Nucleotide Sequence Analysis of a Candidate Gene for Ataxia-Telangiectasia Group D (ATDC)

Leonhardt, Edith A.; Kapp, Leon N.; Young, Barbara R.; Murnane, John P.

doi:10.1006/geno.1994.1022

Cited by 50 publications

(31 citation statements)

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“…Chromatin Extraction-HEK 293 cells expressing either ATDC or ATDC⌬C (lacking amino acids 348 -588) were irradiated with 10 Gy and incubated for different times (1,3,6, and 24 h). Proteins bound to chromatin were released by treatment with 0.2 N HCl and analyzed by Western blotting.…”

Section: Methodsmentioning

confidence: 99%

“…To determine whether IR induces ATDC nuclear translocation, HEK 293 cells expressing ATDC or ATDC⌬C were treated with IR (10 Gy) and the cytoplasmic and nuclear fractions were isolated at various time points (1,3,6, and 24 h) following IR. We observed an increase in ATDC in the nuclear fraction starting at 1 h and increasing until 24 h after IR, which also corresponded to a decrease in the cytoplasmic portion of ATDC (Fig.…”

Section: Atdc Is Present In the Cytoplasm And Nucleus And Requires Itmentioning

confidence: 99%

“…Ataxia telangiectasia group D complementing (ATDC), also known as TRIM29, was identified for its capacity to induce resistance to IR in cells derived from patients with ataxia telangiectasia, a disorder characterized by ATM deficiency (6). ATDC (TRIM29) is a member of the tripartite motif (TRIM) protein family, which is defined by a conserved RING domain, one or two B-box domains, and a coiled-coil region (7).…”

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confidence: 99%

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ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

Yang

Palmbos

Wang

et al. 2015

Journal of Biological Chemistry

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Background: ATDC/TRIM29 promotes resistance to ionizing radiation, but the factor(s) that mediate this effect are incompletely understood. Results: ATDC/TRIM29 binds to RNF8, promoting DNA repair and resistance to IR. Conclusion: Following DNA damage, ATDC/TRIM29 is phosphorylated and interacts with RNF8, promoting DNA repair and cell survival. Significance: The interaction between ATDC/TRIM29 and RNF8 is novel and is important for the DNA damage response.

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Section: Methodsmentioning

confidence: 99%

Section: Atdc Is Present In the Cytoplasm And Nucleus And Requires Itmentioning

confidence: 99%

mentioning

confidence: 99%

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ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

Yang

Palmbos

Wang

et al. 2015

Journal of Biological Chemistry

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“…Although genetic linkage evidence did not support the hypothesis of genetic heterogeneity, the possibility of a cluster of genes at the 11q22-q23 locus could not be ruled out (McConvill et al 1994). The gene responsible for complementation of the D group (ATDC) was also mapped to chromosome 11q22-q23; however, the detailed location of the gene was outside of the major AT region for the other three AT groups (Kapp et al 1992;Leonhardt et al 1994). The candidate gene responsible for ATDC was cloned and analyzed but no mutation, so far, has been reported in this gene in ATD patients (Leonhardt et al 1994).…”

mentioning

confidence: 99%

“…The gene responsible for complementation of the D group (ATDC) was also mapped to chromosome 11q22-q23; however, the detailed location of the gene was outside of the major AT region for the other three AT groups (Kapp et al 1992;Leonhardt et al 1994). The candidate gene responsible for ATDC was cloned and analyzed but no mutation, so far, has been reported in this gene in ATD patients (Leonhardt et al 1994). Linkage analysis by suggested genetic heterogeneity with possible gene loci in the STMY-D11S132 interval for groups A and C and in the more distal D11S147-D11S133 interval for group D. In addition, Sanal et al (1992) concluded that at least two distinct loci, A and D, existed with perhaps a third locus very near the AT-A gene.…”

mentioning

confidence: 99%

Identification and characterization of a new gene physically linked to the ATM gene.

Imai¹,

Yamauchi²,

Seki³

et al. 1996

Genome Res.

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Ataxia telangiectasia [AT} is an autosomal recessive disease of unknown etiology associated with cerebellar ataxia, oculocutaneous telangiectasia, immunodeficiency, and hypersensitivity to ionizing radiation. Although AT has been divided into four complementation groups by its radioresistant-DNA synthesis phenotype, the ATM gene has been isolated as the candidate gene responsible for all AT groups. We identified a new gene, designated NPAT, from the major AT locus on human chromosome Ilq22-q23. The gene encoded a 1421-amino-acid protein containing nuclear localization signals and phosphorylation target sites by cyclin-dependent protein kinases associated with E2F. The messenger RNA of NPAT was detected in all human tissues examined, and its genomic sequence was strongly conserved through eukaryotes, suggesting that the NPAT gene may be essential for cell maintenance and may be a member of the housekeeping genes. Analysis of the genomic region of NPAT surprisingly revealed that the gene existed only 0.5 kb apart from the 5' end of the ATM transcript with opposite transcriptional direction, it may be possible to propose the idea that the promoter region could be shared by both housekeeping genes and that each gene could influence the expression of the other.

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Expression of theATDC (ataxia telangiectasia group D-complementing) gene in A431 human squamous carcinoma cells

Green

et al. 1996

Int. J. Cancer

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The ATDC gene was originally identified by its ability to complement the radiosensitivity defect of an ataxia telangiectasia (AT) fibroblast cell line. Because hypersensitivity to ionizing radiation is an important feature of the AT phenotype, we reasoned that ATDC may function generally in the suppression of radiosensitivity. Previous work in our laboratory focused on radiosensitization mechanisms in human squamous carcinoma (SC) cells, especially A431 cells. To establish a basis for investigating the role of ATDC in radiation-responsive signaling pathways in human SC cells, we characterized ATDC message and protein expressions in A431 cells. ATDC message expression was also compared among human epidermoid cells (A431 cells, HaCaT spontaneously immortalized human keratinocytes and normal human epidermal keratinocytes) and a normal human fibroblast cell line (LM217). We made the following major observations: (i) the relative abundance of ATDC message is substantially higher in the epidermoid cells than in the fibroblast cell line, which has a message level comparable to those reported for other fibroblast lines; (ii) ATDC is constitutively phosphorylated on serine/threonine in A431 cells; (iii) in A431 cells, ATDC is a substrate for the serine/threonine protein kinase C (PKC) but not the epidermal growth factor (EGF) receptor tyrosine kinase; and (iv) EGF decreases ATDC message and protein expressions in A431 cells after a 24-hr exposure. The phosphorylation studies suggest that the ability of ATDC to modulate cellular radiosensitivity may be mediated in part through a PKC signaling pathway.

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Nucleotide Sequence Analysis of a Candidate Gene for Ataxia-Telangiectasia Group D (ATDC)

Cited by 50 publications

References 0 publications

ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase

Identification and characterization of a new gene physically linked to the ATM gene.

Expression of theATDC (ataxia telangiectasia group D-complementing) gene in A431 human squamous carcinoma cells

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