High impact information on TAF10

• Human TAFII30 is present in a distinct TFIID complex and is required for transcriptional activation by the estrogen receptor [1].
• The binding of hTAFII28 and hTAFII30 requires distinct domains of hTAFII18 [2].
• Thus, here we describe a novel role of the three mammalian interacting partners in the nuclear localization of TAF10, and our data suggest that a complex network of regulated cytoplasmic associations may exist among these factors and that this network is important for the composition of different TFIID and TFTC-type complexes in the nucleus [3].
• The nuclear import of TAF10 is regulated by one of its three histone fold domain-containing interaction partners [3].
• In human cells, exogenously expressed TAF10 remains rather cytoplasmic and leptomycin B does not affect this localization [3].

Biological context of TAF10

• Using in situ hybridization on human metaphase chromosomes, the TAF2H gene has been localized in the 11p15.2-p15.5 region of the human genome [4].
• Different temperature-sensitive mutations of yTAF(II)25 or chimeras with the human homologue TAF(II)30 arrested cell growth at either the G(1) or G(2)/M cell cycle phase and displayed distinct phenotypic changes and gene expression patterns [5].
• Assignment of the human TAFII30 gene (TAF2H) to human chromosome band 11p15.3 using somatic cell hybrids [6].
• Detection of an EcoRI restriction fragment length polymorphism in the gene encoding the human TBP associated factor II 30 (TAF(II)30) [7].

Anatomical context of TAF10

• The cytoplasmic-nuclear transport of TAF10 is naturally observed during the differentiation of adult male germ cells [3].

Physical interactions of TAF10

• We find that TAF(II)30 has no effect on ER-ERE binding either alone or in combination with ER and HMG-1 [8].

Other interactions of TAF10

• The effect of high-mobility group (HMG) protein HMG-1 and purified recombinant TATA-binding protein-associated factor TAF(II)30 on ER-ERE binding and transcription initiation were assessed by electrophoretic mobility shift assay and in vitro transcription from an ERE-containing template (pERE2LovTATA), respectively [8].
• A number of other elements were found to be located in close proximity to CLN2, including the gene encoding transcription factor TAFII30, the gene encoding intregrin-linked kinase, and an approximately 914-bp fragment that is 82% identical to antithrombin III [9].
• In addition, we found changes on mRNA level for several transcription regulators, including early growth response genes 1 and 2, TAFII30 and topoisomerase I. Furthermore, we show accumulation of mRNA for the phosphatases CD45 and DUSP5 in anti-IgM stimulated BL60-2 cells [10].

Analytical, diagnostic and therapeutic context of TAF10

• Using a combination of protein affinity chromatography and cotransfection and immunoprecipitation assays, we have identified a series of in vitro and intracellular interactions among the novel hTAFIIs and between the novel hTAFIIs and hTAFII30 or TBP [2].

References