that one of the most abundant proteins is a 30-32-kDa polypeptide. This protein was analyzed by sequencing peptides derived following limited proteolysis. Peptide sequences were found to match VDAC2 and VDAC3. VDACs (voltage-dependent, anion-selective channels) or eukaryotic porins are a group of proteins first identified in the mitochondrial outer membrane that are able to form hydrophilic pore structures in membranes. In mammals, three VDAC isoforms (VDAC1, -2, -3) have been identified by cDNA cloning and sequencing. Antibodies against synthetic peptides specific for the three mammal VDAC isoforms were generated in rabbits. Their specificity was demonstrated by immunoblotting using recombinant VDAC1, -2, and -3. In protein extracts of bovine spermatozoa, VDAC1, -2, and -3 were detected by specific antibodies, while only VDAC2 and -3 were found as solubilized proteins derived from purified bovine ODFs. Immunofluorescence microscopy of spermatozoa revealed that anti-VDAC2 and anti-VDAC3 antibodies clearly bound to the sperm flagellum, in particular to the ODF. Transmission electron immunomicroscopy supported the finding that VDAC2 protein is abundant in the ODF. Since the ODF does not have any known membranous structure, it is tempting to speculate that VDAC2 and VDAC3 might have an alternative structural organization and different functions in ODF than in mitochondria.  (+info)

Bax-dependent regulation of Bak by voltage-dependent anion channel 2. (8/42)

Many studies have demonstrated a critical role of Bax in mediating apoptosis, but the role of Bak in regulating cancer cell apoptotic sensitivities in the presence or absence of Bax remains incompletely understood. Using isogenic cells with defined genetic deficiencies, here we show that in response to intrinsic, extrinsic, and endoplasmic reticulum stress stimuli, HCT116 cells show clear-cut apoptotic sensitivities in the order of Bax+/Bak+ > Bax+/Bak- >> Bax-/Bak+ >> Bax-/Bak-. Small interference RNA-mediated knockdown of Bak in Bax-deficient cells renders HCT116 cells completely resistant to apoptosis induction. Surprisingly, however, Bak knockdown in Bax-expressing cells only slightly affects the apoptotic sensitivities. Bak, like Bax, undergoes the N terminus exposure upon apoptotic stimulation in both Bax-expressing and Bax-deficient cells. Gel filtration, chemical cross-linking, and co-immunoprecipitation experiments reveal that different from Bax, which normally exists as monomers in unstimulated cells and is oligomerized by apoptotic stimulation, most Bak in unstimulated HCT116 cells exists in two distinct protein complexes, one of which contains voltage-dependent anion channel (VDAC) 2. During apoptosis, Bak and Bax form both homo- and hetero-oligomeric complexes that still retain some VDAC-2. However, the oligomeric VDAC-2 complexes are diminished, and Bak does not interact with VDAC-2 in Bax-deficient HCT116 cells. These results highlight VDAC-2 as a critical inhibitor of Bak-mediated apoptotic responses.  (+info)

Mitochondria are critically involved in necrotic cell death induced by Ca(2+) overload, hypoxia and oxidative damage. The mitochondrial permeability transition (MPT) pore - a protein complex that spans both the outer and inner mitochondrial membranes - is considered the mediator of this event and has been hypothesized to minimally consist of the voltage-dependent anion channel (Vdac) in the outer membrane, the adenine-nucleotide translocase (Ant) in the inner membrane and cyclophilin-D in the matrix. Here, we report the effects of deletion of the three mammalian Vdac genes on mitochondrial-dependent cell death. Mitochondria from Vdac1-, Vdac3-, and Vdac1-Vdac3-null mice exhibited a Ca(2+)- and oxidative stress-induced MPT that was indistinguishable from wild-type mitochondria. Similarly, Ca(2+)- and oxidative-stress-induced MPT and cell death was unaltered, or even exacerbated, in fibroblasts lacking Vdac1, Vdac2, Vdac3, Vdac1-Vdac3 and Vdac1-Vdac2-Vdac3. Wild-type and Vdac-deficient ...
Erastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS.
In cancer cells the little chemical substances RSL3 and erastin promote a new type of cell death called ferroptosis, which requires iron\reliant accumulation of lipid reactive oxygen species. chemical substance\caused ferroptosis.10, 14 Lipoxygenase are non-heme iron\containing dioxygenases that catalyze Necrostatin 2 S enantiomer IC50 the stereospecific installation of air into polyunsaturated fatty acids (PUFA) such as arachidonic acidity and linoleic acidity.15 Although many choose free fatty acids as a base LOX, some isoforms, including bunny 15\LOX, can oxygenate esterified Necrostatin 2 S enantiomer IC50 polyenoic fatty acids in Necrostatin 2 S enantiomer IC50 cellular membranes. Human being LOX are indicated in a range of cells and many tumors, and possess been suggested as a factor in tumor,16 although the part of LOX in tumor can be unclear. Cancer cells accumulate iron, and iron provisioned from extracellular pathways mediated by transferrin receptors and from intracellular pathways ...
VDAC2山羊多克隆抗体(ab118872)可与人样本反应并经WB, ELISA, IHC实验严格验证。中国75%以上现货,所有产品均提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
Ferroptosis is a form of nonapoptotic cell death involving the iron-dependent production of reactive oxygen species (ROS). Several small molecules that selectively induce ferroptosis in oncogenic RAS (RASV12)-expressing cells have been described, but whether these compounds target a common regulatory pathway is unclear. Yang and colleagues found that erastin, a ferroptosis-inducing compound, caused glutathione depletion, which was necessary for selective lethality of erastin and erastin-induced generation of cytosolic and lipid ROS in RASV12-expressing cells. The depletion of glutathione in erastin-treated cells inactivated glutathione-dependent peroxidases (GPX), which catalyze the reduction of hydrogen peroxide and organic hydroperoxides and require glutathione as a cofactor. Because RSL3, another ferroptosis-inducing compound, increased lipid ROS production in the absence of glutathione depletion, a chemoproteomic approach was used to identify RSL3 targets in RASV12-expressing cells. RSL3 was ...
Mouse Monoclonal Anti-VDAC1 Antibody (2A8). Mitochondria Marker. Validated: WB, ELISA. Tested Reactivity: Human. 100% Guaranteed.
Chicken Polyclonal Anti-VDAC3 Antibody. Validated: WB, ELISA, ICC/IF, IHC, IHC-P. Tested Reactivity: Human, Mouse, Rat, and more. 100% Guaranteed.
The channel-forming protein called VDAC forms the major pathway in the mitochondrial outer membrane and controls metabolite flux across that membrane. The different VDAC isoforms of a species may play different roles in the regulation of mitochondrial functions. The mouse has three VDAC isoforms (VD …
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
Impacts, Issues: When Mitochondria Spin Their Wheels  More than forty disorders related to defective mitochondria are known (such as Friedreichs ataxia); many of those afflicted die young Leah: A professional model
Voltage-dependent anion channel (VDAC) is principally situated in the mitochondrial external membrane and participates in lots of biological procedures. integrity and acrosome response using particular anti-VDAC2 monoclonal antibody for the very first time. The outcomes exhibited that indigenous VDAC2 been around in the membrane the different parts of individual Bentamapimod spermatozoa. The co-incubation of spermatozoa with anti-VDAC2 antibody did not impact the acrosomal integrity and acrosome reaction, but inhibited ionophore "type":"entrez-nucleotide","attrs":"text":"A23187″,"term_id":"833253″,"term_text":"A23187″A23187-induced intracellular Ca2+ increase. Our study suggested that VDAC2 was located in the acrosomal plasma or membrane membrane of individual spermatozoa, and performed putative assignments in sperm features through mediating Ca2+ transmembrane transportation. Launch Voltage-dependent anion route (VDAC), being a membrane route protein, is normally discovered in the ...
Excess superoxide (O2−) and nitric oxide (NO) forms peroxynitrite (ONOO−) during cardiac ischemia reperfusion (IR) injury, which in turn induces protein tyrosine nitration (tyr-N). Mitochondria are both a source of and target for ONOO−. Our aim was to identify specific mitochondrial proteins that display enhanced tyr-N after cardiac IR injury, and to explore whether inhibiting O2−/ONOO− during IR decreases mitochondrial protein tyr-N and consequently improves cardiac function. We show here that IR increased tyr-N of 35 and 15 kDa mitochondrial proteins using Western blot analysis with 3-nitrotyrosine antibody. Immunoprecipitation (IP) followed by LC-MS/MS identified 13 protein candidates for tyr-N. IP and Western blot identified and confirmed that the 35 kDa tyr-N protein is the voltage-dependent anion channel (VDAC). Tyr-N of native cardiac VDAC with IR was verified on recombinant (r) VDAC with exogenous ONOO−. We also found that ONOO− directly enhanced rVDAC channel activity, and rVDAC
The structural proximity and functional coupling between the SR (sarcoplasmic reticulum) and mitochondria have been suggested to occur in the heart. However, themolecular architecture involved in the SR–mitochondrial coupling remains unclear. In the present study, we performed various genetic and Ca2+ -probing studies to resolve the proteins involved in the coupling process. By using the bacterial 2-hybrid, glutathione transferase pull-down, co-immunoprecipitation and immunocytochemistry assays, we found that RyR2 (ryanodine receptor type 2), which is physically associated with VDAC2 (voltage-dependent anion channel 2), was co-localized in SR–mitochondrial junctions. Furthermore, a fractionation study revealed that VDAC2 was co-localized with RyR2 only in the subsarcolemmal region. VDAC2 knockdown by targeted short hairpin RNA led to an increased diastolic [Ca2+ ] (calcium concentration) and abolishment of mitochondrial Ca2+ uptake. Collectively, the present study suggests that the ...
VDAC3 antibody, N-term (voltage dependent anion channel 3) for WB. Anti-VDAC3 pAb (GTX47682) is tested in Human samples. 100% Ab-Assurance.
Apoptosis, or programmed cell death, is essential for proper development and functioning of the body systems. During development, apoptosis plays a central role to sculpt the embryo, and in adults, to maintain tissue homeostasis by eliminating redundant, damaged or effete cells. Therefore, a tight regulation of this process is essential. Cell shrinkage associated efflux of K+ and Cl- through plasma membrane ion channels is an early event of apoptosis. However, little is known about these fluxes. The aim of this thesis was to investigate ion channels in the plasma membrane of neurons undergoing apoptosis. We studied differentiated (the mouse hippocampal cell line HT22, the human neuroblastoma cell line SK-N-MC, and rat primary hippocampal neurons) and undifferentiated (rat primary cortical neural stem cells cNSCs) cells with the patch-clamp technique. All cell types displayed a low electrical activity under control conditions. However, during apoptosis in differentiated neurons, we found an ...
Citation: Chalivendra, S.C., Huber, S.C., Sachs, M.M., Rhoads, D.M. 2006. Sucrose synthase interaction with the voltage-dependent anion channel suggests a potential role for the enzyme in inter-organellar signaling. American Society of Plant Biologists [abstract]. Paper no. 36027. Available: http://abstracts.aspb.org/pb2006/public/P36/P36027.html. Interpretive Summary: Technical Abstract: Sucrose synthase (SUS) is a key enzyme in plant sucrose catabolism and uniquely able to mobilize sucrose into multiple pathways involved in metabolic, structural, and storage functions. Our recent work indicates that the biological function of SUS extends beyond its biochemical activity. This inference is based on the following observations: a) tissue-specific, isoform-dependent and metabolically-regulated association of SUS with mitochondria and nuclei and b) isoform-specific and anoxia-enhanced interaction of SUS with the outer mitochondrial membrane protein, VDAC (voltage-dependent anion channel; also known ...
Mitochondria are the key source of ATP that fuels cellular functions, and they are also central in cellular signaling, cell division and apoptosis. Dysfunction of mitochondria has been implicated in a wide range of diseases, including neurodegenerative and cardiac diseases, and various types of cancer. One of the key proteins that regulate mitochondrial function is the voltage-dependent anion channel 1 (VDAC1), the most abundant protein on the outer membrane of mitochondria. VDAC1 is the gatekeeper for the passages of metabolites, nucleotides, and ions; it plays a crucial role in regulating apoptosis due to its interaction with apoptotic and anti-apoptotic proteins, namely members of the Bcl-2 family of proteins and hexokinase ...
Dr. Samantha Morris three December 2018 Publications Evaluation of Wu et al.: Comprehending Global and Local Structure of Single-Cell Datasets. Kong W, Morris SA. Cell… ...
Mitochondrial porin, also known as the voltage-dependent anion channel (VDAC), is a multi-functional channel protein that shuttles metabolites between the mitochondria and the cytosol and implicated in cellular life and death decisions. The inhibition of porin under the control of neuronal Ddc-Gal4 result in short lifespan and in an age-dependent loss in locomotor function, phenotypes that are strongly associated with Drosophila models of Parkinson disease. Loss of porin function was achieved through exploitation of RNAi while derivative lines were generated by homologous recombination and tested by PCR. The expression of human α-synuclein transgene in neuronal populations that include dopamine producing neurons under the control of Ddc-Gal4 produces a robust Parkinson disease model, and results in severely reduced lifespan and locomotor dysfunction. In addition, the porin-induced phenotypes are greatly suppressed when the pro-survival Bcl-2 homologue Buffy is overexpressed in these neurons and ...
The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein forms a heterodimer with BCL2, and functions as an apoptotic activator. This protein is reported to interact with, and increase the opening of, the mitochondrial voltage-dependent anion channel (VDAC), which leads to the loss in membrane potential and the release of cytochrome c. The expression of this gene is regulated by the tumor suppressor P53 and has been shown to be involved in P53-mediated apoptosis. Multiple alternatively spliced transcript variants, which encode different isoforms, have been reported for this gene. Product Name ...
The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form hetero- or homodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein forms a heterodimer with BCL2, and functions as an apoptotic activator. This protein is reported to interact with, and increase the opening of, the mitochondrial voltage-dependent anion channel (VDAC), which leads to the loss in membrane potential and the release of cytochrome c. The expression of this gene is regulated by the tumor suppressor P53 and has been shown to be involved in P53-mediated apoptosis. Multiple alternatively spliced transcript variants, which encode different isoforms, have been reported for this gene. Product Name ...
The protein encoded by this gene belongs to the BCL2 protein family. BCL2 family members form oligomers or heterodimers and act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. This protein localizes to mitochondria, and functions to induce apoptosis. It interacts with and accelerates the opening of the mitochondrial voltage-dependent anion channel, which leads to a loss in membrane potential and the release of cytochrome c. This protein also interacts with the tumor suppressor P53 after exposure to cell stress. [provided by RefSeq, Jul 2008] ...
If an organ has mostly defective mitochondria, the organs function will be suboptimal, but the organ can amplify the least damaged mitochondria for years. This is common in kidney failure and heart failure. Mitochondria usually last about 3 weeks. The choice for mitochondria in life is limited; divide or die. In this fashion, defective power plants are constantly weeded out. Let me give you an example. Take a brain neuron. They usually are as old as we are and are rarely replaced. Their function does not crash if there is a power plant mutation. Instead, its function is diminished to a very small degree over time. The more defective mtDNA is, the more oxidation will be found in the cell. Ironically, this oxidation does not effect proteins, fats, or carbohydrates from the diet, in the cell as we once thought. Studies have been done in damaged organs and cannot find evidence for oxidative damage. What is effected is the generation of transcription factors and genes by the new cellular redox state. ...
TY - JOUR. T1 - Microsporidia interact with host cell mitochondria via voltage-dependent anion channels using sporoplasm surface protein 1. AU - Han, Bing. AU - Ma, Yanfen. AU - Tu, Vincent. AU - Tomita, Tadakimi. AU - Mayoral, Joshua. AU - Williams, Tere. AU - Horta, Aline. AU - Huang, Huan. AU - Weissa, Louis M.. PY - 2019/1/1. Y1 - 2019/1/1. N2 - Microsporidia are opportunistic intracellular pathogens that can infect a wide variety of hosts ranging from invertebrates to vertebrates. During invasion, the microsporidian polar tube pushes into the host cell, creating a protective microenvironment, the invasion synapse, into which the sporoplasm extrudes. Within the synapse, the sporoplasm then invades the host cell, forming a parasitophorous vacuole (PV). Using a proteomic approach, we identified Encephalitozoon hellem sporoplasm surface protein 1 (EhSSP1), which localized to the surface of extruded sporoplasms. EhSSP1 was also found to interact with polar tube protein 4 (PTP4). Recombinant ...
Originally discovered in mitochondrial membrane fractions from Paramecium aurelia, VDAC is a highly conserved protein found in the MOM from all eukaryotes studied (Sampson et al., 1997). In mice and humans, the VDAC has three isoforms, VDAC1, VDAC2, and VDAC3, of approximately 30 kDa. Each VDAC forms a barrel in the membrane with staves comprised of β-strands (Colombini, 2004). VDAC refolded from inclusion bodies forms 19-stranded β-barrels as analyzed by NMR and X-ray crystallography, although another model proposes that this three-dimensional structure is non-native and functional VDAC forms 13-stranded barrels (Bayrhuber et al., 2008; Hiller et al., 2008; Ujwal et al., 2008; Colombini, 2009).. Beyond discrepancies concerning the number of strands, the VDAC β-barrel encloses an aqueous channel of ∼2.5 nm in internal diameter surrounded by a wall of 1 nm. In the open state, the VDAC is permeable to nonelectrolyte solutes of molecular mass up to 5 kDa (Colombini, 1980; Colombini et al., ...
Emerging evidence suggested mitophagy activation mitigates ethanol-induced liver injury. However, the effect of ethanol on mitophagy is inconsistent. Importantly, the understanding of mitophagy status after chronic ethanol consumption is limited. This study evaluated the effect of quercetin, a naturally-occurring flavonoid, on chronic ethanol-induced mitochondrial damage focused on mitophagy. An ethanol regime to mice for 15 weeks (accounting for 30% of total calories) led to significant mitochondrial damage as evidenced by changes of the mitochondrial ultrastructure, loss of mitochondrial membrane potential and remodeling of membrane lipid composition, which was greatly attenuated by quercetin (100 mg/kg.bw). Moreover, quercetin blocked chronic ethanol-induced mitophagy suppression as denoted by mitophagosomes-lysosome fusion and mitophagy-related regulator elements, including LC3II, Parkin, p62 and voltage-dependent anion channel 1 (VDAC1), paralleling with increased FoxO3a nuclear translocation. AMP
The innate immune system plays a critical role in both the initial response to an invading pathogen, which frequently limits or contains pathogen replication and dissemination, and the induction of an effective adaptive immune response, which is most often the primary mechanism for pathogen clearance. The characteristics of the innate immune response are determined in part by the pathogen initiating the response but can also be influenced by the type of cell in which the response is generated. In this report, we examined the functional PRR-mediated pathways present in human neuronal cells and differentiated primary rat neurons, with a particular focus on those pathways previously identified as being important for antiviral innate immune responses in other cell types. We drew four main conclusions. First, human neuronal cells possess functional TLR3-, TLR4-, RIG-I-, and MDA5-mediated PRR pathways whose activity was maturation-dependent. Second, both extracellular and transfected poly(I-C) induced ...
Academic Dissertations;Academic Dissertations--South Carolina;Tubulin Modulators;Tubulin;Neoplasms--metabolism;Voltage-Dependent Anion ...
Ferroptosis is a non-apoptotic form of regulated cell death. It is distinct from other regulated cell death phenotypes, such as apoptosis and necroptosis. Ferroptosis is characterized by extensive lipid peroxidation, which can be suppressed by iron chelators or lipophilic antioxidants. Mechanistically, Ferroptosis inducers are divided into two classes: (1) inhibitors of cystine import via system xc− (e.g., Erastin), which subsequently causes depletion of glutathione (GSH), and (2) covalent inhibitors (e.g., (1S, 3R)-RSL3) of glutathione peroxidase 4 (GPX4). Since GPX4 reduces lipid hydroperoxides using GSH as a co-substrate, both compound classes ultimately result in loss of GPX4 activity, followed by elevated levels of lipid reactive oxygen species (ROS) and consequent cell death. Ferroptosis is an iron- and ROS-dependent form of regulated cell death (RCD). Misregulated Ferroptosis has been implicated in multiple physiological and pathological processes, including cancer cell death, ...
Study; VDACS; sources, scale, and prevention of food waste in the Commonwealth; report. Directs the Virginia Department of Agriculture and Consumer Services (VDACS) to study, in consultation with the Department of Environmental Quality and stakeholders, the sources, scale, and prevention of food waste in the Commonwealth. In conducting its study, VDACS shall (i) assess the total annual statewide rate of preventable food waste received by landfills within the Commonwealth; (ii) identify the industry sectors within the Commonwealth that contribute to preventable food waste, and determine their rate of contribution to such waste; (iii) identify alternative uses of food that is wasted; and (iv) recommend policies to reduce the annual rate of preventable food waste in the Commonwealth with data-driven reduction targets and timelines, including food donation requirements for certain food waste from grocery stores and restaurants. The provisions of the bill are contingent on funding in a general appropriation
Abstract: Background and Objectives: The initiating steps and precise pathway of breast tumorigenesis are poorly understood and it is unclear if Ductal Carcinoma In Situ (DCIS) progresses to invasive ductal carcinoma (IDCA) of the breast. This study was undertaken to identify proteins that are differentially expressed between IDCA and DCIS and that may predict the invasive potential of breast tumors. Methodology: It is utilized that the two-dimensional difference in gel electrophoresis technology (2D-DIGE) and tandem mass spectrometry (LC-MS/MS) to perform proteomic analysis of IDCA (MCF-7 and BT-474) and DCIS (HCC-1500 and HCC-38) cell lines. Results: Identified 10 proteins that were differentially expressed between IDCA and DCIS (≥2-fold difference; p≤0.05) and classified the proteins according to their Gene Ontology (GO). Out of these proteins, 60 kDa mitochondrial heat shock protein (HSPD1), Heat Shock Protein Beta 1 (HSPB1) and the voltage-dependent anion-selective channel protein 1 ...
The generation of action potentials in excitable cells requires selective ion channels that open and close upon changes in membrane potential. Initially, cell excitability was mainly studied in neuronal axons, and in this particular cell compartment, electrical excitability is almost exclusively governed by cation channels. For many years, voltage-dependent anion channels were thought to be of no relevance for cell excitability and considered mere "background" or "leakage" channels involved in housekeeping functions. Skeletal muscle was the first excitable tissue shown to exhibit a significant anion conductance (Hodgkin and Horowicz, 1959). Although the resting muscle chloride conductance largely exceeds the resting potassium conductance, chloride ions do not contribute to the resting membrane potential under physiological conditions. Variations of external [Cl−] cause only a transient change in membrane potential that results in rapid redistribution of anions and return of the transmembrane ...
India and its Doctors have always been at the forefront of ground breaking medical procedures and research especially in the field of assisted reproduction and Surrogacy.. According to Dr.Samit Sekhar, who is IVF and Surrogacy program director at the Kiran Infertility centre "Genetic diseases are a group of hereditary abnormalities due to a mutation in the mothers mitochondria, these diseases can affect one part of the body or multiple parts including the brain, kidneys, muscles, heart, eyes, and ears".. What this relatively simple technique will do is to take only the healthy genetic material from the embryo of a woman with defective mitochondria and a second embryo is then stripped of its key DNA but still retains its healthy mitochondria. Finally, the fertilized embryo is placed in the womb of the mother. This is excellent news for families with mitochondrial disease. This will give women who carry these diseased genes more reproductive choices! Earlier they had no choice but to opt for an ...
Hexokinase II is often highly expressed in poorly differentiated and rapidly growing tumors that exhibit a high rate of aerobic glycolysis. Hexokinase II binds to the mitochondrial membrane through its interaction with the outer membrane voltage-dependent anion channel (VDAC), preferentially at contact sites between the outer and inner mitochondrial membrane. This location is thought to be important for the integration of glycolysis with mitochondrial energy metabolism. VDAC is a critical component of the mitochondrial phase of apoptosis and its interaction with Bcl-2 family proteins controls the rate of release of mitochondrial intermembrane space proteins that activate the execution phase of apoptosis. The proteins involved in the contact sites also constitute the mitochondrial permeability transition, one of the mechanisms by which mitochondrial protein release can be mediated. Hexokinase II binding to VDAC suppresses the release of intermembrane space proteins and inhibits apoptosis, thereby ...
Nitric oxide (NO) dependent mitochondrial hyperpolarization (MHP) and enhanced calcium fluxing underlie aberrant T cell activation in Systemic Lupus Erythematosus. Activity of mTOR, which senses the mitochondrial membrane potential, is increased in lupus T cells, which promotes HRES-1/Rab4 expression. Rab4 overexpression enhances recycling and lysosomal degradation of immune synapse components, including CD4 and TCRζ. We investigated activity of the NO-MHP-mTOR-Rab4 signaling pathway in lupus-prone mice. Overexpression of Rab4 and loss of TCRζ were detected prior to disease onset of NZB/NZW (F1) mice at 5 months. Increased NO production, mitochondrial transmembrane potential, and mitochondrial mass were present after disease onset at 11 months. MRL/lpr mice exhibited increased expression of the mitochondrial voltage-dependent anion channel 1(VDAC1) protein, transaldolase (TAL), Rab4, mTOR activation, and enhanced CD3 and CD4 recycling at 2-3 months, prior to disease development. In conclusion, ...
We show that the ISE1 gene encodes a mitochondria-localized DEAD-box RNA helicase. Absence of functional ISE1 leads to increased intercellular transport of large dextrans during Arabidopsis embryogenesis. In support of the role of ISE1 in PD-mediated intercellular transport, PD are altered in ise1 mutant embryos; specifically, ise1 mutants have more branched and twinned PD than wild-type embryos, suggesting that PD biogenesis may be up-regulated in ise1-1 mutants. Further, the ise1 phenotype can be recapitulated in mature leaf tissues by silencing the ISE1 gene; ISE1-silenced tissues exhibit increased intercellular movement of TMV P30-2XGFP. Thus, the pathway or process disrupted by the loss of ISE1 function affects transport via PD in mature and embryonic tissues. We show that ISE1 is localized to mitochondria and that the N terminus of ISE1 contains a mitochondria-targeting sequence. The disruption of mitochondrial function in ise1 mutants is supported by the failure of their mitochondria to ...
It has been reported that high [Ca2+] is required for the Ca2+ transmission between endo/sarcoplasmic reticulum (E(S)R) and mitochondria, since MCU has very low affinity for Ca2+ [37], [38]. Several tethering proteins support the close apposition between the subcellular organelles [39], [40] and the interaction between Ca2+ releasing channels (IP3R and RyR) in E(S)R and Ca2+ pathways (VDACs) across the mitochondrial outer membrane could mediate high [Ca2+] microdomains around the uniplex [41], [42], [43]. Considering each RyRs and VDACs clustered in the microdomain [43], [44], [45], it opens the possibility of MCU clustering at the microdomain for efficient permeation across the mitochondrial inner membrane. In fact, we observed that MCU NTD forms an oligomer in the crystals and in the solution (Fig EV3A and B, Appendix Fig S3). Furthermore, MCU NTDs form helical oligomers in a similar manner to both the crystals of T4 lysozyme‐MCU NTD and MCU NTD‐E, suggesting that a crystal packing ...
It has been reported that high [Ca2+] is required for the Ca2+ transmission between endo/sarcoplasmic reticulum (E(S)R) and mitochondria, since MCU has very low affinity for Ca2+ [37], [38]. Several tethering proteins support the close apposition between the subcellular organelles [39], [40] and the interaction between Ca2+ releasing channels (IP3R and RyR) in E(S)R and Ca2+ pathways (VDACs) across the mitochondrial outer membrane could mediate high [Ca2+] microdomains around the uniplex [41], [42], [43]. Considering each RyRs and VDACs clustered in the microdomain [43], [44], [45], it opens the possibility of MCU clustering at the microdomain for efficient permeation across the mitochondrial inner membrane. In fact, we observed that MCU NTD forms an oligomer in the crystals and in the solution (Fig EV3A and B, Appendix Fig S3). Furthermore, MCU NTDs form helical oligomers in a similar manner to both the crystals of T4 lysozyme‐MCU NTD and MCU NTD‐E, suggesting that a crystal packing ...
As we age, our cells increasingly struggle to recycle the mitochondria - the powerhouse of the cells - and are no longer able to carry out their vital function and thus gets accumulated in the cell.. This degradation affects the health of many tissues, including muscles, which gradually weaken over the years and leads to age-related various diseases.. Urolithin A has been found to re-establish the cells ability to recycle the components of the defective mitochondria.. "Its the only known molecule that can relaunch the mitochondrial clean-up process, otherwise known as mitophagy," said Patrick Aebischer, President, Ecole Polytechnique Federale de Lausanne - a research institute in Switzerland.. "Its a completely natural substance, and its effect is powerful and measurable," Aebischer added.. For the study, the team tested their hypothesis on the nematode C.elegans - roundworm - which is considered elderly, after just 8-10 days.. The lifespan of worms exposed to urolithin A increased by more ...
TY - JOUR. T1 - Pore-forming proteins and adaptation of living organisms to environmental conditions. AU - Andreeva-Kovalevskaya, Zh I.. AU - Solonin, A. S.. AU - Sineva, E. V.. AU - Ternovsky, V. I.. PY - 2008/12/1. Y1 - 2008/12/1. N2 - Pore-forming proteins are powerful "tools" for adaptation of living organisms to environmental conditions. A wide range of these proteins isolated from various sources, from viruses to mammals, has been used for the analysis of their role in the processes of intra- and inter-species competition, defense, attack, and signaling. Here we review a large number of pore-forming proteins from the perspective of their functions, structures, and mechanisms of membrane penetration. Various mechanisms of cell damage, executed by these proteins in the course of formation of a pore and after its passing to conducting state, have been considered: endo- and exocytosis, lysis, necrosis, apoptosis, etc. The role of pore-forming proteins in evolution is discussed. The relevance ...
Nonapoptotic forms of cell death may facilitate the selective elimination of some tumor cells or be activated in specific pathological states. The oncogenic RAS-selective lethal small molecule erastin triggers a unique iron-dependent form of nonapoptotic cell death that we term ferroptosis. Ferropto …
Complete information for VDAC1P7 gene (Pseudogene), Voltage Dependent Anion Channel 1 Pseudogene 7, including: function, proteins, disorders, pathways, orthologs, and expression. GeneCards - The Human Gene Compendium
Bak小鼠单克隆抗体[AT8B4](ab104124)可与小鼠, 人样本反应并经WB, ELISA, ICC/IF实验严格验证。中国75%以上现货,所有产品提供质保服务,可通过电话、电邮或微信获得本地专属技术支持。
Perform reliable PCR with Bio-Rads VDAC2 primer pair, for Human. Designed for EvaGreen-based detection with digital PCR (ddPCR).
Perform reliable PCR with Bio-Rads VDAC3 primer pair, for Human. Designed for EvaGreen-based detection with digital PCR (ddPCR).
... Existem dois tipos de respostas imunes adaptativas, denominadas imunidade humoral e imunidade mediada por
The metabolic programs of functionally distinct T cell subsets are tailored to their immunologic activities. While quiescent T cells use oxidative phosphorylation (OXPHOS) for energy production, and effector T cells (Teffs) rely on glycolysis for proliferation, the distinct metabolic features of regulatory T cells (Tregs) are less well established. Here we show that the metabolic sensor LKB1 is critical to maintain cellular metabolism and energy homeostasis in Tregs. Treg-specific deletion of Lkb1 in mice causes loss of Treg number and function, leading to a fatal, early-onset autoimmune disorder. Tregs lacking Lkb1 have defective mitochondria, compromised OXPHOS, depleted cellular ATP, and altered cellular metabolism pathways that compromise their survival and function. Furthermore, we demonstrate that the function of LKB1 in Tregs is largely independent of the AMP-activated protein kinase, but is mediated by the MAP/microtubule affinity-regulating kinases and salt-inducible kinases. Our ...
... - Abstract. CASTANO LL, Rodrigo et al. Dilatación endoscópica y aplicación de esteroides intralesionales en las estenosis esofágicas por cáusticos y.
Chandra D, Choy G, Daniel PT, Tang DG (May 2005). "Bax-dependent regulation of Bak by voltage-dependent anion channel 2". The ... Voltage-dependent anion-selective channel protein 2 is a protein that in humans is encoded by the VDAC2 gene on chromosome 10. ... Li Z, Wang Y, Xue Y, Li X, Cao H, Zheng SJ (Feb 2012). "Critical role for voltage-dependent anion channel 2 in infectious ... Alvira CM, Umesh A, Husted C, Ying L, Hou Y, Lyu SC, Nowak J, Cornfield DN (Nov 2012). "Voltage-dependent anion channel-2 ...
"Affixing N-terminal α-helix to the wall of the voltage-dependent anion channel does not prevent its voltage gating". The ... "Mapping of residues forming the voltage sensor of the voltage-dependent anion-selective channel". Proceedings of the National ... Voltage-dependent anion-selective channel 1 (VDAC-1) is a beta barrel protein that in humans is encoded by the VDAC1 gene ... "Entrez Gene: VDAC1 voltage-dependent anion channel 1". Reina S, Palermo V, Guarnera A, Guarino F, Messina A, Mazzoni C, De ...
"Bcl-XL interacts with Apaf-1 and inhibits Apaf-1-dependent caspase-9 activation". Proceedings of the National Academy of ... and have been shown to regulate outer mitochondrial membrane channel (VDAC) opening. VDAC regulates mitochondrial membrane ... 275 (2): 1439-48. doi:10.1074/jbc.275.2.1439. PMID 10625696. Qin W, Hu J, Guo M, Xu J, Li J, Yao G, Zhou X, Jiang H, Zhang P, ... Bcl-2-like 1 or BCL2L1 is a human gene. Through alternative splicing, it encodes both of the human proteins Bcl-xL and Bcl-xS. ...
Arbel, Nir; Shoshan-Barmatz, Varda (2010-02-26). "Voltage-dependent anion channel 1-based peptides interact with Bcl-2 to ... mitochondrial membrane of the animal cell where they are thought to form a complex with the voltage-dependent anion channel ... Kinnally KW, Antonsson B (May 2007). "A tale of two mitochondrial channels, MAC and PTP, in apoptosis". Apoptosis. 12 (5): 857- ... Martinez-Caballero S, Dejean LM, Jonas EA, Kinnally KW (June 2005). "The role of the mitochondrial apoptosis induced channel ...
This protein is reported to interact with, and increase the opening of, the mitochondrial voltage-dependent anion channel (VDAC ... BAX is believed to interact with, and induce the opening of the mitochondrial voltage-dependent anion channel, VDAC. ... 2 (3): 238-40. doi:10.4161/auto.2730. PMID 16874066. [permanent dead link] Weng C, Li Y, Xu D, Shi Y, Tang H (March 2005). " ... Bcl-2 family members share one or more of the four characteristic domains of homology entitled the Bcl-2 homology (BH) domains ...
It interacts with and accelerates the opening of the mitochondrial voltage-dependent anion channel, which leads to a loss in ... Moreover, BAK1 is believed to induce the opening of the mitochondrial voltage-dependent anion channel, leading to release of ... and do not directly modulate voltage-dependent anion channel activity". Proceedings of the National Academy of Sciences of the ... 3 (2): E43-6. doi:10.1038/35055145. PMID 11175758. Lin B, Kolluri SK, Lin F, Liu W, Han YH, Cao X, Dawson MI, Reed JC, Zhang XK ...
Voltage-dependent anion channels are a class of porin ion channel located on the outer mitochondrial membrane. There is debate ... "Mapping of residues forming the voltage sensor of the voltage-dependent anion-selective channel". Proc. Natl. Acad. Sci. USA. ... Voltage-Dependent Anion Channels at the US National Library of Medicine Medical Subject Headings (MeSH) This article ... De Pinto, V.; Messina, A.; Lane, D. J. R.; Lawen, A. (2010). "Voltage-dependent anion-selective channel (VDAC) in the plasma ...
... voltage-dependent anion channels MeSH D12.776.157.530.400.500.520.500 -- voltage-dependent anion channel 1 MeSH D12.776.157.530 ... 520.750 -- voltage-dependent anion channel 2 MeSH D12.776.157.530.400.600 -- potassium channels MeSH D12.776.157.530.400.600. ... trpp cation channels MeSH D12.776.157.530.400.901.888 -- trpv cation channels MeSH D12.776.157.530.450.074 -- anion transport ... potassium channels, tandem pore domain MeSH D12.776.157.530.400.600.900 -- potassium channels, voltage-gated MeSH D12.776. ...
Voltage-dependent anion-selective channel protein 3 (VDAC3) is a protein that in humans is encoded by the VDAC3 gene on ... "Entrez Gene: voltage-dependent anion channel 3". Lee MJ, Kim JY, Suk K, Park JH (May 2004). "Identification of the hypoxia- ... De Pinto V, Messina A, Lane DJ, Lawen A (May 2010). "Voltage-dependent anion-selective channel (VDAC) in the plasma membrane". ... Hinsch KD, De Pinto V, Aires VA, Schneider X, Messina A, Hinsch E (Apr 2004). "Voltage-dependent anion-selective channels VDAC2 ...
... voltage-dependent anion channels MeSH D12.776.543.550.425.730.520.500 -- voltage-dependent anion channel 1 MeSH D12.776.543.550 ... voltage-dependent anion channels MeSH D12.776.543.585.400.730.520.500 -- voltage-dependent anion channel 1 MeSH D12.776.543.585 ... 520.750 -- voltage-dependent anion channel 2 MeSH D12.776.543.550.425.750 -- potassium channels MeSH D12.776.543.550.425.750. ... 520.750 -- voltage-dependent anion channel 2 MeSH D12.776.543.585.400.750 -- potassium channels MeSH D12.776.543.585.400.750. ...
Crompton M, Virji S, Ward JM (Dec 1998). "Cyclophilin-D binds strongly to complexes of the voltage-dependent anion channel and ... 67 (2): 109-27. doi:10.1006/geno.2000.6242. PMID 10903836. Andersen JS, Lyon CE, Fox AH, Leung AK, Lam YW, Steen H, Mann M, ... 258 (2): 729-35. doi:10.1046/j.1432-1327.1998.2580729.x. PMID 9874241. Bowles KR, Zintz C, Abraham SE, Brandon L, Bowles NE, ... 367 (Pt 2): 541-8. doi:10.1042/BJ20011672. PMC 1222909 . PMID 12149099. Bowles KR, Zintz C, Abraham SE, Brandon L, Bowles NE, ...
Schwarzer C, Barnikol-Watanabe S, Thinnes FP, Hilschmann N (2002). "Voltage-dependent anion-selective channel (VDAC) interacts ... Implication in dynein-dependent vesicle transport". J. Biol. Chem. 273 (46): 30065-8. doi:10.1074/jbc.273.46.30065. PMID ... 2004). "Receptor (CD155)-dependent endocytosis of poliovirus and retrograde axonal transport of the endosome". J. Virol. 78 (13 ... Strovel ET, Wu D, Sussman DJ (2000). "Protein phosphatase 2Calpha dephosphorylates axin and activates LEF-1-dependent ...
Schwarzer C, Barnikol-Watanabe S, Thinnes FP, Hilschmann N (2002). "Voltage-dependent anion-selective channel (VDAC) interacts ... "Voltage-dependent anion-selective channel (VDAC) interacts with the dynein light chain Tctex1 and the heat-shock protein PBP74 ... Bauch A, Campbell KS, Reth M (1998). "Interaction of the CD5 cytoplasmic domain with the Ca2+/calmodulin-dependent kinase ... 3.0.CO;2-L. PMID 9692886. Mueller S, Cao X, Welker R, Wimmer E (2002). "Interaction of the poliovirus receptor CD155 with the ...
"Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death". Nature Cell Biology. 9 (5): 550-555. ... Initial experiments by Szabó and Zoratti proposed the MPT may comprise Voltage Dependent Anion Channel (VDAC) molecules. ... MPT induction is also due to the dissipation of the difference in voltage across the inner mitochondrial membrane (known as ... I. Binary structure and voltage dependence of the pore". FEBS Letters. 330 (2): 201-205. doi:10.1016/0014-5793(93)80273-w. PMID ...
... the voltage-dependent anion channel". The Journal of Biological Chemistry. 268 (3): 1835-41. PMID 8420959. Aleshin AE, Zeng C, ... which is the ATP-dependent phosphorylation of glucose to G6P. Physiological levels of G6P can regulate this process by ... "Cloning and functional expression in yeast of two human isoforms of the outer mitochondrial membrane channel, ... 31 (2): 197-212. doi:10.1016/s0047-6374(85)80030-0. PMID 4058069. Wang F, Wang Y, Zhang B, Zhao L, Lyubasyuk V, Wang K, Xu M, ...
Family Voltage-dependent anion channel Aquaporin Porins at the US National Library of Medicine Medical Subject Headings (MeSH) ... CS1 maint: Extra text: authors list (link) Besnard M, Martinac B, Ghazi A (1997). "Voltage-dependent Porin-like Ion Channels in ... and also display a greater voltage-dependent role during metabolism. Archaea also contain ion channels that have originated ... Porins are water-filled pores and channels found in the membranes of bacteria and eukaryotes. Porin-like channels have also ...
Bax is believed to interact with, and induce the opening of the mitochondrial voltage-dependent anion channel, VDAC. ... or tumor necrosis factor-dependent cell death requires caspase-3". J. Biol. Chem. 276 (24): 21907-15. doi:10.1074/jbc. ... "Caspase-8 activation and bid cleavage contribute to MCF7 cellular execution in a caspase-3-dependent manner during ... Bcl-2 proteins act as anti- or pro-apoptotic regulators that are involved in a wide variety of cellular activities. BID is a ...
... or voltage dependent anion channel. This association confers hexokinase direct access to ATP generated by mitochondria, which ... The addition of a charged phosphate group at the 6-position of hexoses also ensures 'trapping' of glucose and 2-deoxyhexose ... and 2-fluoro-2-deoxyglucose) within cells, as charged hexose phosphates cannot easily cross the cell membrane. Hexokinases I ...
... and no permeability to anions. Channel open probability is voltage- and cytoplasmic Ca2+-independent. The generalized transport ... The mammalian NS channel proteins have been implicated in platelet derived growth factor (PDGF)-dependent single channel ... They are also the non-selective (NS) cation channels of the mammalian cytoplasmic membrane. NSCC2 channels are believed to ... These channels are essentially closed in serum deprived tissue-culture cells and are specifically opened by exposure to PDGF. ...
They are associated with the major outer membrane porins (in prokaryotes) and with the voltage-dependent anion channel (in ... PBR forms a multimeric complex with the voltage-dependent anion channel (VDAC) and adenine nucleotide carrier. Molecular ... association with the voltage-dependent anion channel and the adenine nucleotide carrier". Proc. Natl. Acad. Sci. U.S.A. 89 (8 ... 45 (2): 201-11. PMID 8114671. Zeng X, Kaplan S (November 2001). "TspO as a modulator of the repressor/antirepressor (PpsR/AppA ...
This interaction is important for rapid uptake of calcium by mitochondria through Voltage dependent anion channels (VDACs), ... RNA-dependent protein kinase (PKR)-like ER kinase), PERK contributes to apoptosis twofold by sustaining the levels of pro- ... This increased connectivity also caused an abnormality in Ca+2 signaling between neurons. Also with regard to the role in MAMs ... MAMS play an important role in Ca+2 Homeostasis, phospholipid and cholesterol metabolism. Research has associated the ...
The PTP is composed of the voltage-dependent anion channel (VDAC), the inner membrane protein adenine nucleotide translocator ( ... 2001). "Defective Cytochrome c-dependent Caspase Activation in Ovarian Cancer Cell Lines Due to Diminished or Absent Apoptotic ... 2001). "Apaf-1 Protein Deficiency Confers Resistance to Cytochrome c-dependent Apoptosis in Human Leukemic Cells". Journal of ... Bcl-2 was the first oncogene found to cause cancer-inhibiting apoptosis. It is over expressed in tumors and is resistant to ...
"Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death". Nature Cell Biology. 9 (5): 550-5. ... Hassouna A, Matata BM, Galiñanes M (Nov 2004). "PKC-epsilon is upstream and PKC-alpha is downstream of mitoKATP channels in the ... Li H, Yang T, Long Z, Cheng J (17 June 2014). "Effect of mitochondrial ATP-sensitive potassium channel opening on the ... Liedtke CM, Yun CH, Kyle N, Wang D (Jun 2002). "Protein kinase C epsilon-dependent regulation of cystic fibrosis transmembrane ...
The voltage dependent anion channel of the mitochondrion is also up regulated. Infection with WSSV differs from other described ... December 2, 2016. Retrieved 2016-12-08. ICTV. "Virus Taxonomy: 2014 Release". Retrieved 15 June 2015. Nadala, E. C. B. Jr.; L. ...
... also blocks homomeric KCNQ1 and KCNQ4 voltage gated potassium channels which contribute to vascular tone with ... in blocking voltage-dependent and calcium-activated potassium currents in hippocampal neurons". The Journal of Pharmacology and ... from addition of the transient anion on the methyl group of the picoline to the more electrophilic carbonyl group. The alcohol ... Sun, J.; Kapur, J. (2012). "M-type potassium channels modulate Schaffer collateral-CA1 glutamatergic synaptic transmission". ...
This gene encodes an alpha-1 subunit of a voltage-dependent calcium channel. Calcium channels mediate the influx of calcium ... calcium channel activity. • metal ion binding. • voltage-gated ion channel activity. • ion channel activity. • protein binding ... high voltage-gated calcium channel activity. • voltage-gated calcium channel activity involved in AV node cell action potential ... voltage-gated calcium channel activity. • voltage-gated calcium channel activity involved in cardiac muscle cell action ...
Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death.. Title. Voltage-dependent anion ... Voltage-Dependent Anion Channel 1, Voltage-Dependent Anion Channel 2, Voltage-Dependent Anion Channels. ... Home Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death. ... is considered the mediator of this event and has been hypothesized to minimally consist of the voltage-dependent anion channel ...
... chloride intracellular channel 4), Authors: Velayuthan C Padmakumar, Stuart H Yuspa. Published in: Atlas Genet Cytogenet Oncol ... angiogenesis endothelial cell morphogenesis voltage-gated ion channel activity chloride channel activity protein binding ... Overexpressed chloride intracellular channel protein CLIC4 (p64H1) is an essential component of novel plasma membrane anion ... angiogenesis endothelial cell morphogenesis voltage-gated ion channel activity chloride channel activity protein binding ...
stunning; slaughtering; proteomics; voltage dependent anion channel 2;chicken muscle. Subjects:. T Technology , TA Engineering ... Over expression of Voltage Dependent Anion Channel 2 (VDAC2) in muscles of electrically stunned chickens ... Abu Samah, Norshahida and Amid, Azura and Yusof, Faridah (2011) Over expression of Voltage Dependent Anion Channel 2 (VDAC2) in ... Voltage dependent anion channel 2 (VDAC2) was identified to be over expressed in the muscle sample of over stunned chicken. The ...
... voltage-dependent anion channel 2), was co-localized in SR-mitochondrial junctions. Furthermore, a fractionation study revealed ... Coupling of ryanodine receptor 2 and voltage-dependent anion channel 2 is essential for Ca2+ transfer from the sarcoplasmic ... Coupling of ryanodine receptor 2 and voltage-dependent anion channel 2 is essential for Ca2+ transfer from the sarcoplasmic ... By using the bacterial 2-hybrid, glutathione transferase pull-down, co-immunoprecipitation and immunocytochemistry assays, we ...
... and voltage-dependent anion channel (VDAC) in the juvenile lung. ... and voltage-dependent anion channel (VDAC) in the juvenile lung ... Maternal undernutrition during early to mid pregnancy and programming of mitochondrial uncoupling protein-2 (UCP2) ... Voltage-dependent anion channel (VDAC), together with uncoupling protein-2 (UCP2) may regulate reactive oxygen species within ... Gnanalingham GM1, Yakubu DP1, Gopalakrishnan GS1, Mostyn A1, Alves-Guerra MC2, Pecqueur C2, Miroux B2, Symonds ME1, Stephenson ...
The channel-forming protein called VDAC forms the major pathway in the mitochondrial outer membrane and controls metabolite ... Voltage-Dependent Anion Channel 1 * Voltage-Dependent Anion Channel 2 * Voltage-Dependent Anion Channels ... The channel-forming protein called VDAC forms the major pathway in the mitochondrial outer membrane and controls metabolite ... Mouse VDAC isoforms expressed in yeast: channel properties and their roles in mitochondrial outer membrane permeability J Membr ...
Voltage-dependent anion-selective channel protein 2. Xenopus laevis (African clawed frog) ... Voltage-dependent anion-selective channel protein 2 UniProtKBInterProInteractive Modelling. 282 aa; Sequence (Fasta) ...
2014). Voltage-dependent anion channels: the wizard of the mitochondrial outer membrane. Biol. Chem. 395, 1435-1442. doi: ... voltage-dependent anion channel 2. VMO-1. vitelline membrane outer layer protein 1. ... 2016). Characterization of oyster voltage-dependent anion channel 2 (VDAC2) suggests its involvement in apoptosis and host ... voltage-dependent anion channel 2-like protein (VDAC2) and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) (Fig. 3). Note that ...
Voltage-dependent anion-selective channel protein 3. Bos taurus. 87.5. 16 (5). KK up regulated. 15.9. 91. ... Voltage-dependent anion-selective channel protein 2. Bos taurus. 120.7. 21 (5). M specific isoform. -. 500. ... Voltage-dependent anion-selective channel protein 2 (VDAC-2) (Outer mitochondrial membrane protein porin 2). ... cAMP-dependent protein kinase type I-alpha regulatory subunit. Bos taurus. 72.3. 12 (5). M specific isoform. -. 524. ...
VDAC3; voltage dependent anion channel 3 [KO:K15041]. 1536 CYBB; cytochrome b-245 beta chain [KO:K21421] [EC:1.-.-.-]. ... VDAC2; voltage dependent anion channel 2 [KO:K15040]. 7419 ... PCBP2; poly(rC) binding protein 2 [KO:K13162]. 30061 SLC40A1; ... Ferritinophagy via NCOA4 is required for erythropoiesis and is regulated by iron dependent HERC2-mediated proteolysis. ... 1-Octadecanoyl-2-(15S-hydroxy-5Z,8Z,11Z,13E-eicosatetraenoyl)-sn-glycero-3-phosphoethanolamine. ...
Chandra D, Choy G, Daniel PT, Tang DG (May 2005). "Bax-dependent regulation of Bak by voltage-dependent anion channel 2". The ... Voltage-dependent anion-selective channel protein 2 is a protein that in humans is encoded by the VDAC2 gene on chromosome 10. ... Li Z, Wang Y, Xue Y, Li X, Cao H, Zheng SJ (Feb 2012). "Critical role for voltage-dependent anion channel 2 in infectious ... Alvira CM, Umesh A, Husted C, Ying L, Hou Y, Lyu SC, Nowak J, Cornfield DN (Nov 2012). "Voltage-dependent anion channel-2 ...
"Affixing N-terminal α-helix to the wall of the voltage-dependent anion channel does not prevent its voltage gating". The ... "Mapping of residues forming the voltage sensor of the voltage-dependent anion-selective channel". Proceedings of the National ... Voltage-dependent anion-selective channel 1 (VDAC-1) is a beta barrel protein that in humans is encoded by the VDAC1 gene ... "Entrez Gene: VDAC1 voltage-dependent anion channel 1". Reina S, Palermo V, Guarnera A, Guarino F, Messina A, Mazzoni C, De ...
voltage-dependent anion channel 2 Assay Type: SYBR® Green Assay Design: exonic Application: Gene Expression Unique Assay ID: ... voltage-dependent anion channel 2 Assay Type: EvaGreen Application: Gene Expression Unique Assay ID: dHsaEG5006665 Info: EG; ... voltage-dependent anion channel 2 Assay Type: Probe Application: Gene Expression Unique Assay ID: dHsaCPE5031642 Info: FAM; ... voltage-dependent anion channel 2 Assay Type: Probe Application: Gene Expression Unique Assay ID: dHsaCPE5031643 Info: HEX; ...
A chemical glycoproteomics platform reveals O-GlcNAcylation of mitochondrial voltage-dependent anion channel 2.  Palaniappan, ... We have previously shown that second-messenger-dependent kinases (cAMP-dependent kinase, protein kinase C) in the olfactory ... The beta 2-adrenergic receptor (beta 2AR) can be constitutively activated by mutations in the third intracellular loop. Whereas ... A constitutively active mutant beta 2-adrenergic receptor is constitutively desensitized and phosphorylated.  Codina, J; ...
Journal Article] Mitochondrial Ca2+ uptake by the voltage-dependent anion channel 2 regulates cardiac rhythmicity.2014. *. ... Journal Article] RING finger protein 121 facilitates the degradation and membrane localization of voltage-gated sodium channels ... Presentation] JSAP1 and JLP regulate kinesin-1-dependent axonal transport to prevent neuronal degeneration.2014. *. Author(s). ... Journal Article] JSAP1/JIP3 and JLP regulate kinesin-1-dependent axonal transport to prevent neuronal degeneration.2015. *. ...
Voltage-dependent anion-selective channel protein 2. P45880. VDAC2_HUMAN. VDAC2. 43. ↓ 5,89. 0.003. 38.6. 7.7. 187. ... Probable ATP-dependent RNA helicase DDX5. P17844. DDX5_HUMAN. DDX5. 37. ↑ 7,01. 0.002. 69.6. 9.1. 109. ... The ion acceleration voltage was 20 kV. Each spectrum was internally calibrated with the masses of two trypsin autolysis ... Lessnick SL, Dacwag CS, Golub TR (2002) The Ewings sarcoma oncoprotein EWS/FLI induces a p53-dependent growth arrest in ...
Phyllanthus inhibits A549 metastasis by suppressing ERK1/2 and hypoxia pathways that led to suppression of various critical ... Phyllanthus was observed to cause antimetastatic activities by inhibiting ERK1/2 pathway via suppression of Raf protein. ... Voltage-dependent anion-selective channel protein 1. -0.37. -0.19. -0.20. N/A ... Hypoxia-inducible factor-1 (HIF-1) is the determining factor for oxygen-dependent gene regulation and is a dimer of HIF-1α and ...
Voltage-Dependent Anion Channel 2 of Arabidopsis thaliana (AtVDAC2) Is Involved in ABA-Mediated Early Seedling Development ... Among four SNPs, only C270T polymorphism showed significant differences in the frequency of the allele (χ2 = 7.809, p = 0.005) ... 2. Key Laboratory of Child Development and Learning Science, Ministry of Education, Southeast University, Nanjing, 210096, ... χ2 = 28.19,p = 3.44e-005). We suggest that BDNF has a possible role in the pathogenesis of autism. The study also show that the ...
Located in the outer mitochondrial membrane, VDAC forms channels that control the flux of ions and metabolites across the ... Located in the outer mitochondrial membrane, VDAC forms channels that control the flux of ions and metabolites across the ... 2013). Direct modulation of the outer mitochondrial membrane channel, voltage-dependent anion channel 1 (VDAC1) by cannabidiol ... Voltage-dependent anion channels control the release of the superoxide anion from mitochondria to cytosol. J. Biol. Chem. 278, ...
Epub 2014 Jul 2. Research Support, N.I.H., Extramural; Research Support, U.S. Govt, Non-P.H.S.; Review ... D) Single chain β-barrel of mitochondrial voltage dependent anion channel VDAC-2 from the MOM of Danio rerio (4BUM). VDAC-2 ... A) Trimer of maltoporin LamB from the OM of E. coli with sucrose in the hydrophilic channel (1AF6). Each monomer of the sugar ... The channel has a cytoplasmic funnel, the central hydrophobic ring, and external funnel filled by the TM2a helical plug ( ...
This gene encodes a member of the voltage-dependent anion channel pore-forming family of proteins that are considered the main ... Available for probe- and dye-based assays in ROX- dependent or ROX-independent real-time PCR detection systems. ... Pseudogenes have been identified on chromosomes 1 2 12 and 21 and alternative splicing results in multiple transcript variants ...
voltage-dependent anion channel 2. VGLL4. 9686. VGLL4. vestigial like 4 (Drosophila). ...
voltage-dependent anion channel 1. 7417. 7417. VDAC2. voltage-dependent anion channel 2. ...
... or voltage-dependent anion channel (VDAC; Cell Signaling) detection was used as confirmation of the purity of the cytosolic ( ... C: representative line-scan images obtained from H9c2 cells overexpressing RyR1 or RyR2 loaded with fluo-3. The time-dependent ... RyR1 overexpression induces Ca2+-dependent mitochondrial ATP production in cardiac H9c2 cells. A: expression and localization ... influx mechanisms are regulated not solely by MCU but also by multiple channels/transporters. We have previously reported that ...
10737788 - Bh4 domain of antiapoptotic bcl-2 family members closes voltage-dependent anion channel.... ... 25131918 - Inverse relationship between raft lrp1 localization and non-raft erk1,2/mmp9 activation.... 22749528 - ...
  • Depletion of the porins Por1 and Por2 destabilized Ups1 and Ups2, decreased CL levels by ~90%, and caused loss of Ups2-dependent phosphatidylethanolamine synthesis, but did not affect Ups2-independent phosphatidylethanolamine synthesis in mitochondria. (tcdb.org)
  • In addition, she found that co-transfecting both SOD1-G93A and Bcl-2 deformed mitochondria, disrupting membranes and causing vacuolization, which did not occur in cells expressing mSOD1 only. (alzforum.org)
  • Naniche and colleagues suspected that the mSOD1-Bcl-2 interaction would have functional consequences for mitochondria, so they isolated the organelles from HEK293T cells for patch-clamp studies of ion conductance. (alzforum.org)
  • But in Bcl-2-positive mitochondria, mSOD1 increased conductance. (alzforum.org)
  • In terms of ATP generation, one mole of glucose generates ∼36 mol of ATP when oxidized completely in mitochondria, whereas metabolism of one mole of glucose to lactate by glycolysis generates only 2 mol of ATP. (aspetjournals.org)
  • This complex system resides in the mitochondria of cells and utilizes oxidizable substrates to fuel the conversion of ADP to ATP and is dependent on molecular oxygen as the final electron acceptor. (syr.edu)
  • Small SOD1-like therapeutic peptides that specifically block formation of the mutSOD1/Bcl-2 complex, recover both aspects of mitochondrial dysfunction: they prevent mitochondrial hyperpolarization and cell loss as well as restore ADP permeability in mitochondria of symptomatic mutSOD1-G93A mice. (jneurosci.org)
  • To design potent compounds that target the key mediators of mutSOD1 toxicity, we dissected the relationship between mutSOD1 and its proposed mitochondrial partners, Bcl-2 and VDAC1 in particular, and analyzed the order of events downstream of mutSOD1 that destabilize the mitochondria. (jneurosci.org)
  • Morphology and structure of mitochondria in mammalian skeletal muscle, heart, and liver are very different ( 2 ). (mcponline.org)
  • Even in moving organelles, such as mitochondria, physical connections with the endoplasmic reticulum (ER) have been observed ( 1 ) as electron-dense structures that bridge the organelles ( 2 ). (sciencemag.org)
  • When facing ER stress, the Sig-1R dissociates from cognate co-chaperone BiP and acts as a free chaperone to stabilize IP3R3s to increase Ca 2+ signaling from ER into mitochondria to facilitate the production of ATP [ 2 ]. (biomedcentral.com)
  • AFG3 ATPase family gene 3-like 2 (S. ce. (broadinstitute.org)
  • These cells do not normally express Bcl-2, so Naniche was able to compare Bcl-2-negative cells to those that she stably transfected with the gene for the pore protein. (alzforum.org)
  • Crystallographic studies have demonstrated that a domain of SpA forms a complex with human Fab via a conformational surface on BCR that involves side chains from four β strands present in framework subdomains of the clan III gene-encoded V H region ( 2 ). (rupress.org)
  • In this report, we explore the role of one bcl-2 gene in nutrient stress responses. (pubmedcentralcanada.ca)
  • We report that starvation of Drosophila larvae lacking the bcl-2 gene, buffy , decreases survival rate by more than twofold relative to wild-type larvae. (pubmedcentralcanada.ca)
  • We show ΔNp63- dependent regulation of HK2 expression, and we use ChIP, validated by p63-Chip sequencing genomewide profiling analysis, and luciferase assays to demonstrate the presence of one p63-specific responsive element within the 15th intronic region of the HK2 gene, providing evidence of a direct interaction. (elsevier.com)
  • Mouillesseaux K and Chen JN, 'Mutation in utp15 Disrupts Vascular Patterning in a p53-Dependent Manner in Zebrafish Embryos', PLoS One 6: (2012). (ucla.edu)
  • Upregulated interleukin (IL)-1β maturation, IL-18 secretion, and caspase-1 cleavage were observed in MDMs from type 2 diabetic patients after stimulation with various danger molecules (ATP, high-mobility group protein B1, free fatty acids, islet amyloid polypeptide, and monosodium uric acid crystals). (diabetesjournals.org)
  • 2 Department of Cellular and Molecular Pharmacology, University of California at San Francisco, San Francisco, CA 94158, USA. (sciencemag.org)
  • Overexpression of UCP2 decreased reactive oxygen species (ROS) production, which was measured using dihydroethidium because it is specifically oxidized to fluorescent ethidium by the superoxide anion, whereas mice lacking UCP2 exhibited increased ROS relative to wild-type controls. (jneurosci.org)
  • Secreted IFN-α/β induces expression of IFN-stimulated genes that are important for the elimination of viruses ( 2 ). (jimmunol.org)
  • Mutation in IDH1 results in neomorphic activity, producing a different metabolite, 2-hydroxyglutaric acid, whereas wild-type IDH1 normally converts isocitrate to α-ketoglutarate coupled with NADP + /NADPH. (rupress.org)
  • In fact, this long-term immunologic impairment in SpA-treated mice persists despite the fact that central neo-lymphogenesis reestablishes the level of newly formed S107-expressing B cells in the periphery within 1-2 wk after the last SpA treatment ( 5 ). (rupress.org)
  • Finally, unilateral inoculation of sarkosyl-insoluble fractions of GGT homogenates from GGT linked to MAPT P301T, sGGT, and GGT linked to MAPT K317M mutation in the hippocampus, corpus callosum, or caudate/putamen in wild-type mice produces seeding, and time- and region-dependent spreading of phosphorylated, non-oligomeric, and non-truncated 4Rtau and 3Rtau, without GAIs and GOIs but only of coiled bodies. (ibecbarcelona.eu)
  • We have previously shown that second-messenger-dependent kinases (cAMP-dependent kinase, protein kinase C) in the olfactory system are essential in terminating second-messenger signaling in response to odorants. (duke.edu)
  • This will include an assessment of whether loss of L-type calcium channel function can account for failure of EC coupling and whether significant alterations in the 3-dimensional structure and spatial distribution of transverse-tubules, ryanodine and dihydropyridine receptors are involved in the failure of these cells;2) investigate the effect of metabolic inhibition on the function and structure of couplons in rabbit ventricular myocytes. (grantome.com)
  • This will include a measurement of the minimum number of L-type calcium channels in a couplon and the way that metabolic inhibition affects their function. (grantome.com)
  • E7820 inhibits angiogenesis by suppressing integrin alpha 2, a cell adhesion molecule expressed on endothelial cells. (cancer.gov)
  • Most differentiated, nonproliferating cells aerobically metabolize glucose to pyruvate, which is then oxidized in the mitochondrial matrix by the tricarboxylic acid cycle to yield CO 2 and NADH with minimal production of lactate. (aspetjournals.org)
  • Neuroprotective effects of 2,3,5,4'-tetrahydoxystilbene-2-O-β-D-glucoside from Polygonum multiflorum against glutamate-induced oxidative toxicity in HT22 cells. (semanticscholar.org)
  • Taken together, these data suggest that NLRP3 inflammasome activation is elevated in myeloid cells from type 2 diabetic patients and that antidiabetic treatment with metformin contributes to modulation of inflammasome activation in type 2 diabetes. (diabetesjournals.org)
  • dependent due to the cumulative effect of the drug, Antioxidants are found in every living cell where the accumulation of Cis produces obvious and all biological species and scavenge reactive necrotic changes within the tissues of the affected oxygen within cells. (who.int)
  • We show that genetic manipulation of uncoupling protein-2 (UCP2) directly affects substantia nigra dopamine cell function. (jneurosci.org)
  • The Sig-1R has also been implicated as an ion channel regulator in amyotrophic lateral sclerosis (ALS), a neurodegenerative disease that affects motor neurons. (biomedcentral.com)
  • Phyllanthus was observed to cause antimetastatic activities by inhibiting ERK1/2 pathway via suppression of Raf protein. (biomedcentral.com)
  • Key mechanisms of hyperglycemia-induced inflammation include nuclear factor-κB-dependent production of proinflammatory cytokines, Toll-like receptor (TLR) expression, increased oxidative stress, and inflammasome activation ( 4 , 5 ). (diabetesjournals.org)
  • In addition, a series of adaptive responses induced by cisplatin that maintain tumor cell homeostasis and interfere with apoptotic signaling, including metabolic reprogramming, autophagy and oxidative stress, can lead to cisplatin resistance ( 1 , 2 ). (spandidos-publications.com)
  • It was recently shown that motor neurons have the highest levels of Sig-1Rs in the central nervous system (CNS), and that Sig-1Rs may help direct the flow of ions through potassium channels [ 5 ]. (biomedcentral.com)