TY - JOUR. T1 - The role of mitochondrial porins and the permeability transition pore in learning and synaptic plasticity. AU - Weeber, Edwin J.. AU - Levy, Michael. AU - Sampson, Margaret J.. AU - Anflous, Keltoum. AU - Armstrong, Dawna L.. AU - Brown, Sarah E.. AU - David Sweatt, J.. AU - Craigen, William J.. PY - 2002/5/24. Y1 - 2002/5/24. N2 - Mitochondrial outer membrane permeability is conferred by a family of porin proteins. Mitochondrial porins conduct small molecules and constitute one component of the permeability transition pore that opens in response to apoptotic signals. Because mitochondrial porins have significant roles in diverse cellular processes including regulation of mitochondrial ATP and calcium flux, we sought to determine their importance in learning and synaptic plasticity in mice. We show that fear conditioning and spatial learning are disrupted in porin-deficient mice. Electrophysiological recordings of porin-deficient hippocampal slices reveal deficits in long and ...
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
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 ...
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 ...
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 ...
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 …
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, ...
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] ...
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 ...
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 ...
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 ...
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 ...
Mitochondria have emerged recently as effective targets for novel anti-cancer drugs referred to as mitocans. We propose that the molecular mechanism of induction of apoptosis by mitocans, as exemplified by the drug a-tocopheryl succinate, involves generation of reactive oxygen species (ROS). ROS then mediate the formation of disufide bridges between cytosolic Bax monomers, resulting in the formation of mitochondrial outer membrane channels. ROS also cause oxidation of cardiolipin, triggering the release of cytochrome c and its translocation via the activated Bax channels. This model may provide a general mechanism for the action of inducers of apoptosis and anticancer drugs, mitocans, targeting mitochondria via ROS production ...
The human lymphocyte toxins granzyme B (hGrzB) and perforin cooperatively induce apoptosis of virus-infected or transformed cells: perforin pores enable entry of the serine protease hGrzB into the cytosol, where it processes Bid to selectively activate the intrinsic apoptosis pathway. Truncated Bid (tBid) induces Bax/Bak-dependent mitochondrial outer membrane permeability and the release of cytochrome c and Smac/Diablo. To identify cellular proteins that regulate perforin/hGrzB-mediated Bid cleavage and subsequent apoptosis, we performed a gene-knockdown (KD) screen using a lentiviral pool of short hairpin RNAs embedded within a miR30 backbone (shRNAmiR ...
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 ...
Water bath stunning is a common practice in commercial slaughterhouses. Such treatment is economic and in line with animal welfare practice. However, the conditions applied for the stunning process may vary from a slaughterhouse to another slaughterhouse. Such a loose regulation on the stunning procedure has opened up doors for food adulteration such as over dose stunning. In this study, a simple and reliable approach using proteomics have been developed to study the effect of different currents and voltages in stunning on the protein expression of the chickens. Protein profiles of the chickens were constructed in order to detect any differences in protein expression and modifications. The different voltage studied were 10 V, 40 V and 70 V while the values for current studied were 0.25 A, 0.5 A, and 0.75 A. After the proteomics analyses using 2D Platinum ImageMaster 6.0 and Matrix-assisted laser desorption ionization- time of flight (MALDI TOF) spectrometry identification, Voltage dependent ...
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 ...
Regions of near apposition amongst the endoplasmic reticulum (ER) and mitochondria have been noticed for numerous yrs and are imagined to be required for lipid and calcium trade amongst the two organelles [one,two,three,four,five,6]. Just lately, interactions amongst proteins in the ER membrane and the outer mitochondrial membrane that could act as tethers among the two organelles have been described. In mammals, two sets of interactions have been described. The first entails an conversation in between the ER calcium channel IP3R (inositol one,4,5-triphosphate receptor) and the mitochondrial VDAC (voltage dependent anion channel) protein that also consists of a chaperone [seven]. In the 2nd, ERlocalized Mfn2 tethers mitochondria to the ER by homotypic and heterotypic interactions with Flumatinibmitochondrially localized Mfn2 or Mfn1 [eight]. In Saccharomyces cerevisiae the ER-mitochondria come upon composition (ERMES) has been proven to tether the two organelles [nine,10]. The ERMES is composed ...
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., ...
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
Glioblastoma has a 5-year survival of less than 5% and is responsible for more years of life lost than any other malignancy, making it a challenging therapeutic problem. Healthy cells mainly rely on oxidative phosphorylation to catabolize glucose, while glioblastoma cells use aerobic glycolysis. The first step in glycolysis, conversion of glucose to glucose-6-phosphate using ATP, is catalyzed by hexokinase and glioblastoma tumors employ an isoform (HKII) that is bound to mitochondria via interaction with the outer-membrane voltage dependent anion channel. The prevailing theory is that this localization affords HKII preferential access to the mitochondrial ATP via inner-membrane adenine nucleotide translocase (ANT) to rapidly phosphorylate and trap glucose, thus initiating glycolysis across the cell cytosol. We have tested this hypothesis using a novel water-soluble organoarsenical, PENAO, to inactivate ANT (1). Treatment of glioblastoma cell lines and primary glioma initiating cells with PENAO ...
VDAC3 antibody, N-term (voltage dependent anion channel 3) for WB. Anti-VDAC3 pAb (GTX47682) is tested in Human samples. 100% Ab-Assurance.
Voltage dependent anion channel required for acidification and functions of the Golgi apparatus that may function in counter-ion conductance.
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 ...
EM (fig. S1, C to H) and biochemical fractionation (fig. S2) experiments show the localization of StAR and GRP78 in the ER, MAM, and mitochondria. Because GRP78 is a highly abundant chaperone at the ER that interacts with StAR, it is likely facilitating its folding and subsequent activity (17). We next knocked down the expression of GRP78 by small interfering RNA (siRNA) in COS-1 cells (Fig. 1C) or adenosine 3′,5′-monophosphate (cAMP)-stimulated MA-10 cells (Fig. 1D) and identified changes in StAR expression by Western blotting. In the absence of GRP78, the expression of StAR was greatly reduced, but the negative control siRNA had no effect, suggesting that GRP78 is responsible for StAR expression. As expected, the absence of GRP78 did not affect the expression of mitochondrial VDAC2 or the ER proteins PACS2 and calnexin (Caln) (Fig. 1, C and D). As shown in Fig. 1E, pregnenolone synthesis in MA-10 cells decreased from 25 ng/ml in control cells to 2 ng/ml in the absence of GRP78. The ...
Erastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS.
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… ...
MULAN is a mitochondrial outer membrane (MOM) protein with a cytosolic-facing C-terminal RING-finger.A) MULAN colocalizes with MT-RFP/MT-GFP. NIH3T3 cells were
Eesti Teadusinfosüsteem koondab informatsiooni teadus- ja arendusasutuste, teadlaste, teadusprojektide ning erinevate teadustegevuste tulemuste kohta.
Maternal nutrient restriction at specific gestational stages compromises fetal growth and development, in particular, fetal adipose tissue deposition. The extent to which nutritional supplementation can promote growth and development of specific fetal organs is unknown. This study aimed to determine whether protein supplementation of the maternal diet at defined stages of gestation promoted the abundance of the key mitochondrial proteins; uncoupling protein 1 (UCP1), cytochrome c and the voltage dependent anion channel (VDAC) in fetal adipose tissue.. Twenty-nine twin-bearing ewes of similar body weight and parity were randomly allocated to 4 feeding groups from 10d gestation. All ewes received a control diet, which was supplemented with fishmeal in 3 of the groups during early i.e. 10d-40d, mid i.e. 40d-70d or late i.e. 110d-140d gestation. Each ewe was then humanely euthanased with an overdose of barbiturate (100 mg/kg pentobarbital sodium: Euthanal) at 140d gestation to enable sampling of ...
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
Read "The Pro-Apoptotic Proteins, Bid and Bax, Cause a Limited Permeabilization of the Mitochondrial Outer Membrane That Is Enhanced by Cytosol, The Journal of Cell Biology" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
Reactome is pathway database which provides intuitive bioinformatics tools for the visualisation, interpretation and analysis of pathway knowledge.
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。
TY - JOUR. T1 - The peripheral benzodiazepine receptor modulates Ca2+ transport through the VDAC in rat heart mitochondria. AU - Tamse, C. T.. AU - Lu, X.. AU - Mortel, E. G.. AU - Cabrales, E.. AU - Feng, W.. AU - Schaefer, Saul. PY - 2008. Y1 - 2008. N2 - The voltage-dependent anion channel (VDAC) is a key mitochondrial protein involved in the transport of calcium. Its function is, in part, regulated by associated proteins such as the 18 kD peripheral benzodiazepine receptor (PBR). We tested the hypothesis that an endogenous ligand of the PBR, hemin, could modulate calcium transport by modifying VDAC conductance. In isolated rat cardiac mitochondria, hemin (0-10 μM) exhibited multiple, time-dependent effects. Initially, hemin reduced the calcium uptake rate in a dose-dependent manner, an effect independent of the mitochondrial permeability transition (MPT) as it was not altered by cyclosporine A (CsA). However, subsequent to this inhibitory effect on calcium influx, hemin facilitated MPT as ...
The open-channel conductance properties of a voltage-gated channel from sarcoplasmic reticulum were studied in planar phospholipid membranes. The channel is ideally selective for K+ over Cl- and for K+ over Ca++. In symmetrical 1 M solutions, the single-channel conductance (in pmho) falls in the order: K+ (214) , NH4+ (157) , Rb+ (125) , Na+ (72) , La+ (8.1) , Cs+ (, 3). In neutral bilayers, the channel conductance saturates with ion activity according to a rectangular hyperbolic relation, with half-saturation activities of 54 mM for K+ and 34 mM for Na+. Under symmetrical salt conditions, the K+:Na+ channel conductance ratio increases with salt activity, but the permeability ratio, measured by single-channel bi-ionic potentials, is constant between 20 mM and 2.5 M salt; the permeability ratio is equal to the conductance ratio in the limit of low-salt concentration. The channel conductance varies , 5% in the voltage range -100 to +70 mV. The maximum conductance varies K+ and Na+ is only weakly ...
Academic Dissertations;Academic Dissertations--South Carolina;Tubulin Modulators;Tubulin;Neoplasms--metabolism;Voltage-Dependent Anion ...
In this issue of Circulation Research, Das et al19 report that GSK-3 inhibitors induce dephosphorylation of VDAC, thereby reducing adenine nucleotide (such as ATP) transport across the outer mitochondrial membrane. The action of the GSK-3 inhibitors on VDAC not only preserves ATP by blocking mitochondrial consumption of ATP generated through anaerobic glycolysis but also prevents mitochondrial Ca2+ overloading and oxidative stress by reducing mitochondrial membrane potential. Interestingly, this effect of GSK-3 inhibition appears to be independent of mPTP opening.. The findings of Das et al19 suggest that inhibition of GSK-3 may facilitate hypoxic adaptation during ischemia through dephosphorylation of VDAC. Under hypoxic conditions, generation of ATP shifts from oxidative phosphorylation in the mitochondria to glycolysis in the cytoplasm, a phenomenon known as metabolic adaptation described by Louis Pasteur in the 19th century. This process is controlled by transcription factors, such as ...
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The plant SLAC1 anion channel controls turgor pressure in the aperture-defining guard cells of plant stomata, thereby regulating the exchange of water vapour and photosynthetic gases in response to environmental signals such as drought or high levels of carbon dioxide. Here we determine the crystal structure of a bacterial homologue (Haemophilus influenzae) of SLAC1 at 1.20 Å resolution, and use structure-inspired mutagenesis to analyse the conductance properties of SLAC1 channels. SLAC1 is a symmetrical trimer composed from quasi-symmetrical subunits, each having ten transmembrane helices arranged from helical hairpin pairs to form a central five-helix transmembrane pore that is gated by an extremely conserved phenylalanine residue. Conformational features indicate a mechanism for control of gating by kinase activation, and electrostatic features of the pore coupled with electrophysiological characteristics indicate that selectivity among different anions is largely a function of the energetic ...
TTYH1, 0.1 mg. TTYH1 is a member of the tweety family of proteins, a family of chloride anion channels containing five transmembrane regions.
Forms a channel through the mitochondrial outer membrane and also the plasma membrane. The channel at the outer mitochondrial membrane allows diffusion of small hydrophilic molecules; in the plasma membrane it is involved in cell volume regulation and apoptosis. It adopts an open conformation at low or zero membrane potential and a closed conformation at potentials above 30-40 mV. The open state has a weak anion selectivity whereas the closed state is cation-selective. May participate in the formation of the permeability transition pore complex (PTPC) responsible for the release of mitochondrial products that triggers apoptosis ...
Recombinant Translocase of Outer Mitochondrial Membrane 22 Homolog (Yeast) (TOMM22) Protein (rho-1D4 tag). Species: Human. Source: Insect Cells. Order product ABIN3074708.
Gem1p is a single-pass outer mitochondrial membrane protein with its NH2 terminus exposed to the cytoplasm. (A) WCE from JSY7000 (GEM1) expressing GFP-Gem1p was
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.