scholarly journals Nuclear receptor binding protein 1 regulates intestinal progenitor cell homeostasis and tumour formation

2012 ◽  
Vol 31 (11) ◽  
pp. 2486-2497 ◽  
Author(s):  
Catherine H Wilson ◽  
Catriona Crombie ◽  
Louise van der Weyden ◽  
George Poulogiannis ◽  
Alistair G Rust ◽  
...  
Keyword(s):  
Nuclear Receptor ◽  
Receptor Binding ◽  
Progenitor Cell ◽  
Binding Protein ◽  
Cell Homeostasis ◽  
Tumour Formation ◽  
Receptor Binding Protein

Nuclear receptor-binding protein 1: a novel tumour suppressor and pseudokinase

2013 ◽  
Vol 41 (4) ◽  
pp. 1055-1060 ◽  
Author(s):  
Jason S. Kerr ◽  
Catherine H. Wilson
Keyword(s):  
Nuclear Receptor ◽  
Receptor Binding ◽  
Kinase Activity ◽  
Binding Protein ◽  
Kinase Domain ◽  
Present Review ◽  
Critical Components ◽  
Receptor Binding Protein

Pseudokinases are a class of kinases which are structurally designated as lacking kinase activity. Despite the lack of kinase domain sequence conservation, there is increasing evidence that a number of pseudokinases retain kinase activity and/or have critical cellular functions, casting aside previous notions that pseudokinases simply exist as redundant kinases. Moreover, a number of recent studies have implicated pseudokinases as critical components in cancer formation and progression. The present review discusses the interactions and potential functions that nuclear receptor-binding protein 1, a pseudokinase recently described to have a tumour-suppressive role in cancer, may play in cellular homoeostasis and protein regulation. The recent findings highlighted in the present review emphasize the requirement to fully determine the function of pseudokinases in vitro and in vivo, the understanding of which may ultimately uncover new directions for drug discovery.

Nuclear receptor binding protein 2 is induced during neural progenitor differentiation and affects cell survival

2008 ◽  
Vol 39 (1) ◽  
pp. 32-39 ◽  
Author(s):  
J. Larsson ◽  
M. Forsberg ◽  
K. Brännvall ◽  
X.-Q. Zhang ◽  
M. Enarsson ◽  
...  
Keyword(s):  
Cell Survival ◽  
Nuclear Receptor ◽  
Receptor Binding ◽  
Binding Protein ◽  
Neural Progenitor ◽  
Receptor Binding Protein

scholarly journals Nuclear Receptor Binding Protein 2 Is Downregulated in Medulloblastoma, and Reduces Tumor Cell Survival upon Overexpression

Cancers ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1483
Author(s):  
Anqi Xiong ◽  
Ananya Roy ◽  
Argyris Spyrou ◽  
Holger Weishaupt ◽  
Voichita D. Marinescu ◽  
...  
Keyword(s):  
Cell Lines ◽  
Nuclear Receptor ◽  
Receptor Binding ◽  
Growth Regulation ◽  
Binding Protein ◽  
Histone Deacetylation ◽  
Adult Brain ◽  
Tissue Array ◽  
Receptor Binding Protein

Pseudokinases, comprising 10% of the human kinome, are emerging as regulators of canonical kinases and their functions are starting to be defined. We previously identified the pseudokinase Nuclear Receptor Binding Protein 2 (NRBP2) in a screen for genes regulated during neural differentiation. During mouse brain development, NRBP2 is expressed in the cerebellum, and in the adult brain, mainly confined to specific neuronal populations. To study the role of NRBP2 in brain tumors, we stained a brain tumor tissue array for NRPB2, and find its expression to be low, or absent, in a majority of the tumors. This includes medulloblastoma (MB), a pediatric tumor of the cerebellum. Using database mining of published MB data sets, we also find that NRBP2 is expressed at a lower level in MB than in the normal cerebellum. Recent studies indicate that MB exhibits frequent epigenetic alternations and we therefore treated MB cell lines with drugs inhibiting DNA methylation or histone deacetylation, which leads to an upregulation of NRBP2 mRNA expression, showing that it is under epigenetic regulation in cultured MB cells. Furthermore, forced overexpression of NRBP2 in MB cell lines causes a dramatic decrease in cell numbers, increased cell death, impaired cell migration and inhibited cell invasion in vitro. Taken together, our data indicate that downregulation of NRBP2 may be a feature by which MB cells escape growth regulation.

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