HGNC Approved Gene Symbol:AATF
Cytogenetic location:17q12 Genomic coordinates(GRCh38) :17:36,948,954-37,056,871 (from NCBI)
AATF is a nuclear protein involved in the regulation of gene transcription and cell proliferation (Di Padova et al., 2003).
By yeast 2-hybrid analysis using RPB11 (604150), a core subunit of RNA polymerase II, as bait, followed by 5-prime RACE,Fanciulli et al. (2000) cloned AATF, which they called CHE1, from a skeletal muscle cDNA library. The deduced 558-amino acid protein has a calculated molecular mass of about 62.3 kD. CHE1 contains a canonical leucine zipper motif and 3 nuclear receptor-binding LxxLL consensus sequences distributed throughout the protein. Northern blot analysis detected a 2.1-kb transcript expressed at high levels in heart, skeletal muscle, and testis, and at lower levels in all other tissues analyzed.
By differential display for genes downregulated by TGFB (190180) in an intestinal crypt epithelial cell line,Lindfors et al. (2000) cloned AATF. The AATF transcript contains several 4-nucleotide repeats, and the deduced 560-amino acid protein contains a leucine zipper motif, several phosphorylation sites, a nuclear localization signal, and 3 nuclear receptor LxxLL binding motifs. Northern blot analysis detected a 2.4-kb transcript in all normal tissues examined.
Monaco et al. (2003) cloned mouse Che1, which encodes a deduced 526-amino acid protein. Northern blot analysis detected ubiquitous expression, with highest levels in heart, brain, lung, and testis.
By mutation analysis,Fanciulli et al. (2000) determined that the leucine-rich C-terminal alpha motif of RPB11 bound CHE1. They found that CHE1 bound the retinoblastoma susceptibility gene, RB1 (614041), by 2 distinct domains in vitro and in vivo. CHE1 countered the growth suppression function of RB1 by reversing the inhibitory effect of RB1 on E2F1 (189971), a transcription factor critical for G1/S transition.
Using mouse fibroblasts cotransfected with promoter reporter constructs and with human CHE1,Monaco et al. (2003) demonstrated that overexpression of CHE1 inhibited the activity of its own promoter. Chromatin immunoprecipitation assays confirmed that CHE1 exerted its inhibitory effect by binding its own promoter.
Di Padova et al. (2003) found that CHE1 expression was downregulated in several tumors, including colon and kidney carcinomas, compared with matched normal tissues. CHE1 overexpression inhibited proliferation in 2 colon carcinoma cell lines by activating the cyclin-dependent kinase inhibitor WAF1 (CDKN1A;116899) in a p53 (190070)-dependent manner and by promoting growth arrest at the G1 phase of the cell cycle. CHE1 activated WAF1 by displacing histone deacetylase-1 (HDAC1;601241) from the Sp1 (189906)-binding sites of the WAF1 promoter and accumulating histone H3 (see602810) on these sites. Downregulation of CHE1 by interfering RNA inhibited WAF1 transactivation and increased cell proliferation.Di Padova et al. (2003) concluded that CHE1 is a general HDAC1 competitor.
Monaco et al. (2003) determined that the mouse Aatf gene contains 13 exons and spans 35 kb. The promoter region contains no TATA or CAAT boxes.
By FISH,Lindfors et al. (2000) mapped the AATF gene to chromosome 17q11.2-q12, centromeric to the ERBB2 gene (164870).Monaco et al. (2003) mapped the mouse Aatf gene to chromosome 11, near the Lim1 gene (601999).
Di Padova, M., Bruno, T., De Nicola, F., Iezzi, S., D'Angelo, C., Gallo, R., Nicosia, D., Corbi, N., Biroccio, A., Floridi, A., Passananti, C., Fanciulli, M.Che-1 arrests human colon carcinoma cell proliferation by displacing HDAC1 from the p21(WAF1/CIP1) promoter. J. Biol. Chem. 278: 36496-36504, 2003. [PubMed:12847090,related citations] [Full Text]
Fanciulli, M., Bruno, T., Di Padova, M., De Angelis, R., Iezzi, S., Iacobini, C., Floridi, A., Passananti, C.Identification of a novel partner of RNA polymerase II subunit 11, Che-1, which interacts with and affects the growth suppression function of Rb. FASEB J. 14: 904-912, 2000. [PubMed:10783144,related citations] [Full Text]
Lindfors, K., Halttunen, T., Huotari, P., Nupponen, N., Vihinen, M., Visakorpi, T., Maki, M., Kainulainen, H.Identification of novel transcription factor-like gene from human intestinal cells. Biochem. Biophys. Res. Commun. 276: 660-666, 2000. [PubMed:11027528,related citations] [Full Text]
Monaco, L., Passananti, C., Fanciulli, M.Genomic structure and transcriptional regulation of Che-1, a novel partner of Rb. Gene 321: 57-63, 2003. [PubMed:14636992,related citations] [Full Text]
Alternative titles; symbols
HGNC Approved Gene Symbol: AATF
Cytogenetic location: 17q12 Genomic coordinates(GRCh38) : 17:36,948,954-37,056,871(from NCBI)
AATF is a nuclear protein involved in the regulation of gene transcription and cell proliferation (Di Padova et al., 2003).
By yeast 2-hybrid analysis using RPB11 (604150), a core subunit of RNA polymerase II, as bait, followed by 5-prime RACE, Fanciulli et al. (2000) cloned AATF, which they called CHE1, from a skeletal muscle cDNA library. The deduced 558-amino acid protein has a calculated molecular mass of about 62.3 kD. CHE1 contains a canonical leucine zipper motif and 3 nuclear receptor-binding LxxLL consensus sequences distributed throughout the protein. Northern blot analysis detected a 2.1-kb transcript expressed at high levels in heart, skeletal muscle, and testis, and at lower levels in all other tissues analyzed.
By differential display for genes downregulated by TGFB (190180) in an intestinal crypt epithelial cell line, Lindfors et al. (2000) cloned AATF. The AATF transcript contains several 4-nucleotide repeats, and the deduced 560-amino acid protein contains a leucine zipper motif, several phosphorylation sites, a nuclear localization signal, and 3 nuclear receptor LxxLL binding motifs. Northern blot analysis detected a 2.4-kb transcript in all normal tissues examined.
Monaco et al. (2003) cloned mouse Che1, which encodes a deduced 526-amino acid protein. Northern blot analysis detected ubiquitous expression, with highest levels in heart, brain, lung, and testis.
By mutation analysis, Fanciulli et al. (2000) determined that the leucine-rich C-terminal alpha motif of RPB11 bound CHE1. They found that CHE1 bound the retinoblastoma susceptibility gene, RB1 (614041), by 2 distinct domains in vitro and in vivo. CHE1 countered the growth suppression function of RB1 by reversing the inhibitory effect of RB1 on E2F1 (189971), a transcription factor critical for G1/S transition.
Using mouse fibroblasts cotransfected with promoter reporter constructs and with human CHE1, Monaco et al. (2003) demonstrated that overexpression of CHE1 inhibited the activity of its own promoter. Chromatin immunoprecipitation assays confirmed that CHE1 exerted its inhibitory effect by binding its own promoter.
Di Padova et al. (2003) found that CHE1 expression was downregulated in several tumors, including colon and kidney carcinomas, compared with matched normal tissues. CHE1 overexpression inhibited proliferation in 2 colon carcinoma cell lines by activating the cyclin-dependent kinase inhibitor WAF1 (CDKN1A; 116899) in a p53 (190070)-dependent manner and by promoting growth arrest at the G1 phase of the cell cycle. CHE1 activated WAF1 by displacing histone deacetylase-1 (HDAC1; 601241) from the Sp1 (189906)-binding sites of the WAF1 promoter and accumulating histone H3 (see 602810) on these sites. Downregulation of CHE1 by interfering RNA inhibited WAF1 transactivation and increased cell proliferation. Di Padova et al. (2003) concluded that CHE1 is a general HDAC1 competitor.
Monaco et al. (2003) determined that the mouse Aatf gene contains 13 exons and spans 35 kb. The promoter region contains no TATA or CAAT boxes.
By FISH, Lindfors et al. (2000) mapped the AATF gene to chromosome 17q11.2-q12, centromeric to the ERBB2 gene (164870). Monaco et al. (2003) mapped the mouse Aatf gene to chromosome 11, near the Lim1 gene (601999).
Di Padova, M., Bruno, T., De Nicola, F., Iezzi, S., D'Angelo, C., Gallo, R., Nicosia, D., Corbi, N., Biroccio, A., Floridi, A., Passananti, C., Fanciulli, M.Che-1 arrests human colon carcinoma cell proliferation by displacing HDAC1 from the p21(WAF1/CIP1) promoter. J. Biol. Chem. 278: 36496-36504, 2003. [PubMed: 12847090] [Full Text: https://doi.org/10.1074/jbc.M306694200]
Fanciulli, M., Bruno, T., Di Padova, M., De Angelis, R., Iezzi, S., Iacobini, C., Floridi, A., Passananti, C.Identification of a novel partner of RNA polymerase II subunit 11, Che-1, which interacts with and affects the growth suppression function of Rb. FASEB J. 14: 904-912, 2000. [PubMed: 10783144] [Full Text: https://doi.org/10.1096/fasebj.14.7.904]
Lindfors, K., Halttunen, T., Huotari, P., Nupponen, N., Vihinen, M., Visakorpi, T., Maki, M., Kainulainen, H.Identification of novel transcription factor-like gene from human intestinal cells. Biochem. Biophys. Res. Commun. 276: 660-666, 2000. [PubMed: 11027528] [Full Text: https://doi.org/10.1006/bbrc.2000.3480]
Monaco, L., Passananti, C., Fanciulli, M.Genomic structure and transcriptional regulation of Che-1, a novel partner of Rb. Gene 321: 57-63, 2003. [PubMed: 14636992] [Full Text: https://doi.org/10.1016/s0378-1119(03)00834-5]
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