Identification of apoptosis-related PLZF target genes

Bernardo, María Victoria; Yelo, Estefania; Gimeno, Lourdes; Campillo, José A.; Parrado, Antonio

doi:10.1016/j.bbrc.2007.05.085

Cited by 36 publications

(34 citation statements)

References 16 publications

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“…Furthermore, NKT cells are not dependent on PLZF to undergo proliferation, as has been shown in PLZF-deficient mice (16,17). Indeed, PLZF has been reported to inhibit cell cycle progression (45,46) and to cause cell quiescence (47) and suppression of cell growth (48). Therefore, it is possible that the NKT cell proliferative burst is actually dependent on the rapid downregulation of PLZF that we reported (16).…”

Section: Discussionsupporting

confidence: 61%

PLZF Induces the Spontaneous Acquisition of Memory/Effector Functions in T Cells Independently of NKT Cell-Related Signals

Kovalovsky

Alonzo

Uche

et al. 2010

The Journal of Immunology

102

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The broad complex, tramtrack, bric-a-brac–zinc finger (BTB-ZF) transcription factor promyelocytic leukemia zinc finger (PLZF) is required for development of the characteristic innate/effector functions of NKT cells. In this study, we report the characterization and functional analysis of transgenic mouse T cells with forced expression of PLZF. PLZF expression was sufficient to provide some memory/effector functions to T cells without the need for Ag stimulation or proliferation. The acquisition of this phenotype did not require the proliferation typically associated with T cell activation. Furthermore, PLZF transgenic cells maintained a diverse TCR repertoire, indicating that there was no preferential expansion of specific clones. Functionally, PLZF transgenic CD4 and CD8 lymphocytes were similar to wild type memory cells, in that they had similar requirements for costimulation and exhibited a similar pattern of cytokine secretion, with the notable exception that transgenic T cells produced significantly increased levels of IL-17. Whereas transgene-mediated PLZF expression was not sufficient to rescue NKT cell development in Fyn- or signaling lymphocytic activation-associated protein (SAP)-deficient mice, the acquisition of memory/effector functions induced by PLZF in conventional T cells was independent of Fyn and SAP. These data show that PLZF is sufficient to promote T cell effector functions and that PLZF acts independently of SAP- and Fyn-mediated signaling pathways.

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Section: Discussionsupporting

confidence: 61%

PLZF Induces the Spontaneous Acquisition of Memory/Effector Functions in T Cells Independently of NKT Cell-Related Signals

Kovalovsky

Alonzo

Uche

et al. 2010

The Journal of Immunology

102

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“…Although PLZF has little effect on apoptosis in HEK293 cells, PLZF can induce apoptosis and increase p21 expression in Jurkat cells, as reported by others in hematopoietic cells (Fig. 10) (36). Interestingly in Jurkat cells, PLZF repressed TP53 very weakly and also showed little effect on acetylation of p53.…”

Section: Discussionmentioning

confidence: 55%

Role of Promyelocytic Leukemia Zinc Finger (PLZF) in Cell Proliferation and Cyclin-dependent Kinase Inhibitor 1A (p21WAF/CDKN1A) Gene Repression

Choi

Kim

Jeon

et al. 2014

Journal of Biological Chemistry

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Background: Promyelocytic leukemia zinc finger (PLZF) is transcription repressor that recruits nuclear co-repressors at the target promoters. PLZF is overexpressed in various human solid tumors, such as clear cell renal carcinoma, glioblastoma, and seminoma. Results: PLZF represses transcription of CDKN1A by inhibition of p53 acetylation, Sp1 binding. Conclusion: PLZF causes cellular transformation and increases cell proliferation by repressing transcription of CDKN1A. Significance: PLZF can act as a proto-oncogene depending on the cell types.

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“…A fragment of PLZF (aa322-528) was confirmed as an interacting partner of LYRIC/ AEG-1 through a b-galactosidase assay ( Figure 1b). PLZF is a transcriptional repressor associated with growth suppression and apoptosis (Shaknovich et al, 1998;Bernardo et al, 2007), regulating many genes including c-myc Bernardo et al, 2007). PLZF contains a BTB/POZ domain at the N terminus amino acids 34-96 (aa34-96), an RD2 domain (aa200-300) and 9 DNA-binding zinc fingers at the C terminus (aa404-652; Figure 1).…”

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confidence: 99%

“…LYRIC/AEG-1 has been shown to be overexpressed during tumourigenesis (Li et al, 2008;Hu et al, 2009;Thirkettle et al, 2009) and our results suggest that this may lead to a reduction in PLZF-mediated repression. This would increase oncogene expression such as c-myc and a decrease in genes involved in apoptosis (Bernardo et al, 2007) (Figure 4d). C-myc has been shown to bind the promoter region of LYRIC/AEG-1 and regulate its expression (Lee et al, 2006).…”

mentioning

confidence: 99%