Mouse BTEB3, a new member of the basic transcription element binding protein (BTEB) family, activates expression from GC-rich minimal promoter regions

Martin, Karen; Cooper, Wendy N.; Metcalfe, James C.; Kemp, Paul R.

doi:10.1042/0264-6021:3450529

Cited by 27 publications

(36 citation statements)

References 16 publications

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“…5). By contrast, the expression of Bteb3, a closely related Bteb1 family member (41), showed a tendency to increase (p ϭ 0.1) in Bteb1 Ϫ/Ϫ uteri. At 8 -10 weeks of age, there was no difference in the uterine expression of these genes in WT and Bteb1 Ϫ/Ϫ mice, the exception being Bteb3, whose uterine mRNA levels were higher (p Ͻ0.05) in Bteb1 Ϫ/Ϫ than WT.…”

Section: Increased Incidence Of Neonatal Lethality For Bteb1 ϫ/ϫmentioning

confidence: 76%

Subfertility, Uterine Hypoplasia, and Partial Progesterone Resistance in Mice Lacking the Krüppel-like Factor 9/Basic Transcription Element-binding Protein-1 (Bteb1) Gene

Simmen

Eason

McQuown³

et al. 2004

Journal of Biological Chemistry

119

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Progesterone receptor (PR), a ligand-activated transcription factor, is a key regulator of cellular proliferation and differentiation in reproductive tissues. The transcriptional activity of PR is influenced by co-regulatory proteins typically expressed in a tissue-and cellspecific fashion. We previously demonstrated that basic transcription element-binding protein-1 (BTEB1), a member of the Sp/Krü ppel-like family of transcription factors, functionally interacts with the two PR isoforms, PR-A and PR-B, to mediate progestin sensitivity of target genes in endometrial epithelial cells in vitro. Here we report that ablation of the Bteb1 gene in female mice results in uterine hypoplasia, reduced litter size, and increased incidence of neonatal deaths in offspring. The reduced litter size is solely a maternal genotype effect and results from fewer numbers of implantation sites, rather than defects in ovulation. In the early pregnant uterus, Bteb1 expression in stromal cells temporally coincides with PR-A isoform-dependent decidual formation at the time of implantation. Expression of two implantation-specific genes, Hoxa10 and cyclin D3, was decreased in uteri of early pregnant Bteb1-null mutants, whereas that of Bteb3, a related family member, was increased, the latter possibly compensating for the loss of Bteb1. Progesterone responsiveness of several uterine genes was altered with Bteb1-null mutation. These results identify Bteb1 as a functionally relevant PR-interacting protein and suggest its selective modulation of cellular processes that are regulated by PR-A in the uterine stroma.

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Section: Increased Incidence Of Neonatal Lethality For Bteb1 ϫ/ϫmentioning

confidence: 76%

Subfertility, Uterine Hypoplasia, and Partial Progesterone Resistance in Mice Lacking the Krüppel-like Factor 9/Basic Transcription Element-binding Protein-1 (Bteb1) Gene

Simmen

Eason

McQuown³

et al. 2004

Journal of Biological Chemistry

119

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“…FKLF2/RFLAT-1/BTEB3 (hereafter referred to as FKLF2) is a recently cloned member of the Sp1/KLF family of transcription factors (21)(22)(23). FKLF2 is a phosphorylated protein and is expressed in a variety of tissues (21)(22)(23).…”

mentioning

confidence: 99%

“…FKLF2 is a phosphorylated protein and is expressed in a variety of tissues (21)(22)(23). Our previous studies (21) have shown that FKLF2 activates the human ␥ globin promoter and to a lesser degree the ⑀ and ␤ globin promoters as well as several erythroid-specific promoters.…”

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confidence: 99%

Functional Interaction between Coactivators CBP/p300, PCAF, and Transcription Factor FKLF2

Song¹,

Keller²,

Murata³

et al. 2002

Journal of Biological Chemistry

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The Sp1/KLF family of factors regulates diverse cellular processes, including growth and development. Fetal Krü ppel-like factor (FKLF2) is a new member of this family. In this study, we characterized the coactivators involved in FKLF2 transcriptional activation. Our results show that both CBP/p300 and p300/CBP-associated factor (PCAF) enhance FKLF2 transcriptional activity. We demonstrate that the acetyltransferase activity of PCAF but not that of CBP/p300 is required for stimulating FKLF2 transcription activity. We further show that p300 and PCAF act cooperatively in stimulating FKLF2 transcriptional activation. FKLF2 interacts with both CBP and PCAF through specific domains, and CBP and PCAF acetylate FKLF2. Both CBP/p300 and PCAF stimulate FKLF2 DNA binding activity. The integrity of the acetyltransferase domain of PCAF but not that of CBP/p300 is required for stimulating FKLF2 DNA binding activity. These results demonstrate that CBP/p300 and PCAF stimulate FKLF2 transcriptional activity at least by enhancing its DNA binding. The acetyltransferase activities of CBP/p300 and PCAF play a distinct role in stimulating FKLF2 transcription and DNA binding.The Sp1/KLF family of transcription factors regulates diverse cellular processes, including cell growth and differentiation, and is essential for early embryonic development (1-3). This family of proteins is characterized by the presence of three highly homologous C2H2 type zinc fingers near the C terminus that bind GC/GT boxes. Amino acid sequences in the transcription activation/repression domains are less conserved among family members. This family of proteins exhibits a different affinity for the GC/GT boxes in different promoters and possesses transcriptional activation, repression, or both functions. Because the GC/GT boxes are one of the most common regulatory elements in promoters of many cellular and viral genes, the characterization of the modulation of their transcriptional activities by different coactivators will provide significant insight into the mechanism by which this family of factors regulates gene expression.Sp1 and EKLF, 1 an erythroid-specific factor that is required for the expression of the adult type ␤ globin gene (4 -7), are the best studied in this family. EKLF interacts with CBP (8) as well as ERC-1 (EKLF coactivator remodeling complex 1). ERC-1 is a SWI/SNF-related chromatin remodeling complex and is required for generating a DNase I-hypersensitive, transcriptionally active ␤ promoter on a chromatin template in vitro (9). EKLF was also demonstrated to interact with the corepressors mSin3A and HDAC1 and repress transcription (10). The glutamine-rich activation domain of Sp1 makes direct contact with the TAF110 subunit of the TFIID complex and mediates transcriptional activation (11). In addition, the transcriptional cofactor complex CRSP (cofactor required for Sp1 activation) has also been shown to be required for Sp1 transcriptional activation in vitro (12). CBP/p300 and PCAF function as coactivators for a variety of transcriptional ...

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“…Moreover, the migration of the speci®c complex is faster than the speci®c Sp1 complex, suggesting that an Sp1-like nuclear protein with smaller molecular weight bound to CycY. Several di erent members of the Sp family, Sp1, 2, 3, 4, and three more distantly related factors, BTEB (basic transcription element binding protein), BTEB2 and BTEB3 have been isolated (Lania et al, 1997;Martin et al, 2000). The BTEB family is of particular interest because BTEB is smaller than Sp1, and BTEBcontaining complexes run ahead of Sp1-containing complexes in EMSA gels (Chen and Davis, 1999).…”

Section: Discussionmentioning

confidence: 99%

Cyclopentenone causes cell cycle arrest and represses cyclin D1 promoter activity in MCF-7 breast cancer cells

Hsiang

Straus

2002

Oncogene

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Evidence indicates that overexpression of cyclin D1 is an important event in malignant transformation of breast cancer cells. Therefore, cyclin D1 is a potential target for mechanistically-based chemoprevention/treatment of breast cancer. Treatment of serum-stimulated quiescent MCF-7 breast cancer cells with cyclopentenone (2-cyclopenten-1-one) blocked progression through G 1 and into S phase. Growth arrest of the cyclopentenone-treated cells in G 1 was associated with changes in the levels of several proteins that control the cell cycle, including a dramatic decrease in cyclin D1 protein expression. Cyclopentenone also decreased the abundance of cyclin D1 mRNA and nuclear transcripts, indicating that it regulated cyclin D1 expression at the transcriptional level. Cyclopentenone selectively inhibited the activity of the cyclin D1 and cyclin A promoters but not the activity of several other control promoters. Deletion analysis indicated that the cyclopentenone response element was located in the cyclin D1 core promoter. Additional functional studies showed that a sequence within the core promoter (CycY, located downstream from the initiator element) played an important role in activation of the cyclin D1 promoter in MCF-7 cells. Electrophoretic mobility shift assays demonstrated speci®c binding of the transcription factor BTEB to the CycY site. The cyclopentenone response element did not correspond to the CycY site but rather mapped to the initiator element itself. The overall results suggest that cyclopentenone interferes with the transcription initiation complex that assembles over the cyclin D1 initiator element, leading to selective inhibition of cyclin D1 gene transcription.

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Mouse BTEB3, a new member of the basic transcription element binding protein (BTEB) family, activates expression from GC-rich minimal promoter regions

Cited by 27 publications

References 16 publications

Subfertility, Uterine Hypoplasia, and Partial Progesterone Resistance in Mice Lacking the Krüppel-like Factor 9/Basic Transcription Element-binding Protein-1 (Bteb1) Gene

Subfertility, Uterine Hypoplasia, and Partial Progesterone Resistance in Mice Lacking the Krüppel-like Factor 9/Basic Transcription Element-binding Protein-1 (Bteb1) Gene

Functional Interaction between Coactivators CBP/p300, PCAF, and Transcription Factor FKLF2

Cyclopentenone causes cell cycle arrest and represses cyclin D1 promoter activity in MCF-7 breast cancer cells

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