A gene family of HMG-box transcription factors with homology to TCF-1

Castrop, J; Norren, Klaske van; Clevers, Hans

doi:10.1093/nar/20.3.611

Cited by 51 publications

(37 citation statements)

References 4 publications

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“…For example, development of tooth germs that normally express both genes is arrested in I£P-1-defi cient mice, whereas no obvious phenotype was detected in the inner ear despite exclusive expression of LEF-1. Two other candidate genes, termed TCF-3 and TCF-4, which contain HMG boxes virtually identical to those in LEF-1 and TCF-1, have also been identified (Castrop et al 1992). It is possible that these genes might compensate for the absence of LEF-1 in organs not affected by the mutation, although we cannot rule out that expression of LEF-1 is dispensable in these organs.…”

Section: Discussionmentioning

confidence: 94%

Development of several organs that require inductive epithelial-mesenchymal interactions is impaired in LEF-1-deficient mice.

Genderen¹,

Okamura²,

Fariñas³

et al. 1994

Genes Dev.

891

690

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Lymphoid enhancer factor 1 (LEF-1) is a sequence-specific DNA-binding protein that is expressed in pre-B and T lymphocytes of adult mice, and in the neural crest, mesencephalon, tooth germs, whisker follicles, and other sites during embryogenesis. We have generated mice carrying a homozygous germ-line mutation in the LEF-1 gene that eliminates its protein expression and causes postnatal lethality. The mutant mice lack teeth, mammary glands, whiskers, and hair but show no obvious defects in lymphoid cell populations at birth. The I£F-l-deficient mice also lack the mesencephalic nucleus of the trigeminal nerve, the only neural crest-derived neurons normally present within the brain, but no deficiency can be detected in other neural crest-derived neuronal populations. Together, the pattern of these defects suggest an essential role for LEF-1 in the formation of several organs and structures that require inductive tissue interactions.

show abstract

Section: Discussionmentioning

confidence: 94%

Development of several organs that require inductive epithelial-mesenchymal interactions is impaired in LEF-1-deficient mice.

Genderen¹,

Okamura²,

Fariñas³

et al. 1994

Genes Dev.

891

690

View full text Add to dashboard Cite

show abstract

“…A degenerate PCR approach was used to identify mRNA sequences of the LEF/ TCF transcription factor family expressed in these cells. The degenerate primers encoding sequences in the highly conserved high mobility group domain of LEF/TCF were as described previously (40). In addition, we used a nested primer to increase the selectivity toward specific PCR products.…”

Section: Identification Of Tcf-4mentioning

confidence: 99%

Regulation and Possible Function of β-Catenin in Human Monocytes

Thiele

Wasner²,

Müller

et al. 2001

The Journal of Immunology

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In this study, we demonstrate that adherence factors, serum constituents, LPS, and zymosan are capable of inducing a cellular accumulation of β-catenin in human monocytes. Whereas adherence-dependent accumulation of β-catenin can be blocked by wortmannin, an inhibitor of phosphatidylinositol 3-kinase, accumulation induced by the remaining stimuli cannot be prevented by inhibition of phosphatidylinositol 3-kinase, implying the involvement of β-catenin in other not yet described signal transduction pathways. A role of β-catenin in adherence-dependent processes by interacting with classical cadherins can be excluded as we could not detect cadherins in monocytes. To test whether it is possible that β-catenin interacts with LEF/TCF (lymphoid enhancer factor/T cell factor) transcription factors, we studied the expression of this protein family. TCF-4 was identified as the LEF/TCF transcription factor present in human monocytes. However, neither cellular induction of β-catenin nor cotransfection experiments with β-catenin conducted in the monocytic cell line THP-1 resulted in the activation of a LEF/TCF-dependent promoter, suggesting the requirement of additional signals. Concurrent with this suggestion, we found that LPS and zymosan, two physiological inducers of β-catenin, caused an increase in the expression of genes that are positively regulated by β-catenin.

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“…Since that time, several more family members have been identified and found to play central roles in development. In mammals, chicken, and Xenopus, four members of the family have been identified: T-cell factor-1 (Tcf1, which has since been renamed Tcf7 in human and will be referred to henceforth using this nomenclature), Lymphoid Enhancer Factor-1 (Lef1), Tcf3 and Tcf4 (Travis et al, 1991;van de Wetering et al, 1991;Waterman et al, 1991;Castrop et al, 1992;Korinek et al, 1998b;Roel et al, 2003). Four members of this family have also been described in zebrafish: Lef1, Tcf3 (Headless), Tcf3b, and Tcf4 (Dorsky et al, 1999(Dorsky et al, , 2003Kim et al, 2000;Young et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Expression pattern of zebrafishtcf7 suggests unexplored domains of Wnt/?-catenin activity

et al. 2005

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Tcf/Lef transcription factors play an important role in mediating canonical Wnt signaling. When bound by ␤-catenin, Tcf/Lef proteins either activate or de-repress gene transcription. In zebrafish, four members have been identified: Lef1, Tcf3, Tcf3b, and Tcf4. Here, we report the cloning and expression of the tcf7 gene. Forms of Tcf7 expressed in the embryo contain two highly conserved regions: an N-terminal ␤-catenin binding domain and a C-terminal HMG domain. Tcf7 lacks a putative Groucho corepressor binding site, suggesting that, like Lef1, it functions as a transcriptional activator. We isolated three C-terminal splice variants of tcf7 corresponding to human B, C, and D isoforms. tcf7 expression overlaps with lef1 expression maternally, in the tail bud, fin buds, and paraxial mesoderm, and we expect that the two genes function redundantly in those areas. tcf7 is also expressed in nonoverlapping areas such as the prechordal mesoderm, dorsal retina, and median fin fold, suggesting unique functions. Developmental Dynamics 233: 233-239, 2005.

show abstract

A gene family of HMG-box transcription factors with homology to TCF-1

Cited by 51 publications

References 4 publications

Development of several organs that require inductive epithelial-mesenchymal interactions is impaired in LEF-1-deficient mice.

Development of several organs that require inductive epithelial-mesenchymal interactions is impaired in LEF-1-deficient mice.

Regulation and Possible Function of β-Catenin in Human Monocytes

Expression pattern of zebrafishtcf7 suggests unexplored domains of Wnt/?-catenin activity

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