Disease relevance of BTG1

• The BTG1 gene locus has been shown to be involved in a t(8;12)(q24;q22) chromosomal translocation in a case of B-cell chronic lymphocytic leukemia [1].
• Importantly, knockdown of BTG1 reduced antisense Bcl-2-mediated cytotoxicity in breast cancer cells [2].
• CONCLUSION: Flutamide treatment might up-regulate CDKN1A and BTG1 expression in prostate cancer cells [3].
• Identification of B-cell translocation gene 1 as a biomarker for monitoring the remission of acute myeloid leukemia [4].

High impact information on BTG1

• During erythroid differentiation, increased arginine methylation coincided with BTG1 expression [5].
• FoxO3a regulates erythroid differentiation and induces BTG1, an activator of protein arginine methyl transferase 1 [5].
• Expression of BTG1 in primary mouse bone marrow cells blocked the outgrowth of erythroid colonies, which required a domain of BTG1 that binds protein arginine methyl transferase 1 [5].
• BTG1 expression is maximal in the G0/G1 phases of the cell cycle and is down-regulated when cells progress throughout G1 [1].
• Furthermore, transfection experiments of NIH3T3 cells indicate that BTG1 negatively regulates cell proliferation [1].

Biological context of BTG1

• BTG1 and BTG2 belong to a family of functionally related genes involved in the control of the cell cycle [6].
• In vitro the hCAF-1/BTG1 complex formation was dependent on the phosphorylation of a putative p34cdc2 kinase site on BTG1 (Ser-159) [7].
• Taken together, these results indicate that formation of the hCAF-1/BTG1 complex is driven by phosphorylation at BTG1 (Ser-159) and implicates this complex in the signalling events of cell division that lead to changes in cellular proliferation associated with cell-cell contact [7].
• In support of this hypothesis, we showed that the endogenous induction of BTG1 and BTG2 after genotoxic treatment was correlated with a modulation of protein methylation [8].
• The BTG1 open reading frame is 60% homologous to PC3, an immediate early gene induced by nerve growth factor in rat PC12 cells [1].

Anatomical context of BTG1

• In conclusion, ANA is a fourth member of the Tob/BTG1 family that might play roles in neurogenesis in the central nervous system [9].
• Human carbon catabolite repressor protein (CCR4)-associative factor 1: cloning, expression and characterization of its interaction with the B-cell translocation protein BTG1 [7].
• Cell synchrony experiments with primary cultures of rat aortic smooth-muscle cells (RSMCs) demonstrated that message and protein levels of rat CAF-1 (rCAF-1) were up-regulated under conditions of cell contact, as previously reported for BTG1 [Wilcox, Scott, Subramanian, Ross, Adams-Burton, Stoltenborg and Corjay (1995) Circulation 92, I34-I35] [7].
• We have previously shown that BTG1 stimulates myoblast differentiation [10].
• In this study, we report that BTG1 is essentially expressed at cell confluence and in differentiated myotubes [11].

Associations of BTG1 with chemical compounds

• Immunoprecipitation experiments performed in cells or using in vitro-synthesized proteins and GST pull-down assays established that BTG1 directly interacts with T3 and all-trans retinoic acid receptors and with avian MyoD (CMD1) [12].
• BTG1: a triiodothyronine target involved in the myogenic influence of the hormone [11].
• Overexpression of BTG1 mRNA was also observed in the CR state of all-trans-retinoic acid (ATRA)-treated AML-M3 patients and ATRA-treated HL-60 cells [4].

Other interactions of BTG1

• Using a polymerase chain reaction-mediated cloning procedure, we have identified a novel member, termed ANA (from Abundant in Neuroepithelium Area), of Tob/BTG1 family of antiproliferative genes [9].
• The protein expressions of CDKN1A and BTG1 play an important role in inhibiting the proliferation of cancer cells [3].
• The CDKN1A and BTG1 gene mRNA expression was confirmed to be higher in the experimental group by RT-PCR, while p53 mRNA expression had no significant changes [3].
• In addition, SEA enhanced urothelial expression of B-cell translocation protein (BTG1) and human proliferating cell nuclear antigen (PCNA) mRNAs [13].
• Regulation of protein tyrosine phosphatase 4a1, B-cell translocation gene 2, nuclear receptor subfamily 4a1 and diacylglycerol O-acyltransferase 1 by follicle stimulating hormone in the rat ovary [14].

Analytical, diagnostic and therapeutic context of BTG1

• Western blot and immunohistochemical analysis showed that rCAF-1 localizes to the nucleus of contact-inhibited RSMCs, where it was physically associated with BTG1, as determined by co-immunoprecipitation with anti-hCAF-1 antisera [7].
• Sequence and Northern blot analyses indicate that BTG1 and PC3 are not cognate genes [1].
• In situ hybridization and immunodetection studies demonstrated that BTG1 localized to specific macrophage-rich regions of lesions in both Watanabe heritable hyperlipidemic rabbits and humans [15].

References