Disease relevance of Nubp2

• Interestingly, both regions are syntenic with human chromosome 16p13.1-p13.3, suggesting that a chromosomal breakage between Nubp2 and Nubp1 probably occurred during the evolution of mouse chromosomes [1].
• The effect of dl-alpha-tocopheryl (vitamin E) succinate in combination with Prostaglandin A2 (PGA2) and sodium butyrate on mouse neuroblastoma cells (NBP2) in culture, according to the criteria of growth inhibition and morphological differentiation (neurite formation), was studied [2].
• d- and dl-alpha-tocopheryl succinate inhibited growth and caused morphological changes in mouse melanoma (B-16), mouse neuroblastoma (NBP2), and rat glioma (C-6) cells in culture [3].
• The presence of 1% ethanol in culture medium during heat treatment (40 degrees C for 8 hours and 43 degrees C for 15 minutes) was sufficient to enhance the effect of hyperthermia on murine neuroblastoma cells (NBP2) in culture, on the criteria of growth (number of viable cells per dish) and survival (colony formation) [4].

High impact information on Nubp2

• Nubp1 and Nubp2 also interact with each other [5].
• Motor protein KIFC5A interacts with Nubp1 and Nubp2, and is implicated in the regulation of centrosome duplication [5].
• Monolayer cultures of C-1300 murine neuroblastoma (clone NBP2) were treated with the following compounds in ethanol: dexamethasone, triamcinolone acetonide, hydrocortisone, cortexolone, androstenedione, testosterone, estradiol-17 beta; or with the phosphodiesterase inhibitor Ro20-1724 [4-(3-butoxy-4-methoxybenzyl)-2-imidazolidinone] [6].
• For a better understanding of these events, we use a murine neuroblastoma cell line (NBP2) that terminally differentiates into mature neurons in response to elevated levels of cAMP [7].
• Our data suggest that increased levels of cAMP function through not only CREB but also other signaling pathways that account for the additional cAMP-induced effects, including irreversible differentiation and onset of apoptosis during partial inhibition of proteasome in NBP2 cells [7].

Chemical compound and disease context of Nubp2

• The effect of methylmercuric chloride (CH3HgCl) on the levels of gangliosides in mouse neuroblastoma cells (NBP2) in culture was studied [8].
• The role of adenosine 3',5'-cyclic monophosphate (cAMP) and sodium butyrate in modifying the effect of heat on murine neuroblastoma cells (NBP2) in culture was evaluated on the criterion of survival [9].
• Clonal lines of murine neuroblastoma (NBP2) and rat glioma (C6) were used to investigate the effects of methylmercuric chloride (CH3HgCl) [10].
• Immortalized rat mesencephalic cells (1RB3AN27) produced dopamine (DA) at a level that was higher than produced by undifferentiated or differentiated murine neuroblastoma cells (NBP2) in culture [11].

Biological context of Nubp2

• Mouse Nubp2 is mapped to the t-complex region of mouse Chromosome 17, whereas Nubp1 is mapped to the proximal region of mouse Chromosome 16 [1].
• The effect of dl-alpha-tocopheryl (vitamin E) succinate in modifying the radiation response of mouse neuroblastoma (NBP2) and mouse fibroblast (L-cells) cells in culture was studied on the criterion of growth inhibition (due to cell death and inhibition of cell division) [12].

Associations of Nubp2 with chemical compounds

• The 1RB3AN27 cells were more effective in reducing the rate of methamphetamine-induced turning in rats with unilateral 6-OHDA lesion of the nigrostriatal system than differentiated NBP2 cells [11].
• We then enriched for two populations of NBP2 cells; one expressing high levels of d2EGFP (HG) and the other expressing low levels of d2EGFP (LG) in the absence of doxycycline [13].
• Their potency for growth inhibition in NBP2 clone reflected the order of: BrACh (ED50: 2 microM) greater than BETA (7.8 microM) congruent to BPTA congruent to (greater than 10 microM) congruent to TA-BETA congruent to OPTA [14].
• Although elevation of intracellular levels of cyclic AMP in NBP2 clone invariably stimulates neurite formation and TH activity, these functions were increased in certain sera without a significant increase in the cellular cyclic AMP levels [15].

References