ZNF552, a novel human KRAB/C2H2 zinc finger protein, inhibits AP-1- and SRE-mediated transcriptional activity

Deng, Yuan; Liu, Bisheng; Fan, Xiongwei; Wang, Yuequn; Ming, Tang; Mo, Xiaoyang; Li, Yongqing; Ying, Zaochu; Wan, Yongqi; Luo, Na; Zhou, Junmei; Wu, Xiushan; Yuan, Wuzhou

doi:10.5483/bmbrep.2010.43.3.193

Cited by 7 publications

(7 citation statements)

References 21 publications

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“…Recent experimental studies have demonstrated that several KRAB-containing proteins such as zinc finger protein 552 (ZNF552) (407 amino acids at length with one KRAB domain at the amino terminal and seven C2H2 zinc finger motifs at the carboxyl terminal), ZNF328 (792 amino acids at length with a N-terminal KRAB domain and classic C-terminal C2H2 zinc finger motifs), and ZNF649 (505 amino acids of protein with N-terminal KRAB domain and C-terminal C2H2 zinc finger motifs) significantly inhibited serum response element (SRE) and AP-1 activities in COS-7 kidney fibroblast cells [124,125,126]. AP-1 is one key transcription factor for redox signaling pathway.…”

Section: Molecular Mechanisms Of Zinc As An Anti-oxidative Stress mentioning

confidence: 99%

Molecular Mechanisms of Zinc as a Pro-Antioxidant Mediator: Clinical Therapeutic Implications

2019

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The essentiality of zinc as a trace mineral in human health has been recognized for over five decades. Zinc deficiency, caused by diet, genetic defects, or diseases, can cause growth retardation, delayed sexual maturation, depressed immune response, and abnormal cognitive functions in humans. Zinc supplementation in zinc-deficient individuals can overcome or attenuate these abnormalities, suggesting zinc is an essential micro-nutrient in the body. A large number of in vitro and in vivo experimental studies indicate that zinc deficiency also causes apoptosis, cellular dysfunction, deoxyribonucleic acid (DNA) damage, and depressed immune response. Oxidative stress, due to the imbalance of reactive oxygen species (ROS) production and detoxification in the anti-oxidant defense system of the body, along with subsequent chronic inflammation, is believed to be associated with many chronic degenerative diseases such as diabetes, heart diseases, cancers, alcohol-related disease, macular degenerative disease, and neuro-pathogenesis. A large number of experimental studies including cell culture, animal, and human clinical studies have provided supportive evidence showing that zinc acts as an anti-oxidative stress agent by inhibition of oxidation of macro-molecules such as (DNA)/ribonucleic acid (RNA) and proteins as well as inhibition of inflammatory response, eventually resulting in the down-regulation of (ROS) production and the improvement of human health. In this article, we will discuss the molecular mechanisms of zinc as an anti-oxidative stress agent or mediator in the body. We will also discuss the applications of zinc supplementation as an anti-oxidative stress agent or mediator in human health and disease.

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Section: Molecular Mechanisms Of Zinc As An Anti-oxidative Stress mentioning

confidence: 99%

Molecular Mechanisms of Zinc as a Pro-Antioxidant Mediator: Clinical Therapeutic Implications

2019

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“…19 Many zinc finger proteins have been demonstrated to be involved in transcription. 20 ZNF432 has been found to be associated with inflammatory bowel disease, at P= 8.3 × 10 −5 . 21 Thus, further study of these zinc finger proteins may provide insight on the mechanisms by which inhaled corticosteroids influence bronchodilator response.…”

Section: Discussionmentioning

confidence: 98%

Inhaled corticosteroid treatment modulates ZNF432 gene variant’s effect on bronchodilator response in asthmatics

Himes

Lasky‐Su

et al. 2014

Journal of Allergy and Clinical Immunology

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Background Single nucleotide polymorphisms (SNPs) influence a patient's response to inhaled corticosteroids and β2-agonists, and the effect of treatment with inhaled corticosteroids is synergistic with the effect of β2-agonists. We hypothesized that use of inhaled corticosteroids could influence the effect of SNPs associated with bronchodilator response. Objective To assess whether, among asthma subjects, the association of SNPs with bronchodilator response is different between those treated with inhaled corticosteroids vs. those on placebo. Methods A genome-wide association analysis was conducted using 581 white subjects from the Childhood Asthma Management Program (CAMP). Using data for 449,540 SNPs, we conducted a gene by environment analysis in PLINK with inhaled corticosteroid treatment as the environmental exposure and bronchodilator response as the outcome measure. We attempted to replicate the top 12 SNPs in the Leukotriene Modifier Or Corticosteroid or Corticosteroid-Salmeterol (LOCCS) Trial. Results The combined P-value for the CAMP and LOCCS populations was 4.81E-08 for rs3752120, which is located in the zinc finger protein gene ZNF432, and has unknown function. Conclusions Inhaled corticosteroids appear to modulate the association of bronchodilator response with variant(s) in the ZNF432 gene among adults and children with asthma. Clinical Implications Clinicians who treat asthma patients with inhaled corticosteroids should be aware that the patient's genetic makeup likely influences response as measured in lung function. Capsule Summary Our study suggests that inhaled corticosteroids could influence the effect of multiple SNPs associated with bronchodilator response across the genome.

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“…The ZNF proteins have a large number of motifs that include Cys2-His2, GATA, RanBP, A20, LIM, MYND, RING, PHD, and TAZ. Of these, the most common motifs are the Cys 2 -His 2 domain-containing ZNF proteins [4,5]. On the other hand, another conserved domain present in one-third of all ZNF proteins [6] is Krüppel-associated box (KRAB) [7].…”

Section: Introductionmentioning

confidence: 99%

Expression of ZNF695 Transcript Variants in Childhood B-Cell Acute Lymphoblastic Leukemia

Rosa¹,

Villegas-Ruíz²,

Caballero-Palacios³

et al. 2019

Genes

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B-cell acute lymphoblastic leukemia is the most commonly diagnosed childhood malignancy worldwide; more than 50% of these cases are diagnosed in Mexico. Although the five-year survival rate is >80%, 30% of patients experience relapse with poor prognosis. Cancer-associated gene expression profiles have been identified in several malignancies, and some transcripts have been used to predict disease prognosis. The human transcriptome is incompletely elucidated; moreover, more than 80% of transcripts can be processed via alternative splicing (AS), which increases transcript and protein diversity. The human transcriptome is divided; coding RNA accounts for ~2%, and the remaining 98% is noncoding RNA. Noncoding RNA can undergo AS, promoting the diversity of noncoding transcripts. We designed specific primers to amplify previously reported alternative transcript variants of ZNF695 and showed that six ZNF695 transcript variants are co-expressed in cancer cell lines. The amplicons were sequenced and identified. Additionally, we analyzed the expression of these six transcript variants in bone marrow from B-cell acute lymphoblastic leukemia patients and observed that ZNF695 transcript variants one and three were the predominant variants expressed in leukemia. Moreover, our results showed the co-expression of coding and long noncoding RNA. Finally, we observed that long noncoding RNA ZNF695 expression predicted survival rates.

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ZNF552, a novel human KRAB/C2H2 zinc finger protein, inhibits AP-1- and SRE-mediated transcriptional activity

Cited by 7 publications

References 21 publications

Molecular Mechanisms of Zinc as a Pro-Antioxidant Mediator: Clinical Therapeutic Implications

Molecular Mechanisms of Zinc as a Pro-Antioxidant Mediator: Clinical Therapeutic Implications

Inhaled corticosteroid treatment modulates ZNF432 gene variant’s effect on bronchodilator response in asthmatics

Expression of ZNF695 Transcript Variants in Childhood B-Cell Acute Lymphoblastic Leukemia

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