Disease relevance of Arhgef16

• Analysis of cells transfected by the oncogenes of other tumors and tumor cell lines indicates that the transforming gene of the HL-60 leukemia cell line is closely related to oncogenes of a Burkitt's lymphoma, an acute myelogenous leukemia, an adenocarcinoma of the colon, a neuroblastoma, and two sarcomas [1].
• These secondary neuroblastoma transfectants were injected into young mice and grew out into fibrosarcomas [2].
• Muscarinic response to acetylcholine in neuroblastoma times glioma hybrid cells [3].
• Amplified DNA with limited homology to myc cellular oncogene is shared by human neuroblastoma cell lines and a neuroblastoma tumour [4].
• We demonstrate that SV infection of baby hamster kidney (BHK-2), mouse neuroblastoma (N18), and rat prostatic adenocarcinoma (AT-3) cells results in programmed cell death, whereas SV infection of bcl-2-transfected AT-3 cells results in long-term persistent productive infection [5].

Psychiatry related information on Arhgef16

• Treatment with r-interferon gamma or rIL-2 on days 1 through 3 after C1300-NRB inoculation significantly prolonged the mean tumor latency period, decreased the tumor growth rate, and enhanced in vitro NK killing of C1300-NRB and YAC-1 [6].
• Two (P117L; M146L) familial Alzheimer's disease (FAD)-causing presenilin-1 (PS1) mutations have been tested fortheir effect in stably transfected mouse neuroblastoma (N2a) cell lines [7].
• The following four parameters were considered: 1) dose of injected cells, 2) type of injected tumour (NB or T-L), 3) age of mice after individuation of three groups of animals (group A, 4-9 weeks old, group B, 9-20 weeks old, group C, > 20 weeks old), 4) injected cell line within the same tumour type [8].
• Administrations of ABPP (200 mg/kg or 500 mg/kg) at intervals of 2 days and the injection of IFN (25,000 IU/mouse) 3 hr before each administration of ABPP to neuroblastoma-bearing A/J mice reduced the mortality and completely cured 40% of the mice in each combined therapy group [9].

High impact information on Arhgef16

• YARS localizes to axonal termini in differentiating primary motor neuron and neuroblastoma cultures [10].
• The introduction of human chromosome 17 suppresses the tumourigenicity of a neuroblastoma cell line in the absence of any effects on in vitro growth and the neurofibromatosis type 1 (NF1) gene may be responsible [11].
• The oncogene is unrelated to transforming sequences detected in a variety of other types of human tumor cell lines derived from colonic and lung carcinoma and from neuroblastoma [12].
• Antisera were prepared from mice bearing tumors induced by transformed cells derived by transfection of DNAs from various tumor cell types unrelated to rat neuroblastoma [2].
• In neuroblastoma, an embryonal tumour derived from the neural crest, Id2 is overexpressed in cells carrying extra copies of the N-myc gene [13].

Chemical compound and disease context of Arhgef16

• Morphine elevates levels of cyclic GMP in a neuroblastoma X glioma hybrid cell line [14].
• Morphine antagonises action of prostaglandin in neuroblastoma and neuroblastoma times glioma hybrid cells [15].
• The mouse neuroblastoma-rat glioma hybrid cell line NG108-15 was used to study the acute and chronic interaction of ethanol with intact neural cells [16].
• Renin and angiotensin: the complete system within the neuroblastoma x glioma cell [17].
• Since most normal rapidly dividing cells do not have surface dopamine receptors, we propose this approach for the selective targeting of toxicity for neuroblastoma cells [18].

Biological context of Arhgef16

• We show here that a DNA domain detectable by partial homology to the myc oncogene is amplified up to 140-fold in cell lines derived from different human neuroblastomas and in a neuroblastoma tumour, but not in other tumour cells showing cytological evidence for gene amplification [4].
• Recent studies have shown that mevinolin, a competitive inhibitor of the reductase, inhibits cell proliferation and induces differentiation in cultured C1300 (Neuro-2A) murine neuroblastoma cells [19].
• METHODS: Three neuroblastoma cell lines (human LAN-5, human SK-N-SH, and murine N1E-115) were used in these experiments; cells from two of the lines (SK-N-SH and N1E-115) were also studied after being stably transfected with a plasmid containing a full-length DR-nm23 complementary DNA [20].
• A casein kinase II-related activity is involved in phosphorylation of microtubule-associated protein MAP-1B during neuroblastoma cell differentiation [21].
• Thus, we suggest that the observed phosphorylation of a protein identified as MAP-1B during neurite outgrowth is mainly due to the activation of a casein kinase II-related activity in differentiating neuroblastoma cells [21].

Anatomical context of Arhgef16

• Here, in an effort to identify cell-surface antigens associated with the neoplastic process, we have generated hybridomas which secrete monoclonal antibodies that react specifically with cell-surface determinants found on NIH 3T3 cells transformed by transfection with a group of rat neuroblastoma oncogenes [22].
• When added to mouse neuroblastoma cultures, the potent tumor promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) inhibits spontaneous neurite formation as well as that induced in response to serum deprivation, prostaglandin E1, 5-bromo-2'-deoxyuridine, and papaverine [23].
• Amiloride, a potassium sparing diuretic, has now been shown to selectively block the low threshold calcium channel in mouse neuroblastoma and chick dorsal root ganglion neurons [24].
• A complementary DNA clone containing the coding sequence of one of these rapidly responding channels, a 5HT3 subtype of the serotonin receptor, has been isolated by screening a neuroblastoma expression library for functional expression of serotonin-gated currents in Xenopus oocytes [25].
• Clonal neuroblastoma x glioma hybrid cells frequently formed synapses with clonal mouse striated muscle cells [26].

Associations of Arhgef16 with chemical compounds

• Enhancement of the electrical excitability of neuroblastoma cells by valinomycin [27].
• L-Dopa methyl ester: prolongation of survival of neuroblastoma-bearing mice after treatment [28].
• Since melanocytes arise from the neural crest embryologically, the effect of L-dopa methyl ester, a soluble analog, on the murine C1300 neuroblastoma was studied [28].
• Targeted enhancement of the biological activity of the antineoplastic agent, neocarzinostatin. Studies in murine neuroblastoma cells [18].
• The antibody 3F8, an IgG3 murine monoclonal antibody (MoAb) against disialoganglioside GD2, could target iodine-131 (131I) to established subcutaneous human neuroblastoma (NB) xenografts in BALB/c nude mice [29].

Physical interactions of Arhgef16

• Murine neuroblastoma clone N1E-115 possesses receptors that specifically bind the tridecapeptide neurotensin, mediate the formation of intracellular cyclic GMP, and stimulate inositol phospholipid hydrolysis [30].
• The morphological differentiation of mouse neuroblastoma cells induced by 1 mM alpha-FMO plus 0.2 mM Bt2cAMP was accompanied by increases of the regulatory subunit of the type I cAMP-binding protein and acetylcholinesterase activity [31].
• The present article investigates chronic opioid regulation of the stimulatory adenylate cyclase-coupled prostaglandin E1 (PGE1) receptor system in neuroblastoma x glioma (NG108-15) hybrid cells [32].
• These results suggest that m2- and m4-receptors in transformed NL308 cells coupled to PTX-sensitive G-protein which is capable of mobilizing intracellular Ca2+ and activate IK(Ca), whereas m1 and m3 receptors activate a similar process through a different, PTX-insensitive G-protein [33].
• Allogeneic class I major histocompatibility complex gene transfer in murine neuroblastoma in vivo [34].

Enzymatic interactions of Arhgef16

• Furthermore, the phosphopeptide patterns of brain MAP-1B phosphorylated in vitro by either purified casein kinase II or an extract obtained from differentiating neuroblastoma cells are identical to each other and similar to that of in vivo phosphorylated neuroblastoma MAP-1B [21].

Regulatory relationships of Arhgef16

• We determined the expression and the phosphorylation of the RB family gene products during the DMSO-induced differentiation of the N1E-115 murine neuroblastoma cells [35].
• Inhibition of Tcof1 expression by siRNA induced morphological changes in neuroblastoma cells that mimic differentiation [36].
• Here we studied ET-1-induced changes in intracellular calcium (Ca2+in) in Fura-2 loaded mouse neuroblastoma-rat dorsal root ganglion hybrid cells (ND7/104) [37].
• Role of signal transduction systems in neurotensin receptor down-regulation induced by agonist in murine neuroblastoma clone N1E-115 cells [38].
• Dishevelled promotes neurite outgrowth in neuronal differentiating neuroblastoma 2A cells, via a DIX-domain dependent pathway [39].

Other interactions of Arhgef16

• To define the nature of the "dominant negative" effect of the PS1 aspartate variants, we stably expressed PS1 harboring aspartate to alanine substitutions at codons 257 (D257A) or 385 (D385A), singly or in combination (D257A/D385A), in mouse neuroblastoma, N2a cells [40].
• RESULTS: P10(4) exerted a potent cytotoxic activity on different neuroblastoma and melanoma cell lines through induction of both extrinsic and intrinsic caspase cascades and subsequent apoptosis [41].
• Here we demonstrate that the early induction of apoptosis in a model of lyssavirus-infected neuroblastoma cells involves a TRAIL-dependent pathway requiring the activation of caspase-8 but not of caspase-9 or caspase-10 [42].
• In our model, Fas ligand (CD95L) appears to play a limited role in lyssavirus-mediated neuroblastoma cell death [42].
• To generalize this observation, we attempted to quantify AChE(R) and AChE(T) after organophosphate intoxication in the mouse brain and compared the observed effects with those of stress induced by swimming or immobilization; we also analyzed the effects of heat shock and AChE inhibition on neuroblastoma cells [43].

Analytical, diagnostic and therapeutic context of Arhgef16

• Three-dimensional chromatin distribution in neuroblastoma nuclei shown by confocal scanning laser microscopy [44].
• METHODS: Neuroblastoma xenografts derived from the tumors of six different patients were established subcutaneously in immune-deprived mice [45].
• BACKGROUND: Advanced (stage 4) cases of neuroblastoma, a childhood cancer of the nervous system, are associated with high relapse rates, even after intensive chemotherapy, radiotherapy, and autologous bone marrow transplantation [46].
• A neuroblastoma protein related to the brain microtubule-associated protein, MAP-1B, as determined by immunoprecipitation and coassembly with brain microtubules, becomes phosphorylated when N2A mouse neuroblastoma cells are induced to generate microtubule-containing neurites [21].
• Quantitative densitometry of neuroblastoma extracts electrophoresed on SDS-polyacrylamide gels confirmed the constancy of tubulin [47].

References