Morphoregulatory activities of NCAM and N-cadherin can be accounted for by G protein-dependent activation of L- and N-type neuronal Ca2+ channels

Doherty, Patrick; Ashton, Sandra V.; Moore, Stephen E.; Walsh, Frank S.

doi:10.1016/0092-8674(91)90569-k

Cited by 382 publications

(273 citation statements)

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“…19 Of note, NCAM has been shown in some instances to function via transmembrane signaling. 20 On the other hand, the mechanisms of the upregulation of this molecule in the majority of patients with MM remain unknown. 21 It is noteworthy that we were able to isolate a subset of MM characterized by a lack of or a weak expression of CD56, a weak expression of CD138, a less aggressive bone disease and a tendency to develop primary or secondary leukemic phase more frequently.…”

Section: Discussionmentioning

confidence: 99%

The absence of CD56 (NCAM) on malignant plasma cells is a hallmark of plasma cell leukemia and of a special subset of multiple myeloma

et al. 1998

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In this study, we show that malignant plasma cells from patients with either primary (n = 12) or secondary (n = 15) plasma cell leukemia (PCL) do not express CD56 at all, neither in the bone marrow nor the peripheral blood in 81% of cases. On the other hand, multiple myeloma (MM) at diagnosis overexpress it in 63 of 94 (67%) cases (P = 0.0001). In three secondary PCL evaluated serially, CD56 was also lacking at diagnosis showing that CD56 is not downregulated at the end stage of the disease but rather not upregulated in this subset of patients. This last concept is strengthened by the observation that 29% of MM patients lacking CD56 or weakly expressing it at diagnosis present a detectable leukemic phase vs 11% only in CD56 + MM (P = 0.06). Forty percent of all the CD56 −/weak malignant plasma cell disorders present or develop a leukemic phase vs only 15% of CD56 + cases (P Ͻ 0.008). CD56 −/weak MM subset is also associated with a significantly less aggressive osteolytic potential (P = 0.012). We conclude that the lack or weak expression of CD56 is a characteristic feature of PCL but also delineates a special subset of MM at diagnosis mainly characterized by a lower osteolytic potential and a trend for malignant plasma cells to circulate in the peripheral blood more overtly.

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Section: Discussionmentioning

confidence: 99%

The absence of CD56 (NCAM) on malignant plasma cells is a hallmark of plasma cell leukemia and of a special subset of multiple myeloma

et al. 1998

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“…For example, a G protein can couple to the insulin-like growth factor-II/mannose 6-phosphate receptor [13], G~o can be associated with a nerve growth cone protein, GAP-43 [14,15], and a pertussis toxin-sensitive G protein has been implicated in neural growth via interaction with a neural cell adhesion molecule and N-cadherin [16]. G=i has also been detected in organelles other than the plasma membrane (e.g.…”

Section: Discussionmentioning

confidence: 99%

Interaction of the protein nucleobindin with G_αi2, as revealed by the yeast two‐hybrid system

et al. 1995

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The heterotrimeric G protein, G~i2, transduces signals from seven membrane spanning receptors to effectors such as adenylyl cyclase and ion channels. The purpose of this study was to identify these or other cellular proteins that interact with G,d2 by use of the yeast two-hybrid system. A human B cell cDNA library was screened by this system using full length Gin2. Four positive colonies were obtained. Two of the four were identified as nucleobindin, a calcium binding protein and a putative antigen to which anti-nuclear antibodies are generated in mice with a disorder that resembles systemic lupus erythematosus. Nucleobindin has a leucinc zipper, EF hands, and a signal peptide sequence and is thought to localize to the nucleus as well as being secreted. The specificity of intehraction between G~2 and nucleobindin was confirmed by an in vitro binding assay using recombinant proteins. Transfeetion of Gai2 and nucleobindin in COS cells increased G~i2 expression relative to cells transfected with Goi2 and mock vector. Our results indicate that the yeast two-hybrid system provides a means to identify novel proteins that interact with G,~ proteins. Nucleobindin appears to represent one of those proteins.

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“…8A) channels leads to activation of protein kinases C and mitogenactivated protein kinases. Ca 2ϩ influx through the voltagegated channels also triggers a variety of cellular events leading to neurite outgrowth via the concerted actions of various Ca 2ϩ -binding proteins (44) and cell adhesion molecules (45,46). The finding that sPLA 2 -X and suboptimal NGF act in synergy in inducing neurite outgrowth (Fig.…”

Section: Spla 2 -X Is Expressed In Peripheral Neuronal Fibers In Var-mentioning

confidence: 99%

Neuronal Expression and Neuritogenic Action of Group X Secreted Phospholipase A2

Masuda

Murakami

Takanezawa

et al. 2005

Journal of Biological Chemistry

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Although individual mammalian secreted phospholipase A 2 (sPLA 2 ) enzymes exhibit unique tissue and cellular distributions, the cell type-specific functions of each enzyme remain largely unknown. In this study, we found by immunohistochemistry that group X sPLA 2 (sPLA 2 -X) is uniquely located in the peripheral neuronal fibers, an observation that was supported by detection of its transcript and protein in the neuronal cell line PC12 and in primary dorsal root ganglia neurons. Adenoviral expression of sPLA 2 -X in PC12 cells facilitated neurite outgrowth, particularly when combined with a suboptimal concentration of nerve growth factor. In neuronally differentiated PC12 cells, sPLA 2 -X was preferentially localized in the Golgi apparatus and growth cones, and proteolytic conversion of the proenzyme to mature enzyme mainly occurred after the secretion process. The neurite-extending ability of sPLA 2 -X depended on the production of its catalytic product, lysophosphatidylcholine. Moreover, nerve growth factor-induced neurite extension of PC12 cells was modestly but significantly attenuated by an anti-sPLA 2 -X antibody or by a small interfering RNA for sPLA 2 -X. These observations suggest the potential contribution of sPLA 2 -X to neuronal differentiation, and possibly repair, under certain conditions.

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Morphoregulatory activities of NCAM and N-cadherin can be accounted for by G protein-dependent activation of L- and N-type neuronal Ca2+ channels

Cited by 382 publications

References 50 publications

The absence of CD56 (NCAM) on malignant plasma cells is a hallmark of plasma cell leukemia and of a special subset of multiple myeloma

The absence of CD56 (NCAM) on malignant plasma cells is a hallmark of plasma cell leukemia and of a special subset of multiple myeloma

Interaction of the protein nucleobindin with G_αi2, as revealed by the yeast two‐hybrid system

Neuronal Expression and Neuritogenic Action of Group X Secreted Phospholipase A2

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Morphoregulatory activities of NCAM and N-cadherin can be accounted for by G protein-dependent activation of L- and N-type neuronal Ca2+ channels

Cited by 382 publications

References 50 publications

The absence of CD56 (NCAM) on malignant plasma cells is a hallmark of plasma cell leukemia and of a special subset of multiple myeloma

The absence of CD56 (NCAM) on malignant plasma cells is a hallmark of plasma cell leukemia and of a special subset of multiple myeloma

Interaction of the protein nucleobindin with Gαi2, as revealed by the yeast two‐hybrid system

Neuronal Expression and Neuritogenic Action of Group X Secreted Phospholipase A2

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Interaction of the protein nucleobindin with G_αi2, as revealed by the yeast two‐hybrid system