Neuron- and myelin-specific monoclonal antibodies recognizing cell-surface antigens of the central and peripheral nervous system

Patsavoudi, Evangelia; Hurel, Catherine; Matsas, Rebecca

doi:10.1016/0306-4522(89)90266-2

Cited by 30 publications

(65 citation statements)

References 24 publications

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“…For cell cloning, the cells were aliquoted into 96-well tissue culture plates in different dilutions, and stable transfectants were selected. Numerous stable cell lines expressing BM88 were isolated as determined by immunofluorescence screening using specific mouse monoclonal and rabbit polyclonal anti-BM88 antibodies (22,25) followed by an appropriate fluorescein-conjugated secondary antibody (Molecular Probes). Two independent clones, C3C1 and C7G5, with the highest BM88 expression, were selected for further studies and were found to behave similarly in all tests performed.…”

Section: Methodsmentioning

confidence: 99%

“…BM88 (Cend1 for cell cycle exit and neuronal differentiation 1, according to NCBI nomenclature at www.ncbi.nih.gov) has been initially identified as a protein expressed in mature neurons (22,23). However, subsequent studies revealed that BM88 marks neuronal cells all along the different stages of the neuronal lineage; it is expressed at low levels in neuronal precursors, and its expression is distinctly up-regulated in young post-mitotic as well as in mature neurons (24,25).…”

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confidence: 99%

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BM88 Is a Dual Function Molecule Inducing Cell Cycle Exit and Neuronal Differentiation of Neuroblastoma Cells via Cyclin D1 Down-regulation and Retinoblastoma Protein Hypophosphorylation

Georgopoulou¹,

Hurel²,

Politis³

et al. 2006

Journal of Biological Chemistry

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Control of cell cycle progression/exit and differentiation of neuronal precursors is of paramount importance during brain development. BM88 is a neuronal protein associated with terminal neuron-generating divisions in vivoThe formation of the nervous system is governed by a delicate balance between cell proliferation, subsequent cell cycle withdrawal, and differentiation to distinctive neuronal phenotypes (1, 2). Current observations have highlighted the existence of mechanisms coupling cell cycle exit and differentiation as well as functional cross-talk between intrinsic factors controlling these two mechanisms. A number of key factors regulating cell cycle progression have been implicated in cell fate determination and differentiation of neuronal precursors, whereas specification-and/or differentiation-inducing molecules are beginning to emerge as cell cycle regulators (3-6). However, there are still important questions regarding the timing control of the proliferation/differentiation switch that remain unanswered.In the central nervous system, control of cell cycle progression plays an essential role in the generation of the appropriate number of neurons and the formation of functional neuronal circuits. When a neuronal progenitor is committed to undergo differentiation, it exits from the G 1 phase of the cell cycle and enters into an irreversible quiescent state referred to as G 0 . The tumor suppressor proteins p53 and pRb 6 are central regulators of this progression (7). p53, when activated, causes G 1 arrest at the G 0 restriction point by inducing expression of p21 and consequent inhibition of D-type cyclins and related cyclin-dependent kinases (8 -10), thus preventing phosphorylation of pRb (7). Under these conditions, hypophosphorylated pRb associates with the E2F family of transcription factors, thus impairing their ability to transactivate genes required for cell cycle progression (11). As a consequence cells do not progress through the G 1 -to-S phase transition. Several studies have indicated that a critical event associated with cell cycle withdrawal and differentiation both in neuronal and non-neuronal cells is the cellular compartmentalization of cyclin D1, which shifts from a predominantly nuclear localization to cytoplasmic sequestration

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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

BM88 Is a Dual Function Molecule Inducing Cell Cycle Exit and Neuronal Differentiation of Neuroblastoma Cells via Cyclin D1 Down-regulation and Retinoblastoma Protein Hypophosphorylation

Georgopoulou¹,

Hurel²,

Politis³

et al. 2006

Journal of Biological Chemistry

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“…From the initial identification of BM88/Cend1 as a component of mature neurons several years ago, 23,24,39 a clearer picture of its biology has emerged as a neuronal-specific regulator of cell cycle exit and differentiation of neuronal precursors in the developing nervous system. We have found that this molecule is expressed in CNS cells all along the neuronal lineage in a characteristic fashion: at low levels in neural stem/progenitor cells and at higher levels in post-mitotic differentiated neurons.…”

Section: Discussionmentioning

confidence: 99%

“…Although, initially, BM88/Cend1 was identified as a protein expressed in post-mitotic neurons, 23,39 subsequent studies revealed that it marks neuronal cells all along the different stages of the neuronal lineage both in rodents and in the chick. 12,27,40 BM88/ Cend1 is expressed at low levels in neuronal progenitors, while its expression is distinctly upregulated in young post-mitoticas well as in mature neurons.…”

Section: The In Vivo Expression Pattern Of Bm88/cend1 Suggests a Rolementioning

confidence: 99%

“…23,24 BM88/Cend1 cloned from porcine, mouse, human and, more recently, chick brain is an integral membrane protein composed of two 22-23 kDa polypeptide chains linked together by disulphide bridges. [25][26][27] It is anchored to the membrane of intracellular organelles, including the outer membrane of mitochondria, the endoplasmic reticulum and other electrolucent vesicles, via a transmembrane domain, in a way that the bulk of the protein faces towards the cytoplasm.…”

Section: Introductionmentioning

confidence: 99%

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Coordination of cell cycle exit and differentiation of neuronal progenitors

Politis

Thomaidou²,

Matsas³

2008

Cell Cycle

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During development, co-ordinate regulation of cell cycle exit and differentiation of neuronal precursors is essential for generation of appropriate number of neurons and proper wiring of neuronal circuits. Recent studies have identified some of the molecules implicated in the regulation of these cellular events, but the complex machinery that orchestrates these processes into a coherent developmental program remains unclear. BM88/Cend1 is a neuronal protein associated in vivo with terminal neuron-generating divisions, marking the exit of proliferative cells from the cell cycle. Genetic studies in neural cell lines, neural stem/progenitor cells using the neurosphere system and in the developing chicken neural tube in vivo have shown that BM88/Cend1 is a dual function molecule co-ordinating cell cycle exit and differentiation of neuronal progenitors. These studies have thus shed light on a molecular determinant that participates, along with other known and possibly still unknown regulators, in the complex processes by which a progenitor cell becomes a mature neuron.

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Gómez

Boutou

Hurel

et al. 1998

Journal of Neuroscience Research

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Previous studies have shown that the BM88 antigen, a novel neuron-specific molecule, promotes the differentiation of mouse neuroblastoma (Neuro 2a) cells. In particular, stably transfected, with the BM88 cDNA, Neuro 2a cells overexpressing the BM88 antigen (Neuro2a-BM88 cells) are morphologically distinct from the nontransfected Neuro 2a cells; they exhibit enhanced process outgrowth and a slower rate of division. In this study we used Neuro2a and the morphologically differentiated Neuro 2a-BM88 cells to compare their responsiveness to growth factors. The growth factors we used were nerve growth factor (NGF), basic-fibroblast growth factor (b-FGF), and glial cell-line derived neurotrophic factor (GDNF). In addition, we used glial conditioned medium derived from either newborn mouse cerebral cortex (NBCC) or aged mouse cerebral hemispheres (MACH), as a source of normal glial factors. Because these cells express the cholinergic phenotype, we used choline acetyltransferase (ChAT) activity as a biochemical marker for comparison. A differential responsiveness to these factors was observed between Neuro 2a and Neuro 2a-BM88. The presence of NGF, 25 ng/ml, in the culture medium did not affect ChAT activity in either cell type. In contrast to NGF, in the presence of b-FGF, 5 ng/ml, the transfected cells, Neuro 2a-BM88, responded with a marked increase in ChAT activity. On the other hand, with GDNF, 1 ng/ml, only Neuro 2a cells showed an increase in ChAT activity. Finally, we found no response to the glial conditioned media, although these media contain several growth factors, including b-FGF. In conclusion, our findings show that overexpression of the neuron-specific antigen BM88 in neuroblastoma cells modifies their properties with respect to growth factor sensitivity, and, hence, the Neuro 2a and Neuro 2a-BM88 are suitable cell models to examine the role of growth factors in neuronal differentiation.

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Neuron- and myelin-specific monoclonal antibodies recognizing cell-surface antigens of the central and peripheral nervous system

Cited by 30 publications

References 24 publications

BM88 Is a Dual Function Molecule Inducing Cell Cycle Exit and Neuronal Differentiation of Neuroblastoma Cells via Cyclin D1 Down-regulation and Retinoblastoma Protein Hypophosphorylation

BM88 Is a Dual Function Molecule Inducing Cell Cycle Exit and Neuronal Differentiation of Neuroblastoma Cells via Cyclin D1 Down-regulation and Retinoblastoma Protein Hypophosphorylation

Coordination of cell cycle exit and differentiation of neuronal progenitors

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