ZNF257

Last update 08 May 2025

Basic Info

Synonyms

BMZF-4, BMZF4, Bone marrow zinc finger 4

+ [2]

Introduction

May be involved in transcriptional regulation.

100 Clinical Results associated with ZNF257

100 Translational Medicine associated with ZNF257

0 Patents (Medical) associated with ZNF257

Literatures (Medical) associated with ZNF257

01 May 2025·International Journal of Biological Macromolecules

Codon usage bias and nucleotide bias are not influenced by the 5′ flanking but by 3′ and intronic region composition in SCID-associated genes

Article

Author: Al-Hussain, Sami A ; Shi, Quan ; Gurjar, Pankaj ; Zaki, Magdi E A ; Zou, Yichun ; Khandia, Rekha ; Kumar, Utsang

Compositional constraints, selectional and mutational forces, nucleotide skews, RNA folding free energy, gene expression, protein properties, and differential expression are a few attributes that define the molecular signatures of any gene. The absence of information regarding these attributes for genes associated with severe combined immunodeficiency disorder (SCID) prompted us to take up this study. The compositional bias influenced codon bias. Overall percent T composition is the lowest among all nucleotides. However, its distribution varies markedly across different codon positions and is not lowest at all codon positions. We, for the first time, determined the influence of intergenic elements and introns on nucleotide and codon bias on genes and found that in SCID-associated genes, the 5' flanking region neither influences the nucleotide nor codon bias, contrary to the intronic and 3' flanking region, which both influence nucleotide and codon bias in SCID associated genes. Codon usage in the SCID-associated gene set significantly differs from the codon usage present in overall human codon usage for 33 out of 59 codons (excluding start, stop, and trp encoding). Analysis of differentially expressed genes revealed that out of the 10 most differentially expressed genes, 07 genes are Zn finger proteins (ZNF728, ZNF726, ZNF676, ZNF667, ZNF439, ZNF257, and ZNF208). Applying the knowledge of codon bias, rare codons, minimum free energy, and codon adaptation index, codon deoptimization was carried out, and ZNF208 was the best suitable candidate. The study opened the area for the identification of peculiar molecular features and the development of more candidates for gene therapy purposes.

01 Dec 1999·Journal of Biological ChemistryQ2 · BIOLOGY

Molecular Cloning of Six Novel Krüppel-like Zinc Finger Genes from Hematopoietic Cells and Identification of a Novel Transregulatory Domain KRNB

Q2 · BIOLOGY

Article

Author: Mao Mao ; Li-Xin Kan ; Kai-Li He ; Qing-Hua Zhang ; Long Yu ; Ze-Guang Han ; Zhu Chen ; Shao-Lin Shi ; Min Ye ; Gang Fu ; Sai-Juan Chen ; Jun Zhou ; Bai-Wei Gu

To clone zinc finger genes expressed in hematopoietic system, we designed primers based on conserved Cys(2)/His(2) zinc finger sequences to amplify corresponding domains from mRNA of normal bone marrow and leukemia cell line NB4. DNA fragments of novel zinc finger genes were chosen and used as probe pool to screen cDNA libraries or subject to rapid amplification of cDNA ends in order to obtain full-length cDNA. Six cDNAs including whole open reading frame of zinc finger proteins, named as ZNF191, ZNF253 (BMZF-1), ZNF255 (BMZF-2), ZNF256 (BMZF-3), ZNF257 (BMZF-4), and ZNF254 (BMZF-5) were obtained. All six belong to the Krüppel-like zinc finger gene family, and typical transcriptional regulatory motifs exist in the N-terminal moiety, such as the SCAN box in ZNF191, and the KRAB domains in ZNF253, ZNF254, ZNF256, and ZNF257. A previously undefined sequence nominated as Krüppel-related novel box, which may represent a new transregulatory motif, was revealed at the N terminus of ZNF255. The transregulatory function of non-zinc finger regions of ZNF191, ZNF253, and ZNF255 were addressed in yeast and mammalian cells. The results indicated that ZNF255 might be a conditional transactivator, whereas ZNF253 and ZNF191 displayed a suppressive effect on the transcription in yeast and/or mammalian systems.

Signal Transduction and Targeted TherapyQ1 · MEDICINE

Integrative analysis of DNA methylation and gene expression identified cervical cancer-specific diagnostic biomarkers

Q1 · MEDICINE

ArticleOA

Author: Zhang, Yunshan ; Zhou, Wei ; Shi, Yi ; Xiang, Rong ; Xu, Wanxue ; Xu, Mengyao ; Wang, Longlong ; Piao, Yongjun

AbstractCervical cancer is the leading cause of death among women with cancer worldwide. Here, we performed an integrative analysis of Illumina HumanMethylation450K and RNA-seq data from TCGA to identify cervical cancer-specific DNA methylation markers. We first identified differentially methylated and expressed genes and examined the correlation between DNA methylation and gene expression. The DNA methylation profiles of 12 types of cancers, including cervical cancer, were used to generate a candidate set, and machine-learning techniques were adopted to define the final cervical cancer-specific markers in the candidate set. Then, we assessed the protein levels of marker genes by immunohistochemistry by using tissue arrays containing 93 human cervical squamous cell carcinoma samples and cancer-adjacent normal tissues. Promoter methylation was negatively correlated with the local regulation of gene expression. In the distant regulation of gene expression, the methylation of hypermethylated genes was more likely to be negatively correlated with gene expression, while the methylation of hypomethylated genes was more likely to be positively correlated with gene expression. Moreover, we identified four cervical cancer-specific methylation markers, cg07211381 (RAB3C), cg12205729 (GABRA2), cg20708961 (ZNF257), and cg26490054 (SLC5A8), with 96.2% sensitivity and 95.2% specificity by using the tenfold cross-validation of TCGA data. The four markers could distinguish tumors from normal tissues with a 94.2, 100, 100, and 100% AUC in four independent validation sets from the GEO database. Overall, our study demonstrates the potential use of methylation markers in cervical cancer diagnosis and may boost the development of new epigenetic therapies.

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ZNF257

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