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Gene Review

BRE  -  brain and reproductive organ-expressed...

Homo sapiens

Synonyms: BRCA1-A complex subunit BRE, BRCA1/BRCA2-containing complex subunit 45, BRCC4, BRCC45, Brain and reproductive organ-expressed protein
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Disease relevance of BRE

  • Thus, overexpression of BRE promotes local tumor growth but not metastasis [1].
  • Similar decreases in BRE expression were observed in RA-treatment of the brain glioma cell U-251 and the promyelocytic cell HL-60 [2].
  • We have shown that the mouse Lewis lung carcinoma D122 stable transfectants of human BRE expression vector developed into local tumor significantly faster than the stable transfectants of empty vector and parental D122, in both the syngeneic C57BL/6 host and nude mice [1].
  • However, BRE expression was downregulated in human adrenal adenoma and pheochromocytoma, whereas its expression was enhanced in abnormal adrenal tissues of rats chronically treated with nitrate or nitrite [3].
  • Decrease in BRE mRNA was also observed in a squamous carcinoma cell, 1483, that showed X-ray resistance and has a more aggressive tumorigenic phenotype, but BRE expression was unchanged in cells after growth inhibition [2].

High impact information on BRE

  • TFIIB possesses sequence-specific DNA-binding ability and interacts with the TFIIB-recognition element (BRE), present in many promoters [4].
  • BRCC36 and BRCC45 are novel components of the complex with sequence homology to a subunit of the signalosome and proteasome complexes [5].
  • An immunoglobulin light chain protein was isolated from the urine of an individual (BRE) with systemic amyloidosis [6].
  • Recombinant BRE VL was isolated, purified to homogeneity, and crystallized by using ammonium sulfate as the precipitant [6].
  • To study the tertiary structure, BRE VL was expressed in Escherichia coli by using a PCR product amplified from the patient BRE's bone marrow DNA [6].

Biological context of BRE

  • Here we report that BRE was identified multiple times in a yeast two-hybrid screen of a murine cerebellar cDNA library, using the juxtamembrane domain of the p55 tumor necrosis factor alpha (TNF) receptor [7].
  • We conclude that in contrast to the truncated Bid that integrates mitochondrial apoptosis to death receptor-triggered apoptotic cascade, BRE inhibits the integration [8].
  • We further demonstrate that BRE mediates antiapoptosis by inhibiting the mitochondrial apoptotic machinery but without translocation to the mitochondria or nucleus or down-regulation of the cellular level of truncated Bid [8].
  • We conclude that the enhanced tumor growth is more likely due to the antiapoptotic activity of BRE than any direct effect of the protein on cell proliferation [1].
  • We have previously identified a new gene, BRE, that is responsive to DNA damage and retinoic acid [3].

Anatomical context of BRE

  • We propose that BRE inhibits, by ubiquitination-like activity, components in or proximal to the death-inducing signaling complexes that are necessary for activation of the mitochondria [8].
  • Differential expression of a stress-modulating gene, BRE, in the adrenal gland, in adrenal neoplasia, and in abnormal adrenal tissues [3].
  • Comparing with normal cells, immortalized human cell lines uniformly express higher levels of BRE [9].
  • In situ hybridization and immunohistochemical staining indicated that BRE was strongly expressed in the zona glomerulosa of the adrenal cortex, which synthesizes and secretes the mineralocorticoid hormones [3].
  • These data indicate that BRE is a house-keeping gene and it may play a role in homeostatis or in certain pathways of differentiation in cells of neural, epithelial and germ line origins [2].

Associations of BRE with chemical compounds

  • A stress-responsive gene highly expressed in brain and reproductive organs (BRE) is down-regulated after UV irradiation, DNA damaging agents, or retinoic acid treatment [7].
  • Here we show that BRE also binds to another death receptor, Fas, and upon overexpression conferred resistance to apoptosis induced by TNF-alpha, anti-Fas agonist antibody, cycloheximide, and a variety of stress-related stimuli [8].
  • Treatment of fibroblast cell with UV and 4-nitroquinoline-1-oxide caused more than 90% and 50% decreases in BRE mRNA, respectively [2].
  • Blocking BRE expression in Leydig cells inhibits steroidogenesis by down-regulating 3beta-hydroxysteroid dehydrogenase [10].
  • Although cAMP production, along with StAR and P450scc mRNA expression, was unaffected in BRE antisense clones, progesterone and testosterone yields were significantly decreased, while pregnenolone was increased in response to human chorionic gonadotropin stimulation or in the presence of 22(R)OH-cholesterol [10].

Other interactions of BRE

  • Dissociation of BRE rapidly from TNF-R1, but not from Fas, upon receptor ligation suggests that this protein interacts with the death inducing signaling complex during apoptotic induction [8].
  • This is particularly true when restricted to patients in whom the BRE clinical grade is 2 (P < 0.001) or for whom there is a lack of HER2 expression (P < 0.002) [11].
  • Further, we find that an activator can disrupt the TFIIB-BRE interaction within a promoter-bound complex [4].
  • As BRE and IGE are benign, idiopathic, age-dependent epilepsies, EJM1 is a candidate locus for the fsw underlying BRE and related disorders [12].
  • We found that cell proliferation was significantly increased after knockdown of BRE, concomitant with reduced p53 and prohibitin expression [13].

Analytical, diagnostic and therapeutic context of BRE

  • The interaction between the p55 receptor and BRE was verified by an in vitro biochemical assay by using recombinant fusion proteins and by co-immunoprecipitation of transfected mammalian cells [7].
  • Sequence analysis demonstrated that the peptide sequence of BRE in hamster shares approximately 99% homology with those of human, monkey and mouse [14].
  • Using multiple-tissue dot-blotting and Northern blotting, BRE was recently found to be strongly expressed in adrenal cortex and medulla, in testis, and in pancreas, whereas low expression was found in the thyroid, thymus, small intestine and stomach [3].
  • BRE MHC I fibres showed no change in size or V(o) after bed-rest; however, P(o) was 19% lower (P < 0.05), resulting in 20 and 30% declines (P < 0.05) in normalized P(o) and power, respectively [15].
  • The characteristic age-dependent focal sharp wave (fsw) found on the EEG in this disorder segregates as an autosomal dominant trait in families with probands with BRE and acts as a neurobiological marker for the increased risk of developing BRE, other benign partial epilepsies of childhood, and other developmental disorders in these families [12].


  1. BRE enhances in vivo growth of tumor cells. Chan, B.C., Li, Q., Chow, S.K., Ching, A.K., Liew, C.T., Lim, P.L., Lee, K.K., Chan, J.Y., Chui, Y.L. Biochem. Biophys. Res. Commun. (2005) [Pubmed]
  2. Identification of a brain- and reproductive-organs-specific gene responsive to DNA damage and retinoic acid. Li, L., Yoo, H., Becker, F.F., Ali-Osman, F., Chan, J.Y. Biochem. Biophys. Res. Commun. (1995) [Pubmed]
  3. Differential expression of a stress-modulating gene, BRE, in the adrenal gland, in adrenal neoplasia, and in abnormal adrenal tissues. Miao, J., Panesar, N.S., Chan, K.T., Lai, F.M., Xia , N., Wang , Y., Johnson, P.J., Chan, J.Y. J. Histochem. Cytochem. (2001) [Pubmed]
  4. Activator-mediated disruption of sequence-specific DNA contacts by the general transcription factor TFIIB. Evans, R., Fairley, J.A., Roberts, S.G. Genes Dev. (2001) [Pubmed]
  5. Regulation of BRCC, a holoenzyme complex containing BRCA1 and BRCA2, by a signalosome-like subunit and its role in DNA repair. Dong, Y., Hakimi, M.A., Chen, X., Kumaraswamy, E., Cooch, N.S., Godwin, A.K., Shiekhattar, R. Mol. Cell (2003) [Pubmed]
  6. Tertiary structure of an amyloid immunoglobulin light chain protein: a proposed model for amyloid fibril formation. Schormann, N., Murrell, J.R., Liepnieks, J.J., Benson, M.D. Proc. Natl. Acad. Sci. U.S.A. (1995) [Pubmed]
  7. BRE: a modulator of TNF-alpha action. Gu, C., Castellino, A., Chan, J.Y., Chao, M.V. FASEB J. (1998) [Pubmed]
  8. A death receptor-associated anti-apoptotic protein, BRE, inhibits mitochondrial apoptotic pathway. Li, Q., Ching, A.K., Chan, B.C., Chow, S.K., Lim, P.L., Ho, T.C., Ip, W.K., Wong, C.K., Lam, C.W., Lee, K.K., Chan, J.Y., Chui, Y.L. J. Biol. Chem. (2004) [Pubmed]
  9. Expression of human BRE in multiple isoforms. Ching, A.K., Li, P.S., Li, Q., Chan, B.C., Chan, J.Y., Lim, P.L., Pang, J.C., Chui, Y.L. Biochem. Biophys. Res. Commun. (2001) [Pubmed]
  10. Blocking BRE expression in Leydig cells inhibits steroidogenesis by down-regulating 3beta-hydroxysteroid dehydrogenase. Miao, J., Chan, K.W., Chen, G.G., Chun, S.Y., Xia, N.S., Chan, J.Y., Panesar, N.S. J. Endocrinol. (2005) [Pubmed]
  11. Prognostic impact of ANX7-GTPase in metastatic and HER2-negative breast cancer patients. Srivastava, M., Bubendorf, L., Raffeld, M., Bucher, C., Torhorst, J., Sauter, G., Olsen, C., Kallioniemi, O.P., Eidelman, O., Pollard, H.B. Clin. Cancer Res. (2004) [Pubmed]
  12. Exclusion of linkage of genetic focal sharp waves to the HLA region on chromosome 6p in families with benign partial epilepsy with centrotemporal sharp waves. Whitehouse, W., Diebold, U., Rees, M., Parker, K., Doose, H., Gardiner, R.M. Neuropediatrics. (1993) [Pubmed]
  13. Comparative proteomic analysis reveals a function of the novel death receptor-associated protein BRE in the regulation of prohibitin and p53 expression and proliferation. Tang, M.K., Wang, C.M., Shan, S.W., Chui, Y.L., Ching, A.K., Chow, P.H., Grotewold, L., Chan, J.Y., Lee, K.K. Proteomics (2006) [Pubmed]
  14. Tissue specific expression and sequence analysis of a stress responsive gene Bre in adult golden hamster (Mesocricetus auratus). Poon, H.K., Chan, J.Y., Lee, K.H., Chow, P.H. Cell Tissue Res. (2004) [Pubmed]
  15. Human single muscle fibre function with 84 day bed-rest and resistance exercise. Trappe, S., Trappe, T., Gallagher, P., Harber, M., Alkner, B., Tesch, P. J. Physiol. (Lond.) (2004) [Pubmed]
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