Functional analysis of a novel KRAB/C2H2 zinc finger protein Mipu1

Jiang, Lei; Tang, Daolin; Wang, Kangkai; Zhang, Huali; Yuan, Cheng; Duan, Dayue Darrel; Xiao, Xianzhong

doi:10.1016/j.bbrc.2007.02.138

Cited by 21 publications

(36 citation statements)

References 20 publications

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“…Approximately one-third of C2H2-ZFPs exhibit KRAB motifs at their N-termini (23). The KRAB domain functions (8). It was reported that preconditioning may downregulate genes that control metabolism, cell-cycle and ion channel activity (25).…”

Section: Discussionmentioning

confidence: 99%

“…Zinc finger protein 667 (ZNF667) is a novel C2H2 zinc finger protein that is upregulated in rat hearts during myocardial IPC (6,7). It was demonstrated that ZNF667 binds to a consensus DNA sequence and represses the reporter gene expression, indicating that ZNF667 may function as a transcriptional repressor (8). To the best of our knowledge, there are no studies available on the ZNF667 expression pattern in brain IPC and the functional role of ZNF667 in IPC has not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

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Zinc finger protein 667 expression is upregulated by cerebral ischemic preconditioning and protects cells from oxidative stress

et al. 2013

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Abstract. Brain ischemic injury is associated with clinical emergencies such as acute ischemic and hemorrhagic stroke, head trauma, prolonged severe hypotension and cardiac arrest. Ischemic preconditioning (IPC) is the most powerful endogenous mechanism against ischemic injury. However, the majority of IPC treatments are invasive and thus impractical in the clinical setting. Identifying the endogenous neuroprotective mechanism induced by IPC is important for developing new strategies to reduce stroke severity. Zinc finger protein 667 (ZNF667) is a novel zinc finger protein that is upregulated by myocardial IPC. However, its functional role in neuronal ischemia has not been elucidated. In this study, the changes of ZNF667 expression on cerebral IPC and its potential neuroprotective function were investigated. The cerebral ischemia model was established by ameliorated four-vessel occlusion in rats. The northern blot results demonstrated that ZNF667 expression was increased in the hippocampus and cortex at 12 and 24 h after cerebral ischemic pretreatment. To investigate the neuroprotective function of ZNF667, enhanced green fluorescent protein (EGFP)-ZNF667 fusion protein was expressed in C2C12 and brain astrocytoma cells and its subcellular localization was detected by confocal microscopy. EGFP-ZNF667 fusion proteins were localized in the nucleus of C2C12 and brain astrocytoma cells, indicating that ZNF667 may act as a transcription factor in neural cells. To mimic oxidative stress associated with ischemia/reperfusion injury, hydrogen peroxide (H 2 O 2 ) was used to treat cells. Cell viability was measured by the lactate dehydrogenase (LDH) and WST-1 assays. A decrease in viability was detected in C2C12 and astrocytoma cells following H 2 O 2 treatment, whereas ZNF667 gene overexpression significantly improved cell viability following H 2 O 2 treatment. These results suggested that ZNF667 plays a neuroprotective role by acting as a transcription factor in cerebral IPC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Zinc finger protein 667 expression is upregulated by cerebral ischemic preconditioning and protects cells from oxidative stress

et al. 2013

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“…The Mipu1 gene was composed of five exons and four introns with an open reading frame of 1827 bp, and mapped to chromosome 1q12.1, encoding a 608 amino acid polypeptide with an N-terminal KRAB domain and 14 C-terminal C 2 H 2 zinc fingers. Jiang et al (5) used a Mipu1 fusion protein, GST-Mipu1, immobilized on glutathione-bound Sepharose beads to capture specific oligonucleotide sequences from a random oligonucleotide library. These studies confirmed that Mipu1 could bind specifically to the consensus sequence 5'-TGTCTTATCG AA-3', with TCTTA as the core sequence, which suggested that Mipu1 might act as a transcriptional repressor.…”

Section: Discussionmentioning

confidence: 99%

“…AY221750). Jiang et al (5) reported that Mipu1 was a nuclear and DNA binding protein that bound a specific DNA sequence, TGTCTTATCGAA, with TCTTA as the core sequence. This suggested that Mipu1 might function as a transcription factor.…”

Section: Introductionmentioning

confidence: 99%

Tissue expression and subcellular localization of Mipu1, a novel myocardial ischemia-related gene

Wang

Zuo

Jiang

et al. 2009

Braz J Med Biol Res

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“…It has also been demonstrated that the Mipu1 protein functions as a transcriptional repressor. This repressive function was mediated via binding to its specific DNA-binding site (5 0 -TGTCTTATCGAA-3 0 ) in the promoter region [7]. Cells stably transfected with Mipu1 are more resistant to oxidative injury compared with vector controls in terms of decreased lactate dehydrogenase release and apoptosis [6].…”

Section: Introductionmentioning

confidence: 99%

Identification and characterization of the minimal promoter of <italic>Mipu1</italic>: the role of GC boxes in the regulation of basal transcription

Lv¹,

Tang²,

Li³

et al. 2009

ABBS

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Mipu1, a novel gene encoding a KRAB/C2H2 zincfinger protein, was first reported to be up-regulated in myocardial ischemia-reperfusion injury, functioning to protect cells against oxidative stress. To map the promoter region of the gene and to understand its regulation, we identified the transcription start site and revealed that the 1366-bp fragment upstream of the transcription start site possesses promoter activity. Deletion constructs of the 5 0 -flanking region of Mipu1 lead to the identification of a minimal promoter, in which neither a TATA box nor a CAAT box was detected. Two GC boxes were found; however, they are the specific binding sites for Sp1-family transcription factors. Mutations in these GC boxes resulted in the total loss of Mipu1 minimal promoter activity. Finally, WP631, an Sp1-family-specific inhibitor, was found to decrease the promoter activity in a dose-dependent manner, indicating that the GC boxes are essential for the activity of the Mipu1 minimal promoter activity.

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Functional analysis of a novel KRAB/C2H2 zinc finger protein Mipu1

Cited by 21 publications

References 20 publications

Zinc finger protein 667 expression is upregulated by cerebral ischemic preconditioning and protects cells from oxidative stress

Zinc finger protein 667 expression is upregulated by cerebral ischemic preconditioning and protects cells from oxidative stress

Tissue expression and subcellular localization of Mipu1, a novel myocardial ischemia-related gene

Identification and characterization of the minimal promoter of <italic>Mipu1</italic>: the role of GC boxes in the regulation of basal transcription

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Functional analysis of a novel KRAB/C2H2 zinc finger protein Mipu1

Cited by 21 publications

References 20 publications

Zinc finger protein 667 expression is upregulated by cerebral ischemic preconditioning and protects cells from oxidative stress

Zinc finger protein 667 expression is upregulated by cerebral ischemic preconditioning and protects cells from oxidative stress

Tissue expression and subcellular localization of Mipu1, a novel myocardial ischemia-related gene

Identification and characterization of the minimal promoter of &lt;italic&gt;Mipu1&lt;/italic&gt;: the role of GC boxes in the regulation of basal transcription

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Identification and characterization of the minimal promoter of <italic>Mipu1</italic>: the role of GC boxes in the regulation of basal transcription