ATF-7, a Novel bZIP Protein, Interacts with the PRL-1 Protein-tyrosine Phosphatase

Peters, Charles S.; Liang, Xianping; Li, Shuixing; Kannan, Subburaj; Peng, Yong; Taub, Rebecca; Diamond, Robert H.

doi:10.1074/jbc.m011562200

Cited by 72 publications

(90 citation statements)

References 66 publications

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“…ATF5 overexpression has also been shown in malignant CLL cells compared to normal B-cells when activated with CD40 ligand (22). As it is well known that many cellular processes such as cell cycle, gene expression, protein synthesis and cellular transport are regulated through phosphorylation, ATF5 has also been identified as a factor which physically interacts with protein-tyrosine phosphatase (PTPase) (20).…”

Section: Discussionmentioning

confidence: 99%

“…ATF5 was the most highly overexpressed gene in the poor outcome group. ATF5, also known as ATFx or ATF7, is a member of the activating transcriptional factor or cAMP response element-binding (ATF/CREB) family of basic leucine zipper (bZIP) protein (19,20). Its role has been shown to regulate the differentiation process (19) and to inhibit apoptosis (21).…”

Section: Discussionmentioning

confidence: 99%

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Molecular basis of aggressive disease in chronic lymphocytic leukemia patients with 11q deletion and trisomy 12 chromosomal abnormalities

et al. 2007

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Abstract. In B-cell chronic lymphocytic leukemia (CLL), Rai stage, immunoglobulin gene mutational status, chromosomal abnormalities, CD38 and ZAP-70 expression were used as prognostic markers. In this study, to understand the molecular basis of chromosomal abnormalities leading to tumor progression, 90 CLL patients were grouped into poor prognosis (with 11q deletion and trisomy 12) and good prognosis (with normal karyotype and 13q deletion) and their clinical outcome was assessed. Gene expression profiles of 35 CLL samples with poor outcome (11q deletion, n=9; trisomy 12, n=5) and good outcome (13q deletion, n=13; normal karyotype, n=8) were analyzed using oligonucleotide microarray. Significance analysis of microarray (SAM) identified 27 differentially expressed genes between these two subgroups with significant overexpression of ATF5 and underexpression of CDC16, PCDH8, SLAM, MNDA and ATF2 in CLL patients with poor outcome. ATF5 gene expression in CLL was further studied because of its role in the regulation of cell cycle progression/differentiation and apoptosis. The overexpression of ATF5 was confirmed by real-time PCR using 39 CLL samples from the poor and good outcome groups. ATF5 was significantly (p<0.001) overexpressed in the poor outcome group. Furthermore, ATF5 expression was significantly higher in the 11q deletion as well as trisomy 12 group alone compared to the 13q deletion and normal karyotype groups. ATF5 overexpression was also associated with significantly (p=0.04) shorter time to treatment. Similarly, expression of five underexpressed genes also correlated with longer time to treatment. Thus, this report demonstrates that ATF5 may be one of the key genes involved in increased proliferation and survival in 11q deletion or trisomy 12, whereas CD16, CD86, SLAM, MNDA and ATF2 may be involved in the decreased proliferation of CLL cells with 13q deletion or normal karyotype.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Molecular basis of aggressive disease in chronic lymphocytic leukemia patients with 11q deletion and trisomy 12 chromosomal abnormalities

et al. 2007

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“…54 ATF7 interacts with the stress activated kinase JNK2, 55 with PRL1 a protein tyrosine phosphatase involved in growth control and E1A. 56,57 The transcriptional activity of ATF7 is potentiated by expression of TAF12, the TAF4 heterodimerization partner, but not by TAF4. 58 TAF12 interacts directly with ATF7 and they associate cooperatively on the ATF7-dependent E-selectin promoter.…”

Section: Taf4 As a Positive And Negative Modulator Of Camp And Retinomentioning

confidence: 99%

New Insights into TAFs as Regulators of Cell Cycle and Signalling Pathways

Davidson

Kobi²,

Fadloun³

et al. 2005

Cell Cycle

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RNA polymerase II general transcription factor TFIID is a macromolecular complex comprising the TATA-binding protein, TBP and 13-14 evolutionary conserved TBP-associated factors, TAFs. Although genetic experiments have shown that TAFs are essential for cell cycle progression in yeast and in rapidly proliferating vertebrate cells in vitro, new experiments indicate they may be dispensible in specific developmental and physiological processes. Moreover, the TAF4 subunit of TFIID negatively regulates proliferation by inhibiting activation of the TGFβ signalling pathway by its paralogue TAF4b. TAF4 is however essential in the retinoic acid and cAMP signalling pathways acting as a cofactor for CREB and the retinoic acid receptor, but is a negative regulator of the ATF7 transcription factor.

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“…Recently, we have used expression profiling to analyze gene expression in interleukin-3 (IL-3)-dependent murine FL5.12 cells following cytokine deprivation (Devireddy et al 2001). Among the most dramatic changes was the decreased expression of ATFx (also known in murine cells as ATF7 [Peters et al 2001] and in human cells as hATF5 [Pati et al 1999]), a member of the ATF/CREB family of transcription factors, raising the possibility that ATFx has a role in cell survival. Here we test this idea and study the role of ATFx in apoptosis.…”

mentioning

confidence: 99%

Inhibition of apoptosis by ATFx: a novel role for a member of the ATF/CREB family of mammalian bZIP transcription factors

Persengiev¹,

Devireddy²,

Green³

2002

Genes Dev.

103

101

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The mammalian ATF/CREB family of transcription factors comprises a large group of basic-region leucine zipper (bZIP) proteins whose members mediate diverse transcriptional regulatory functions. Here we report that expression of a specific mouse ATF gene, ATFx, is down-regulated in a variety of cells undergoing apoptosis following growth factor deprivation. When stably expressed in an interleukin 3 (IL-3)-dependent cell line, ATFx suppresses apoptosis resulting from cytokine deprivation. Conversely, a dominant-negative ATFx mutant induces apoptosis of cells cultured in the presence of growth factors. We also show that 24p3, a secreted lipocalin that induces apoptosis when added to hematopoietic cells, represses ATFx expression. However, constitutive expression of ATFx renders cells resistant to 24p3-mediated apoptosis. Collectively, our results indicate that ATFx is an anti-apoptotic factor, a novel role for an ATF protein.

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ATF-7, a Novel bZIP Protein, Interacts with the PRL-1 Protein-tyrosine Phosphatase

Cited by 72 publications

References 66 publications

Molecular basis of aggressive disease in chronic lymphocytic leukemia patients with 11q deletion and trisomy 12 chromosomal abnormalities

Molecular basis of aggressive disease in chronic lymphocytic leukemia patients with 11q deletion and trisomy 12 chromosomal abnormalities

New Insights into TAFs as Regulators of Cell Cycle and Signalling Pathways

Inhibition of apoptosis by ATFx: a novel role for a member of the ATF/CREB family of mammalian bZIP transcription factors

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