Titlebook: C-Myc in B-Cell Neoplasia; 14th Workshop on Mec Michael Potter (Chief),Fritz Melchers (Director) Book 1997 The Editor(s) (if applicable) an

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Mnt: A Novel Max-interacting Protein and Myc Antagonistls. Likewise, Mnt protein is expressed in many proliferating cell types in culture where both Myc:Max and Mnt:Max complexes are detected. An exception is P19 embryonal carcinoma cells, where Mnt is expressed and in a complex with Max, but Myc proteins are not detected. Mnt is likely to be a key regu

成份

0070-217X nk the National Cancer Institute for sponsoring this workshop and the staff of Cygnus, Inc. , for their outstanding organizational assistance. The organizers ar978-3-642-64560-0978-3-642-60801-8Series ISSN 0070-217X Series E-ISSN 2196-9965

Indolent

Book 1997h of this field. The organizers of the meeting have each contributed review chapters that summarize different aspects of the meeting. We thank the National Cancer Institute for sponsoring this workshop and the staff of Cygnus, Inc. , for their outstanding organizational assistance. The organizers ar

intangibility

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thrombus

Biofuel and Biorefinery Technologiesw levels in normal proliferating cells [2,5]. Minor fluctuations in MYC protein and/or mRNA levels can have dramatic outcomes on cellular physiology. Consequently, mammalian MYC gene expression is subject to tight control at multiple levels.

Myocarditis

https://doi.org/10.1007/978-3-319-43679-1ice harboring a translocated Pvt 1/Ck segment in order to determine whether 1). these mice produce the Pvt 1/Ck fusion product 2). these mice are immunocompromised and 3). these mice develop tumors of a B cell origin.

octogenarian

https://doi.org/10.1007/978-3-319-43679-1tory elements but also the acquisition of different regulatory influences associated with its new, immunoglobulin-associated, chromosomal environment. The focus of this paper is on the nature of IgH associated sequences that impact upon the c-myc oncogene in B cell malignancies.

大方一點

Microbial Extracellular Polymeric Substancescause an increase in p27. Since dexamethasone causes a loss of myc and synergizes with the anti-IgM signal, we suggest that accelerated cell death with this steroid in the presence of anti-IgM is due to a more rapid degradation of this oncogene product. Finally, we propose that c-myc drives the tran

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