VDAC and its interacting partners in plant and animal systems: an overview

Kanwar, Poonam; Samtani, Harsha; Sanyal, Sibaji K.; Srivastava, Ashish Kumar; Suprasanna, Penna; Pandey, Girdhar K.

doi:10.1080/07388551.2020.1756214

Cited by 28 publications

(22 citation statements)

References 206 publications

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“…Interactor Reference VDAC Tubulin, Desmin, Vimentin, plectin, hexokinase and creatine kinases, MtCK, ANT, cardiolipin [10,42,43] Acyl-dihydroxyacetone phosphate reductase Unclear [13] ADP/ATP carrier Previous suggested as dimer, and now convincedly proved as monomers [44] Phosphate carrier ATP synthase, mitochondrial peptidyl-prolyl cis-trans isomerase, NaStEP, Citrate synthase, isocitrate dehydrogenase and oxoglutarate dehydrogenase [25,[45][46][47] Pyruvate carrier Heterodimer [48,49] Tricarboxylate carrier Homodimer [50] Dicarboxylate carrier Homodimer [51] Oxoglutarate carrier Homodimer, BCL2 [52,53] Glutamate transporter Synaptic protein [54] Aspartate/glutamate carrier Homodimer [36,39,55] The association of mitochondrial transport proteins plays an important role in the movement of metabolites across the IMM. For example, although not a member of the MCF, the heteromeric complex of the mitochondrial pyruvate carrier (MPC) is strategically positioned at the intersection between glycolysis in the cytosol and OXPHOS in the mitochondria [48].…”

Section: Mitochondria Carriermentioning

confidence: 99%

“…Moreover VDACs have been reported to interact with diverse partners, including proteins of apoptosis, cell signaling, cytoskeleton-related proteins, and metabolic enzymes (Table 1) [10]. For example, glucose-6-phosphate, which is the product of the hexokinase-catalyzed reaction, was suggested to potentiate ATP release from mitochondria with the recovery of normal metabolism and substrate replacement, was even more increased when hexokinase and glucokinase were dissociated following being bound to VDAC [10,42]. Therefore, the effect of hexokinase dissociation from VDAC is the subject of many studies dealing with the development of potent cancer chemotherapies.…”

Section: Proteins Associated To Mitochondrial Outer Membrane Carriermentioning

confidence: 99%

“…In summary, the old concept that the outer membrane functions as a "molecular size-exclusion filter" for the passage of small hydrophilic molecules through VDAC has been strongly questioned by different observations. First, transport processes can occur in cells deficient of all VDAC isoforms [10]. Secondly, the VDAC channel properties are modulated by a variety of different effectors, suggesting that their specificity is under active control [10].…”

Section: Proteins Associated To Mitochondrial Outer Membrane Carriermentioning

confidence: 99%

“…First, transport processes can occur in cells deficient of all VDAC isoforms [10]. Secondly, the VDAC channel properties are modulated by a variety of different effectors, suggesting that their specificity is under active control [10]. Thirdly, the outer membrane contains, beside VDAC, additional pore-forming proteins that might mediate metabolite flux [10].…”

Section: Proteins Associated To Mitochondrial Outer Membrane Carriermentioning

confidence: 99%

“…Interestingly, as a convergence point, VDACs interact with diverse partners, including those that are broadly functionally classified as apoptosis-, cell signaling-, and cytoskeleton-related proteins, as well as metabolic enzymes [10]. For larger molecules, including proteins, to be translocated involves three machineries: the sorting and assembly machinery (SAM complex), the translocase of the outer membrane (TOM complex), and the mitochondrial distribution and morphology (MDM) complex [11].…”

Section: Introductionmentioning

confidence: 99%

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On the Detection and Functional Significance of the Protein–Protein Interactions of Mitochondrial Transport Proteins

Zhang

Fernie

2020

Biomolecules

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Protein–protein assemblies are highly prevalent in all living cells. Considerable evidence has recently accumulated suggesting that particularly transient association/dissociation of proteins represent an important means of regulation of metabolism. This is true not only in the cytosol and organelle matrices, but also at membrane surfaces where, for example, receptor complexes, as well as those of key metabolic pathways, are common. Transporters also frequently come up in lists of interacting proteins, for example, binding proteins that catalyze the production of their substrates or that act as relays within signal transduction cascades. In this review, we provide an update of technologies that are used in the study of such interactions with mitochondrial transport proteins, highlighting the difficulties that arise in their use for membrane proteins and discussing our current understanding of the biological function of such interactions.

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Section: Mitochondria Carriermentioning

confidence: 99%

Section: Proteins Associated To Mitochondrial Outer Membrane Carriermentioning

confidence: 99%

Section: Proteins Associated To Mitochondrial Outer Membrane Carriermentioning

confidence: 99%

Section: Proteins Associated To Mitochondrial Outer Membrane Carriermentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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On the Detection and Functional Significance of the Protein–Protein Interactions of Mitochondrial Transport Proteins

Zhang

Fernie

2020

Biomolecules

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LRRK2^G2019S Gene Mutation Causes Skeletal Muscle Impairment in Animal Model of Parkinson's Disease

Hu,

Yang,

Song

et al. 2024

J cachexia sarcopenia muscle

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BackgroundWhile the gradually aggravated motor and non‐motor disorders of Parkinson's disease (PD) lead to progressive disability and frequent falling, skeletal muscle impairment may contribute to this condition. The leucine‐rich repeat kinase2 (LRRK2) is a common disease‐causing gene in PD. Little is known about its role in skeletal muscle impairment and its underlying mechanisms.MethodsTo investigate whether the mutation in LRRK2 causes skeletal muscle impairment, we used 3‐month‐old (3mo) and 14‐month‐old (14mo) LRRK2G2019S transgenic (TG) mice as a model of PD, compared with the age‐matched littermate wild‐type (WT) controls. We measured the muscle mass and strength, ultrastructure, inflammatory infiltration, mitochondrial morphology and dynamics dysfunction through behavioural analysis, electromyography (EMG), immunostaining, transmission electron microscopy (TEM) and other molecular biology techniques.ResultsThe 3mo‐TG mice display mild skeletal muscle impairment with spontaneous potentials in EMG (increased by 130%, p < 0.05), myofibre necrosis (p < 0.05) and myosin heavy chain‐II changes (reduced by 19%, p < 0.01). The inflammatory cells and macrophage infiltration are significantly increased (CD8a+ and CD68+ cells up 1060% and 579%, respectively, both p < 0.0001) compared with the WT mice. All of the above pathogenic processes are aggravated by aging. The 14mo‐TG mice EMG examinations show a reduced duration (by 31%, p < 0.01) and increased polyphasic waves of motor unit action potentials (by 28%, p < 0.05). The 14mo‐TG mice present motor behavioural deficits (p < 0.05), muscle strength and mass reduction by 37% and 8% (p < 0.05 and p < 0.01, respectively). A remarkable increase in inflammatory infiltration is accompanied by pro‐inflammatory cytokines in the skeletal muscles. TEM analysis shows muscle fibre regeneration with the reduced length of sarcomeres (by 6%;p < 0.05). The muscle regeneration is activated as Pax7+ cells increased by 106% (p < 0.0001), andmyoblast determination protein elevated by 71% (p < 0.01). We also document the morphological changes and dynamics dysfunction of mitochondria with the increase of mitofusin1 by 43% (p < 0.05) and voltage‐dependent anion channel 1 by 115% (p < 0.001) in the skeletal muscles of 14mo‐TG mice.ConclusionsTaken together, these findings may provide new insights into the clinical and pathogenic involvement of LRRK2G2019 mutation in muscles, suggesting that the diseases may affect not only midbrain dopaminergic neurons, but also other tissues, and it may help overall clinical management of this devastating disease.

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Bombyx mori voltage‐dependent anion‐selective channel induces programmed cell death to defend against Bombyx mori nucleopolyhedrovirus infection

Lv,

Lai,

Gong

et al. 2024

Pest Management Science

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BACKGROUNDVoltage‐dependent anion‐selective channels (VDACs) serve as pore proteins within mitochondrial membrane, aiding in the regulation of cell life and cell death. While the occurrence of cell death is crucial for the defense against virus infection, the function played by VDAC in Bombyx mori, in response to the influence of Bombyx mori nucleopolyhedrovirus (BmNPV), remains unclear.RESULTSBmVDAC was found to be relatively highly expressed both during embryonic development and in the Malpighian tubule and midgut. Additionally, the expression levels of BmVDAC were found to be different among silkworm strains with varying levels of resistance to BmNPV, strongly suggesting a connection between BmVDAC and virus infection. To gain further insight into the function of BmVDAC in BmNPV, we employed RNA interference (RNAi) to silence and overexpressed it by pIZT/V5‐His‐mCherry. The results revealed that BmVDAC is instrumental in developing the resistance of host cells to BmNPV infection in BmN cells, which was further validated to be likely associated with initiating programmed cell death. Furthermore, we evaluated the function of BmVDAC in another insect, Spodoptera exigua. Knockdown of the BmVDAC homolog in S. exigua, SeVDAC, made the larvae more sensitive to BmNPV.CONCLUSIONWe have substantiated the pivotal role of BmVDAC in conferring resistance against BmNPV infection, primarily associated with the initiation of PCD. The findings of this study offer fresh substantiation illuminating the molecular mechanisms governing the silkworm's response to BmNPV infection, thereby innovative approaches for pest biocontrol.This article is protected by copyright. All rights reserved.

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VDAC and its interacting partners in plant and animal systems: an overview

Cited by 28 publications

References 206 publications

On the Detection and Functional Significance of the Protein–Protein Interactions of Mitochondrial Transport Proteins

On the Detection and Functional Significance of the Protein–Protein Interactions of Mitochondrial Transport Proteins

LRRK2^G2019S Gene Mutation Causes Skeletal Muscle Impairment in Animal Model of Parkinson's Disease

Bombyx mori voltage‐dependent anion‐selective channel induces programmed cell death to defend against Bombyx mori nucleopolyhedrovirus infection

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VDAC and its interacting partners in plant and animal systems: an overview

Cited by 28 publications

References 206 publications

On the Detection and Functional Significance of the Protein–Protein Interactions of Mitochondrial Transport Proteins

On the Detection and Functional Significance of the Protein–Protein Interactions of Mitochondrial Transport Proteins

LRRK2G2019S Gene Mutation Causes Skeletal Muscle Impairment in Animal Model of Parkinson's Disease

Bombyx mori voltage‐dependent anion‐selective channel induces programmed cell death to defend against Bombyx mori nucleopolyhedrovirus infection

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LRRK2^G2019S Gene Mutation Causes Skeletal Muscle Impairment in Animal Model of Parkinson's Disease