Richard Jucker

University of Zurich

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Sergio Nasi

Sapienza University of Rome

Maria Isabella Sirinian

Sapienza University of Rome

Laura Soucek

Institució Catalana de Recerca i Estudis Avançats

E. Calef

University of Rome Tor Vergata

Cordula Haas

University of Zurich

Alessandra Marchetti

Policlinico Umberto I

Jack Ballantyne

University of Central Florida

Erin Hanson

Saluda Medical (Australia)

Alberto Fruscalzo

National Academies of Sciences, Engineering, and Medicine

Georgia Mandolesi

San Raffaele University of Rome

Cooperative Institutions

Sapienza University of Rome

University of Rome Tor Vergata

Istituti di Ricovero e Cura a Carattere Scientifico

National Research Council

Institute of Neurobiology and Molecular Medicine

Institute of Molecular Biology and Pathology

Institute of Cell Biology and Neurobiology

University of Zurich

University of Bologna

Istituto Dermopatico dell'Immacolata

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Interplay of the E Box, the Cyclic AMP Response Element, and HTF4/HEB in Transcriptional Regulation of the Neurospecific, Neurotrophin-InduciblevgfGene†

Molecular and Cellular Biology (1997)

Giuliana Di Rocco Maria Pennuto Barbara Illi Nadia Canu Gessica Filocamo

vgf is a neurotrophin response-specific, developmentally regulated gene that codes for a neurosecretory polypeptide. Its transcription in neuronal cells is selectively activated by the neurotrophins nerve growth factor (NGF), brain-derived neurotrophic factor, and neurotrophin 3, which induce survival and differentiation, and not by epidermal growth factor. We studied a short region of the rat vgf promoter which is essential for its regulated expression. A cyclic AMP response element (CRE) within this region is necessary for NGF induction of vgf transcription. Two sites upstream of CRE, an E box and a CCAAT sequence, bind nuclear protein complexes and are involved in transcriptional control. The E box has a dual role. It acts as an inhibitor in NIH 3T3 fibroblasts, together with a second E box located downstream, and as a stimulator in the NGF-responsive cell line PC12. By expression screening, we have isolated the cDNA for a basic helix-loop-helix transcription factor, a homolog of the HTF4/HEB E protein, that specifically binds the vgf promoter E box. The E protein was present in various cell lines, including PC12 cells, and was a component of a multiprotein nuclear complex that binds the promoter in vitro. The E box and CRE cooperate in binding to this complex, which may be an important determinant for neural cell-specific expression.

CAAT box

Serum Response Element

10.1128/mcb.17.3.1244

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Citations (30)

The effect of Ha-ras oncogene expression on EBV immortalized B lymphocytes

Cell Biology International Reports (1990)

Richard Jucker Maria Isabella Sirinian Alessandra Marchetti G DIROCCO Sergio Nasi

Expression (computer science)

10.1016/0309-1651(90)90461-7

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Citations (0)

Study on the participation of neoplastic cells in the development of mouse embryos

Development (1982)

E. Calef Corrado Crimi Alberto Fruscalzo Richard Jucker

To test the ability of cloned committed erythroleukemic cells to participate in development we have injected. Friend leukemia cells (FLC) into C57Bl/6 mouse blastocysts together with Friend leukemia virus (FLV) and we have examined the newborn individuals derived from them. Five animals out of 32 born have FLC-derived neoplasia. The incidence of neoplasia is increased as compared with other similar experiments without the virus. In two of the animals with the FLC neoplasia the disease manifestation is an erythroid leukemia similar to the one obtained directly with the virus in normal DBA/2 mice.

Friend virus

10.1242/dev.70.1.37

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Citations (2)

NGF‐dependent and tissue‐specific transcription of vgf is regulated by a CREB–p300 and bHLH factor interaction

FEBS Letters (2001)

Georgia Mandolesi Silvia Gargano Maria Pennuto Barbara Illi Rosa Molfetta

Neurotrophins support neuronal survival, development, and plasticity through processes requiring gene expression. We studied how vgf target gene transcription is mediated by a critical promoter region containing E‐box, CCAAT and cAMP response element (CRE) sites. The p300 acetylase was present in two distinct protein complexes bound to this region. One complex, containing HEB (ubiquitous basic helix–loop–helix (bHLH)), bound the promoter in non‐neuronal cells and was involved in repressing vgf expression. Neurotrophin‐dependent transcription was mediated by the second complex, specific for neuronal cells, which included CRE binding protein and MASH1 (neuro‐specific bHLH), bound the CCAAT motif, and was target of neurotrophin signalling. The interaction, mediated by p300, of different transcription factors may add specificity to the neurotrophin response.

Basic helix-loop-helix

Transcription

Response element

10.1016/s0014-5793(01)03227-6

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Citations (26)

Induction of the neoplastic phenotype of EBV-established B lymphocytes by the human Ha-ras oncogene.

PubMed (1990)

Sergio Nasi Maria Isabella Sirinian Gaetano Luca Panetta Alessandra Marchetti Richard Jucker

Oncogene Proteins

Immortalised cell line

Lymphoblast

Source

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Citations (1)

Omomyc, a potential Myc dominant negative, enhances Myc-induced apoptosis.

PubMed (2002)

Laura Soucek Richard Jucker Laura Panacchia R. Ricordy Franco Tatò

The Myc basic helix-loop-helix zipper domain determines dimerization with Max and binding to the DNA E-box, both of which play a critical role in Myc regulation of growth, proliferation, tumorigenesis, and apoptosis. The mutant basic helix-loop-helix zipper domain, Omomyc, dimerizes with Myc, sequestering it in complexes unable to bind the E-box, and so acting as a potential dominant negative. Consistent with this, Omomyc reverses Myc-induced cytoskeletal disorganization in C2C12 myoblasts. Surprisingly, however, Omomyc strongly potentiates Myc-induced apoptosis in a manner dependent on Myc expression level. Expression analysis of known Myc target genes indicates that Omomyc inhibits transcriptional activation but enhances repression. These findings suggest that Omomyc can selectively trigger apoptosis in cells overexpressing Myc, possibly through the transcriptional repression of specific genes.

Zipper

Proto-Oncogene Proteins c-myc

Basic helix-loop-helix

C2C12

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Citations (152)

Studies on host-virus genome relationship in Epstein-Barr virus immortalized lymphoblastoid cell lines

Cell Biology International Reports (1986)

Giuseppe Ragona Domenico Frezza Alberto Fruscalzo Richard Jucker Nicola Rossi

Immortalised cell line

Lymphoblast

10.1016/0309-1651(86)90002-0

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Citations (7)

Identification of skin in touch/contact forensic samples by messenger RNA profiling

Forensic science international. Genetics supplement series (2011)

Erin Hanson Cordula Haas Richard Jucker Jack Ballantyne

Human skin

Identification

Profiling (computer programming)

10.1016/j.fsigss.2011.09.015

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Citations (26)

Design and properties of a Myc derivative that efficiently homodimerizes

Oncogene (1998)

Laura Soucek Manuela Helmer‐Citterich Alessandra Sacco Richard Jucker Gianni Cesareni

Proto-Oncogene Proteins c-myc

Basic helix-loop-helix

Transcription

10.1038/sj.onc.1202199

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Citations (184)

Making decisions through Myc

FEBS Letters (2001)

Sergio Nasi Roberta Ciarapica Richard Jucker Jessica Rosati Laura Soucek

c‐Myc is a transcriptional regulator involved in carcinogenesis through its role in growth control and cell cycle progression. Here we attempt to relate its role in stimulating the G1–S transition to the ability to affect functioning of key cell cycle regulators, and we focus on how its property of modulating transcription of a wide range of target genes could explain its capacity to affect multiple pathways leading to proliferation, apoptosis, growth, and transformation.

10.1016/s0014-5793(01)02118-4

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Citations (121)