The cytoplasmic Purkinje onconeural antigen cdr2 down-regulates c-Myc function: implications for neuronal and tumor cell survival

Okano, Hirotaka James; Park, Woong-Y.; Corradi, John P.; Darnell, Robert B.

doi:10.1101/gad.13.16.2087

Cited by 109 publications

(81 citation statements)

References 59 publications

(58 reference statements)

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“…44,45 Similar observations were made in chondrocytes where c-Myc was nuclear in proliferating cells, but was primarily cytoplasmic in mature chondrocytes. 46 In endometrial carcinomas, c-Myc was nuclear in poorly differentiated forms and cytoplasmic in well-differentiated carcinomatous endometrium.…”

Section: Myc-nick Regulates the Microtubule Cytoskeleton And Promotessupporting

confidence: 65%

Post-translational control of Myc function during differentiation

Conacci‐Sorrell

Eisenman

2011

Cell Cycle

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Section: Myc-nick Regulates the Microtubule Cytoskeleton And Promotessupporting

confidence: 65%

Post-translational control of Myc function during differentiation

Conacci‐Sorrell

Eisenman

2011

Cell Cycle

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“…For example, though c-Myc is usually nuclear, it is sequestered in the cytoplasm of Purkinje cells via an interaction with the CDR-2 protein. This interaction is thought to block c-Myc-induced cell death in Purkinje cells (43).…”

Section: Resultsmentioning

confidence: 99%

MondoA, a Novel Basic Helix-Loop-Helix–Leucine Zipper Transcriptional Activator That Constitutes a Positive Branch of a Max-Like Network

Billin

Eilers

Coulter

et al. 2000

Molecular and Cellular Biology

121

158

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Max is a common dimerization partner for a family of transcription factors (Myc (20,27,29,38). Consistent with a role in regulating proliferation and growth, Myc-Max heterocomplexes drive cell growth and division and Myc expression is down-regulated during cellular differentiation. By contrast, Mad-Max complexes inhibit proliferation and are upregulated during cellular differentiation (1, 2, 9, 23, 37). Therefore, via the relative activities of the Myc-Max and Mad-Max heterodimers, the Max transcription factor network is thought to regulate growth and differentiation.Considerable evidence supports the positive effects of the Myc family and the negative effects of the Mad family on cell growth and proliferation. Overexpression of Myc proteins can transform primary rat embryo fibroblasts in cooperation with a number of oncogenes, most notably activated Ras (27). Expression of Mad family genes or Mnt blocks transformation by Myc plus activated Ras (14,16,29,30,34,52). The opposing functions of the Myc and Mad families are also observed in mice null for members of the myc or mad family and in transgenic mice overexpressing c-Myc or Mad1. Mouse embryos null for c-myc arrest development at day 9.5 postcoitum (18), and N-Myc null mice fail to fully develop the heart, lungs, and nervous system (15,40). By contrast, mad1 null animals have defects in the differentiation capacity of granulocyte clusterforming cells (24), and mxi1 null mice show increased proliferation in precursor cell populations of the prostatic epithelium (48). The phenotypes generated by overexpression of myc and mad family genes are reciprocal to those seen in the genetic null animals; c-myc overexpression in murine B cells results in cells that are larger than normal (31), and transgenic mice overexpressing mad1 are smaller than normal (45). Therefore, these phenotypes are entirely consistent with the proposed positive effects of the myc family and the negative effects of the mad family in regulating cell growth and differentiation. These opposing effects of the Myc and Mad families are likely also active in Drosophila melanogaster because flies homozygous for hypomorphic alleles of dmyc are smaller than normal (25) and overexpression of dmyc in wing imaginal discs yields cells that are larger than normal (32).Myc-Max and Mad-Max heterocomplexes both recognize the CACGTG subclass of E-box elements; however, Myc-Max heterocomplexes activate transcription while Mad-Max complexes repress transcription (5, 9, 47). The opposing effects of Myc and Mad may manifest themselves by reciprocally regulating the expression of genes involved in cell growth and proliferation. Consistent with this hypothesis, Myc transcriptional targets include genes involved in metabolism (CAD, ornithine decarboxylase, lactate dehydrogenase A, and dihydrofolate reductase genes) and cell cycle progression (cyclin A, cyclin D2, cyclin E, and telomerase genes) (13,17,26,44). Furthermore, Mxi1 can downregulate ornithine decarboxylase expression (55), and cyclin D2-associated kinase act...

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“…CD30, originally identi®ed as a cell surface marker for Hodgkin's lymphoma cells, is a member of the tumor necrosis factor receptor family (Chiarle et al, 1999). PCD Cdr2 directly binds to c-Myc and may therefore regulate cell growth (Okano et al, 1999). It is also the major auto-antigen that causes paraneoplastic cerebellar degeneration in breast cancer and ovarian cancer patients (Darnell, 1996).…”

Section: Molecular Cloning and Identification Of The Transforming Genesmentioning

confidence: 99%

Genetic screens in mammalian cells by enhanced retroviral mutagens

Liú

Yang

et al. 2000

Oncogene

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Genetic approaches such as retrovirus-mediated mutagenesis and cDNA expression libraries have contributed greatly to our understanding of signal transduction in mammalian cells. However, previously described methods for retroviral insertional mutagenesis are hindered by low mutagenesis rates and diculties in cloning mutated genes. cDNA expression library methods are usually celltype dependent and bias towards abundant and short messages. With the near completion of the genome projects, alternative genetic methods are needed where large numbers of genes can be more easily isolated and biochemically studied. We have developed a novel retrovirus-mediated genetic screening method in cultured cells. To achieve ecient and regulated mutagenesis, we constructed Enhanced Retroviral Mutagen (ERM) vectors that contained several engineered sequences (e.g., an ERM Tag and a splice donor) controlled by a tetracycline-responsive promoter. Endogenous genes can thus be randomly activated and tagged in a conditional system. NIH3T3 cells were used to screen for focusforming genes using the ERM strategy. We showed that these added sequences increased the screening eciency by 410-fold, and allowed more direct identi®cation of the genes targeted. Sequence analysis of *10% of the 4600 focus clones recovered revealed both known oncogenes and novel factors such as protein kinases and GTP/GDP exchange proteins. The ERM strategy should help to facilitate large-scale gene identi®cation in diverse pathways and integrate both genetic (with the completion of the genome projects) and functional information more readily. Oncogene (2000) 19, 5964 ± 5972.

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The cytoplasmic Purkinje onconeural antigen cdr2 down-regulates c-Myc function: implications for neuronal and tumor cell survival

Cited by 109 publications

References 59 publications

Post-translational control of Myc function during differentiation

Post-translational control of Myc function during differentiation

MondoA, a Novel Basic Helix-Loop-Helix–Leucine Zipper Transcriptional Activator That Constitutes a Positive Branch of a Max-Like Network

Genetic screens in mammalian cells by enhanced retroviral mutagens

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