The BM88 Antigen, a Novel Neuron-specific Molecule, Enhances the Differentiation of Mouse Neuroblastoma Cells

Mamalaki, Avgi; Boutou, Effrossyni; Hurel, Catherine; Patsavoudi, Evangelia; Tzartos, Socrates J.; Matsas, Rebecca

doi:10.1074/jbc.270.23.14201

Cited by 34 publications

(101 citation statements)

References 40 publications

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“…The ϳ22-kDa band present in rat and mouse brain, but not in liver mitochondria and SH-SY5Y cells, was identified by nanoESI-MS/MS as BM88 (BM88_MOUSE, Q9JKC6), a neuron-specific protein involved in neuronal differentiation (34) found to be associated with the membrane of intracellular organelles including the limiting membrane of mitochondria (35). Although labeling of BM88 was inhibited by low concentration of Ro 68-3400 (Fig.…”

Section: Affinity Labeling Of Mitochondria With [ 3 H]ro 68-3400: Idementioning

confidence: 98%

The Voltage-dependent Anion Channel Is the Target for a New Class of Inhibitors of the Mitochondrial Permeability Transition Pore

Cesura¹,

Pinard²,

Schubenel³

et al. 2003

Journal of Biological Chemistry

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The relevance of the mitochondrial permeability transition pore (PTP) in Ca 2؉ homeostasis and cell death has gained wide attention. Yet, despite detailed functional characterization, the structure of this channel remains elusive. Here we report on a new class of inhibitors of the PTP and on the identification of their molecular target. The most potent among the compounds prepared, Ro 68-3400, inhibited PTP with a potency comparable to that of cyclosporin A. Since Ro 68-3400 has a reactive moiety capable of covalent modification of proteins, [3 H]Ro 68-3400 was used as an affinity label for the identification of its protein target. In intact mitochondria isolated from rodent brain and liver and in SH-SY5Y human neuroblastoma cells, [ 3 H]Ro 68-3400 predominantly labeled a protein of ϳ32 kDa. This protein was identified as the isoform 1 of the voltage-dependent anion channel (VDAC). Both functional and affinity labeling experiments indicated that VDAC might correspond to the site for the PTP inhibitor ubiquinone 0 , whereas other known PTP modulators acted at distinct sites. While Ro 68-3400 represents a new useful tool for the study of the structure and function of VDAC and the PTP, the results obtained provide direct evidence that VDAC1 is a component of this mitochondrial pore.

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Section: Affinity Labeling Of Mitochondria With [ 3 H]ro 68-3400: Idementioning

confidence: 98%

The Voltage-dependent Anion Channel Is the Target for a New Class of Inhibitors of the Mitochondrial Permeability Transition Pore

Cesura¹,

Pinard²,

Schubenel³

et al. 2003

Journal of Biological Chemistry

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“…Several of the DEGs that enriched to the GO term "regulation of cellular processes" (Fig. 10B) play an important role in neuron survival, such as hepatic and glial cell adhesion molecule (HEPACAM, FC of 11, an axon protein that plays a role in neuron motility [92]), mitogen-activated protein (MAP) kinase 8 interacting protein 1 (JIP1, FC of 10, part of the MAP kinase signal transduction pathway in neurons [93]), FK056-binding protein 8 (FKBP8, FC of 9, inhibiting programmed cell death in neurons [94]), and BM88 antigen (FC of 10, involved in neuron differentiation [95]). of the downregulated DEGs that mapped to the GO processes "regulation of synaptic plasticity," "ion transport," "anion transport," and "endocytosis.…”

Section: Fig 7 Immunohistochemistry Gene Validation Ihc Staining Andmentioning

confidence: 99%

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

Arnold

Girke

Sureshchandra

et al. 2016

J Virol

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Primary infection with varicella-zoster virus (VZV), a neurotropic alphaherpesvirus, results in varicella. VZV establishes latency in the sensory ganglia and can reactivate later in life to cause herpes zoster. The relationship between VZV and its host during acute infection in the sensory ganglia is not well understood due to limited access to clinical specimens. Intrabronchial inoculation of rhesus macaques with simian varicella virus (SVV) recapitulates the hallmarks of VZV infection in humans. We leveraged this animal model to characterize the host-pathogen interactions in the ganglia during both acute and latent infection by measuring both viral and host transcriptomes on days postinfection (dpi) 3, 7, 10, 14, and 100. SVV DNA and transcripts were detected in sensory ganglia 3 dpi, before the appearance of rash. CD4 and CD8 T cells were also detected in the sensory ganglia 3 dpi. Moreover, lung-resident T cells isolated from the same animals 3 dpi also harbored SVV DNA and transcripts, suggesting that T cells may be responsible for trafficking SVV to the ganglia. Transcriptome sequencing (RNA-Seq) analysis showed that cessation of viral transcription 7 dpi coincides with a robust antiviral innate immune response in the ganglia. Interestingly, a significant number of genes that play a critical role in nervous system development and function remained downregulated into latency. These studies provide novel insights into host-pathogen interactions in the sensory ganglia during acute varicella and demonstrate that SVV infection results in profound and sustained changes in neuronal gene expression. IMPORTANCEMany aspects of VZV infection of sensory ganglia remain poorly understood, due to limited access to human specimens and the fact that VZV is strictly a human virus. Infection of rhesus macaques with simian varicella virus (SVV), a homolog of VZV, provides a robust model of the human disease. Using this model, we show that SVV reaches the ganglia early after infection, most likely by T cells, and that the induction of a robust innate immune response correlates with cessation of virus transcription. We also report significant changes in the expression of genes that play an important role in neuronal function. Importantly, these changes persist long after viral replication ceases. Given the homology between SVV and VZV, and the genetic and physiological similarities between rhesus macaques and humans, our results provide novel insight into the interactions between VZV and its human host and explain some of the neurological consequences of VZV infection. V aricella-zoster virus (VZV) is a neurotropic alphaherpesvirus and the causative agent of varicella (chickenpox) (1). VZV establishes latency in the sensory ganglia and can reactivate later in life to cause herpes zoster (shingles), a painful disease that affects almost 1 million individuals in the United States alone (2). VZV is transmitted through the inhalation of virus-laden saliva droplets or by direct contact with the infectious fluid from vesicles...

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“…BM88 has recently emerged as part of a protein interaction network associated with inherited human ataxias, a group of diseases characterized by degeneration of cerebellar Purkinje cells (4). BM88 cloned from mammalian and chick brain (5,6) is an integral membrane protein composed of two 23-kDa polypeptide chains linked together by disulfide bridges. It is anchored to the membrane of intracellular organelles, including the outer membrane of mitochondria and endoplasmic reticulum, via a transmembrane domain so that the bulk of the protein faces toward the cytoplasm (6, 7).…”

mentioning

confidence: 99%

BM88/CEND1 coordinates cell cycle exit and differentiation of neuronal precursors

Politis

Makri²,

Thomaidou³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

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The BM88 Antigen, a Novel Neuron-specific Molecule, Enhances the Differentiation of Mouse Neuroblastoma Cells

Cited by 34 publications

References 40 publications

The Voltage-dependent Anion Channel Is the Target for a New Class of Inhibitors of the Mitochondrial Permeability Transition Pore

The Voltage-dependent Anion Channel Is the Target for a New Class of Inhibitors of the Mitochondrial Permeability Transition Pore

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

BM88/CEND1 coordinates cell cycle exit and differentiation of neuronal precursors

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