The Bin1 Gene Localizes to Human Chromosome 2q14 by PCR Analysis of Somatic Cell Hybrids and Fluorescencein SituHybridization

Negorev, Dmitri; Riethman, Harold; Wechsler‐Reya, Robert J.; Sakamuro, Daitoku; Prendergast, George C.; Simón, Daniela

doi:10.1006/geno.1996.0205

Cited by 25 publications

(19 citation statements)

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“…Fifth, similar to several other important tumor suppressors, Bin1 promotes di erentiation in the myogenic pathway and its inhibition suppresses di erentiation (Wechsler-Reya et al, 1998). Finally, the human Bin1 gene has been mapped to chromosome 2q14 (Negorev et al, 1996), within a mid-2q region that is deleted in *42% of metastatic prostate cancers (Cher et al, 1996), and recent investigations suggest that loss of Bin1 function may contribute to prostate tumor progression (unpublished observations). Evidence from genetic, in vitro biochemical association, and co-localization experiments supports interaction between Bin1 and Myc Wechsler-Reya et al, 1997a) but in vivo physical association and functional interaction had not been documented.…”

Section: Introductionmentioning

confidence: 93%

Bin1 functionally interacts with Myc and inhibits cell proliferation via multiple mechanisms

et al. 1999

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Section: Introductionmentioning

confidence: 93%

Bin1 functionally interacts with Myc and inhibits cell proliferation via multiple mechanisms

et al. 1999

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“…The human Bin1 gene (Wechsler-Reya et al, 1997) is located at chromosome 2q14 (Negorev et al, 1996), which lies within a hotspot for deletion in metastatic prostate cancers (Cher et al, 1996). Loss of an adaptor protein that suppresses the oncogenic properties of c-Myc may be important in prostate cancer since c-Myc deregulation is among the most frequent events in this malignancy .…”

Section: Bin1mentioning

confidence: 99%

New Myc-interacting proteins: a second Myc network emerges

1999

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Despite its intensive investigation for almost two decades, c-Myc remains a fascinating and enigmatic subject. A large and compelling body of evidence indicates that c-Myc is a transcription factor with central roles in the regulation of cell proliferation, dierentiation, and apoptosis, but its exact function has remained elusive. In this review we survey recent advances in the identi®cation and analysis of c-Mycbinding proteins, which suggest insights into the transcriptional roles of c-Myc but which also extend the existing functional paradigms. The C-terminal domain (CTD) of c-Myc mediates interaction with Max and physiological recognition of DNA target sequences, events needed for all biological actions. Recently described interactions between the CTD and other cellular proteins, including YY-1, AP-2, BRCA-1, TFII-I, and Miz-1, suggest levels of regulatory complexity beyond Max in controlling DNA recognition by cMyc. The N-terminal domain (NTD), which includes the evolutionarily conserved and functionally crucial Myc Box sequences (MB1 and MB2), contains the transcription activation domain (TAD) of c-Myc as well as regions required for transcriptional repression, cell cycle regulation, transformation, and apoptosis. In addition to interaction with the retinoblastoma family protein p107, the NTD has been shown to interact with a-tubulin and the novel adaptor proteins Bin1, MM-1, Pam, TRRAP, and AMY-1. The structure of these proteins and their eects on c-Myc actions suggest links to the transcriptional regulatory machinery as well as to cell cycle regulation, chromatin modeling, and apoptosis. Investigations of this emerging NTD-based network may reveal how c-Myc is regulated and how it aects cell fate, as well as providing tools to distinguish the physiological roles of various Myc target genes.

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“…In addition, Bin1 expression is reduced in carcinoma cells derived from malignancies of the breast and other tissues, and introduction of Bin1 into tumor cell lines lacking endogenous expression reduces their proliferative capacity. Finally, the human Bin1 gene maps to chromosome 2q14 (28), a locus within the mid-2q region that is deleted in Ͼ40% of metastatic prostate carcinomas (13). Together, these observations lend strong support to the hypothesis that Bin1 is a tumor suppressor.…”

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A Role for the Putative Tumor Suppressor Bin1 in Muscle Cell Differentiation

Wechsler‐Reya

Elliott

Prendergast

1998

Molecular and Cellular Biology

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Bin1 is a Myc-interacting protein with features of a tumor suppressor. The high level of Bin1 expression in skeletal muscle prompted us to investigate its role in muscle differentiation. Significant levels of Bin1 were observed in undifferentiated C2C12 myoblasts, a murine in vitro model system. Induction of differentiation by growth factor withdrawal led to an upregulation of Bin1 mRNA and to the generation of higher-molecularweight forms of Bin1 protein by alternate splicing. While Bin1 in undifferentiated cells was localized exclusively in the nucleus, differentiation-associated isoforms of Bin1 were found in the cytoplasm as well. To examine the function of Bin1 during differentiation, we generated stable cell lines that express exogenous human Bin1 cDNA in the sense or antisense orientation. Cells overexpressing Bin1 grew more slowly than control cells and differentiated more rapidly when deprived of growth factors. In contrast, C2C12 cells expressing antisense Bin1 showed an impaired ability to undergo differentiation. Taken together, the results indicated that Bin1 expression, structure, and localization are tightly regulated during muscle differentiation and suggested that Bin1 plays a functional role in the differentiation process.

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The Bin1 Gene Localizes to Human Chromosome 2q14 by PCR Analysis of Somatic Cell Hybrids and Fluorescencein SituHybridization

Cited by 25 publications

References 0 publications

Bin1 functionally interacts with Myc and inhibits cell proliferation via multiple mechanisms

Bin1 functionally interacts with Myc and inhibits cell proliferation via multiple mechanisms

New Myc-interacting proteins: a second Myc network emerges

A Role for the Putative Tumor Suppressor Bin1 in Muscle Cell Differentiation

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