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1 June 2001 B-Myc, A Proximal Caput Epididymal Protein, Is Dependent on Androgens and Testicular Factors for Expression
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Abstract

The myc family of transcriptional regulators carries out critical roles in the control of cellular proliferation, differentiation, apoptosis, and tumorigenesis. The B-myc gene is a recently identified myc family member that has not been well characterized. Previously, we have shown that B-Myc inhibits the ability of c-Myc to transform cells and can inhibit cellular proliferation. Because B-myc is primarily expressed in hormonally regulated tissues with predominant expression in the epididymis, we examined in greater detail B-myc expression in the epididymis to ultimately understand potential roles B-myc may play in this and other hormonally regulated tissues. Herein we demonstrate that, in contrast to c-myc, B-myc mRNA and protein expression are highly regionalized with expression predominantly in the proximal caput epididymal region. Furthermore, in situ and immunohistochemical analyses show that within the epididymis B-myc mRNA and protein are specifically expressed by the epithelial cells and that B-Myc protein is localized to both the nuclear and cytosolic compartments. Castration and hormone replacement studies further show that expression of the B-myc mRNA is highly dependent on the presence of androgens and testicular factors. Finally, mRNA turnover studies demonstrate that the B-myc mRNA is relatively unstable with a half-life of 3.5 h. Taken together, the highly restricted and regulated expression of the B-myc gene suggests it may play important regulatory roles in the epididymis and perhaps other hormonally regulated tissues.

Gail A. Cornwall, Rebecca Collis, Qiurong Xiao, Nelson Hsia, and Stephen R. Hann "B-Myc, A Proximal Caput Epididymal Protein, Is Dependent on Androgens and Testicular Factors for Expression," Biology of Reproduction 64(6), 1600-1607, (1 June 2001). https://doi.org/10.1095/biolreprod64.6.1600
Received: 30 August 2000; Accepted: 1 January 2001; Published: 1 June 2001
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