Nmi protein interacts with regions that differ between MycN and Myc and is localized in the cytoplasm of neuroblastoma cells in contrast to nuclear MycN

Bannasch, Detlev; Weis, Isabel; Schwab, Manfred

doi:10.1038/sj.onc.1203090

Cited by 38 publications

(31 citation statements)

References 51 publications

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“…Functional proteomic analysis of prostate cancer cells K Nagano et al (Bannasch et al, 1999). Interestingly, besides cytoplasmic localization, we also observed nuclear localization of the fusion protein.…”

Section: Demonstrated By Sds-page Immunoblottingmentioning

confidence: 64%

Differential protein synthesis and expression levels in normal and neoplastic human prostate cells and their regulation by type I and II interferons

et al. 2003

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In all, 31 differentially regulated proteins were identified by mass spectrometry analysis, several of which are involved in chaperone-assisted protein folding in the endoplasmic reticulum (ER) or in regulated protein degradation. Our results suggest that the exclusion of proteins by the ER quality control system, crosstalk between the EGF-and INF-induced signalling pathways and the regulation of INF-inducible genes are all altered in the prostate cancer cells. The combination of upregulated activity in the growth-promoting PI3K/Akt pathway, suppression of Nmi and overexpression of hnRNP-K and c-myc proteins may explain why the prostate cancer cells were found to be more resistant to the growth inhibitory effects of INFc.

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Section: Demonstrated By Sds-page Immunoblottingmentioning

confidence: 64%

Differential protein synthesis and expression levels in normal and neoplastic human prostate cells and their regulation by type I and II interferons

et al. 2003

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“…In contrast to the proposed nuclear function of Nmi, several studies indicate that Nmi is a cytoplasmic protein (Bannasch et al, 1999;Lebrun et al, 1998;Lee et al, 1999). The endogenous Nmi or ectopically expressed full-length Nmi was found to be localized in the cytoplasm, in punctate speckles, in a number of cell lines.…”

Section: Nmimentioning

confidence: 98%

Modulation of STAT signaling by STAT-interacting proteins

2000

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“…However, a signi®cant contribution was assigned to the central area of N-Myc between amino acids 134 ± 300 which encompasses the interaction domain with Nmi (aa 177 to 298) (Bannasch et al, 1999). Nmi is a predominantly cytoplasmic protein that can be translocated to the nucleus where it augments STATdependent transcription in response to cytokines by interacting with STATs (except STAT2) and enhancing association of CBP/p300 to STATs (Zhu et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

N-myc oncogene overexpression down-regulates IL-6; evidence that IL-6 inhibits angiogenesis and suppresses neuroblastoma tumor growth

et al. 2002

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Angiogenesis is an indispensable prerequisite for the progression and metastasis of solid malignancies. Tumor angiogenesis appears to be governed by alterations of tumor suppressor or oncogenes operant in a broad range of tumors. We have addressed this issue in neuroblastoma, a malignancy characterized by the near-exclusive ampli®cation and overexpression of the N-Myc oncogene. Here, we report that N-Myc overexpression results in down-regulation of interleukin-6 (IL-6) and that IL-6 is an inhibitor of endothelial cell proliferation and VEGF-induced rabbit corneal angiogenesis. STAT3 is instrumental for IL-6 activity as infection with adenoviruses expressing a phosphorylation de®cient STAT3 mutant renders endothelial cells insensitive to the antiproliferative action of IL-6. Finally, though IL-6 does not in¯uence neuroblastoma cell growth, IL-6-expressing xenograft tumors in mice exhibit reduced neovascularization and suppressed growth. Our data shed new light on the mechanisms by which N-myc oncogene ampli®cation enhances the malignant phenotype in neuroblastomas.

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Nmi protein interacts with regions that differ between MycN and Myc and is localized in the cytoplasm of neuroblastoma cells in contrast to nuclear MycN

Cited by 38 publications

References 51 publications

Differential protein synthesis and expression levels in normal and neoplastic human prostate cells and their regulation by type I and II interferons

Differential protein synthesis and expression levels in normal and neoplastic human prostate cells and their regulation by type I and II interferons

Modulation of STAT signaling by STAT-interacting proteins

N-myc oncogene overexpression down-regulates IL-6; evidence that IL-6 inhibits angiogenesis and suppresses neuroblastoma tumor growth

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