Disease relevance of Tcfap2c

• AP-2gamma (Tcfap2c - Mouse Genome Informatics) is a retinoic acid-responsive gene implicated in placental development and the progression of human breast cancer [1].
• A 2.8-kb cDNA encoding a new transcription factor (AP-2.2) has been cloned from mouse P19 embryonal carcinoma cells, in which the corresponding mRNA begins to accumulate 30 min after retinoic acid (RA) addition [2].
• Expression of AP-2.2 in Escherichia coli generated a protein that formed a specific complex with the AP-2 recognition site GCCN3GGC [2].

High impact information on Tcfap2c

• Analysis of embryo cultures suggests that AP-2 gamma is also implicated in the regulation of the adenosine deaminase (ADA) gene, a gene involved in purine metabolism found expressed at the maternal-fetal interface [3].
• Therefore, AP-2 gamma seems to be required in early embryonic development because it regulates the genetic programs controlling proliferation and differentiation of extraembryonic trophectodermal cells [3].
• AP-2 gamma had been implicated in multiple functions during proliferation and differentiation based on its expression pattern in trophoblast, neural crest, and ectoderm cells in murine embryos [3].
• Transcription factor gene AP-2 gamma essential for early murine development [3].
• Site-specific mutations in each of the binding sites eliminated enhancer activity indicating that AP-2 gamma and Dlx 3, together with an additional transcription factor(s) that are conserved between humans and mice, are required for trophoblast-specific expression of 3 beta-HSD VI [4].

Biological context of Tcfap2c

• The majority of Tcfap2c(-/-) mice failed to survive beyond 8.5 days post coitum (d.p.c.). At 7.5 d.p.c., Tcfap2c(-/-) mutants were typically arrested or retarded in their embryonic development in comparison to controls [1].
• Transcriptional activation required the AP-2.2 amino-terminal region that contains a domain rich in proline and glutamine residues [2].
• We have also shown that the AP-2.2 protein, which is highly related to the AP-2 transcription factor, can activate transcription when bound to an AP-2 consensus binding site [Oulad-Abdelghani et al. (1995) Mol. Cell. Biol., submitted] [5].
• AP-2.2 gene expression was weak throughout the brain [6].
• Proteomic identification of AP2 gamma as a rat placental lactogen II trophoblast cell-specific enhancer binding protein [7].

Anatomical context of Tcfap2c

• Redundant activities of Tfap2a and Tfap2c are required for neural crest induction and development of other non-neural ectoderm derivatives in zebrafish embryos [8].
• Here we show that zebrafish tfap2c, encoding AP-2 gamma (Tfap2c), is expressed in non-neural ectoderm including transiently in neural crest [8].
• The pattern of AP-2.2 expression in adult tissues, which is distinct from that of AP-2alpha, is essentially restricted to male and female gonads, to most if not all the squamous epithelia, and to several exocrine glands [2].
• AP-2.2 RNA was also specifically expressed in the presumptive cortical region of the forebrain vesicles [5].
• AP-2.2 transcripts were restricted to the distal mitotic area (the 'progress zone') of the limb buds and of the genital bud [5].

Other interactions of Tcfap2c

• Using a differential subtractive hybridization cloning procedure we have recently identified the AP-2.2 gene as a novel early retinoic acid-induced gene in murine P19 embryonal carcinoma cells [5].

Analytical, diagnostic and therapeutic context of Tcfap2c

• Further electrophoretic mobility shift assays identified AP-2 gamma and the homeodomain protein, Dlx 3, as the transcription factors that specifically bind to FPI and FPIII, respectively [4].
• AP-2 gamma heterozygous mice are viable and display reduced body sizes at birth but are fertile [3].
• We report here the in situ hybridization pattern of expression of AP-2.2 transcripts during mouse embryogenesis [5].
• Chromatin immunoprecipitation assays confirmed AP2 gamma occupancy of the enhancer region in situ in the nuclei of Rcho giant cells [7].

References