The winged-helix transcription factor HNF-3β is required for notochord development in the mouse embryo

Weinstein, Daniel C.; Altaba, Ariel Ruiz i; Chen, William S.; Hoodless, Pamela A.; Prezioso, Vincent R.; Jessell, Thomas M.; Darnell, James

doi:10.1016/0092-8674(94)90523-1

Cited by 745 publications

(495 citation statements)

References 73 publications

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“…This would suggest that HNF-3 and GATA-4 cooperate to control the potential of endoderm to adopt a hepatic gene expression program. With this in mind it is interesting to note that mice lacking either HNF-3␤ or GATA-4 exhibit a severe disruption to foregut morphogenesis by 8.5 dpc (Ang and Rossant, 1994;Weinstein et al, 1994;Kuo et al, 1997;Molkentin et al, 1997). This shared phenotype is consistent with HNF-3 and GATA-4 having cooperative roles in endoderm development.…”

Section: Hnf-3 and The Competence Of Endoderm To Adopt A Hepatic Fatementioning

confidence: 56%

Transcriptional regulation of liver development

Duncan¹

2000

Dev. Dyn.

102

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Section: Hnf-3 and The Competence Of Endoderm To Adopt A Hepatic Fatementioning

confidence: 56%

Transcriptional regulation of liver development

Duncan¹

2000

Dev. Dyn.

102

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“…In mice, FOXA2 is the first to be expressed in the endoderm progenitor during gastrulation, immediately followed by FOXA1 before organogenesis, and finally, FOXA3 is expressed (Sasaki and Hogan, 1993;Zaret, 1999). The targeted null mutation of FOXA1 leads to mice that die very soon after birth due to pancreatic defects, whereas the loss of FOXA2 is embryonically lethal due to the absence of endodermal progenitor cells (Weinstein et al, 1994;Kaestner et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

BRCA1 and FOXA1 proteins coregulate the expression of the cell cycle-dependent kinase inhibitor p27Kip1

et al. 2005

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We have previously shown that the breast cancer susceptibility gene, BRCA1, can transcriptionally activate the p27 Kip1 promoter. The BRCA1-responsive element was defined as a 35 bp region from position À545 to À511. We next determined that within this region is also a potential binding site for the transcription factor Forkhead box (FOX)A1. RNA and protein analysis as well as immunohistochemistry showed that expression of FOXA1 correlated with the expression of the estrogen receptor in a panel of breast cancer cell lines and tissues. In transient transfection reporter assays, FOXA1 could activate the p27 Kip1 promoter. Cotransfection of BRCA1 and FOXA1 resulted in a synergistic activation of the p27 Kip1 promoter. Mutation of the FOXA1 DNA-binding site in the p27 Kip1 promoter-luciferase construct significantly diminished the activity of FOXA1 alone or in combination with BRCA1. Cotransfection of FOXA1 and BRCA1 resulted in a greater amount of each protein compared to transfection of each expression vector alone. The half-life of FOXA1 was increased when coexpressed with BRCA1. Electrophoretic mobility shift assay analysis demonstrated that FOXA1 could bind to a wild-type oligonucleotide containing the FOXA1 binding site in the p27 Kip1 promoter, but this binding was lost upon mutation of this FOXA1 binding site. The protein-DNA binding complex could be supershifted with an antibody directed against FOXA1. The activity of the p27 Kip1 promoter as well as FOXA1 expression was reduced in cells treated with BRCA1 siRNA, thus silencing the expression of BRCA1 protein. In summary, we identified a FOXA1 binding site within the BRCA1-responsive element of the p27 Kip1 promoter and showed that FOXA1 activated the promoter alone and in conjunction with BRCA1. Furthermore, we identified high expression of FOXA1 in breast cancer cell lines and tissues, discovered a role for BRCA1 in the regulation of p27 Kip1 transcription and a possible interaction with BRCA1.

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“…22,23 For example, HNF-3 beta mutant mice cannot form the node or notochord appropriately, producing defects in neurotube and somite organization. 24,25 These mutants also fail to form tissues arising from the gut endoderm, including liver, lung, pancreas and intestine. Thus, there are several lines of evidence that the winged helix family function as genetic regulators of development.…”

Section: Introductionmentioning

confidence: 99%

Forced expression of Genesis, a winged helix transcriptional repressor isolated from embryonic stem cells, blocks granulocytic differentiation of 32D myeloid cells

Yöder

Sutton

et al. 1998

Leukemia

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We recently isolated and characterized a novel member of the winged helix (formerly HNF-3/Forkhead) transcriptional regulatory family, termed Genesis. Genesis was found to be a transcriptional repressor expressed almost exclusively in embryonic stem cells or embryonal carcinoma cells. This expression rapidly declined when these cells were stimulated to differentiate. This expression pattern suggested that Genesis may play a role in cellular differentiation. To explore that possibility in a heterologous system of differentiation, Genesis was stably transduced into the IL-3-dependent myeloid cell line 32D using a retroviral expression vector. 32D cells overexpressing Genesis failed to mature normally when stimulated with G-CSF but continued to proliferate and maintained a primitive phenotype. This finding implicates Genesis in the regulation of development, and also implies that there may be common transcription pathways for many developing tissues.

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The winged-helix transcription factor HNF-3β is required for notochord development in the mouse embryo

Cited by 745 publications

References 73 publications

Transcriptional regulation of liver development

Transcriptional regulation of liver development

BRCA1 and FOXA1 proteins coregulate the expression of the cell cycle-dependent kinase inhibitor p27Kip1

Forced expression of Genesis, a winged helix transcriptional repressor isolated from embryonic stem cells, blocks granulocytic differentiation of 32D myeloid cells

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