预约演示

更新于：2025-05-07

MZF1

更新于：2025-05-07

基本信息

别名

myeloid zinc finger 1、MZF、MZF-1

+ [7]

简介

Binds to target promoter DNA and functions as a transcription regulator. Regulates transcription from the PADI1 and CDH2 promoter. May be one regulator of transcriptional events during hemopoietic development.

关联

项与 MZF1 相关的药物

Solamargine

靶点

MZF1

作用机制

MZF1 inhibitors [+1]

在研机构

原研机构

在研适应症

非在研适应症

最高研发阶段临床前

首次获批国家/地区-

首次获批日期1800-01-20

项与 MZF1 相关的临床试验

NCT01796795

/ Suspended临床2期

A Double-blind, Randomized, Vehicle-controlled, Parallel-group, Phase II Dose-ranging Study to Evaluate the Efficacy and Safety of SR-T100 Gel in Common Warts (CW) Patients.

This phase II study is to evaluate the efficacy of SR-T100 gel in complete clearance of target warts at different concentrations (1.0% and 2.3% of SM in Solanum undatum plant extract) in patients with CW.

开始日期2030-09-01

申办/合作机构

德英生物科技股份有限公司

NCT04184011

/ Unknown statusN/A

A Prospective Registry Study to Evaluate the Long-Term Efficacy and Safety of Superficial Radiation Therapy (SRT) for the Treatment of Recurrent Keloid Scars

Keloid formation in response to skin trauma inflicts about 18 million individuals. A key impediment in successful treatment of keloids is that the predominant treatments, particularly surgical excision and shaving, tend to initiate the regrowth of the keloid at the excision site, and therefore, recurrence rates are high. There is much evidence to demonstrate that following surgical excision procedures with a course of radiation therapy can significantly reduce recurrence rates to as little as 10% or below. This prospective study is to evaluate this claim.

开始日期2019-08-15

申办/合作机构

Sensus Healthcare, Inc.

NCT03693924

/ Unknown statusN/A

A Retrospective Registry Study to Evaluate the Long-Term Efficacy and Safety of Superficial Radiation Therapy (SRT) for the Treatment of Recurrent Keloid Scars.

开始日期2018-11-15

申办/合作机构

Sensus Healthcare, Inc.

100 项与 MZF1 相关的临床结果

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100 项与 MZF1 相关的转化医学

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0 项与 MZF1 相关的专利（医药）

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251

项与 MZF1 相关的文献（医药）

2025-12-31·Bioengineered

Statement of Retraction: Extracellular vesicles derived from HBMSCs improved myocardial infarction through inhibiting zinc finger antisense 1 and activating Akt/Nrf2/HO-1 pathway

Article

2025-04-01·Translational Oncology

Single-cell insights into HNSCC tumor heterogeneity and programmed cell death pathways

Article

作者: Chai, Yuanhao ; Zhang, Ziwei ; Shao, Wenwen ; Zhang, Jianlin

BACKGROUNDHead and neck squamous cell carcinoma (HNSCC) is a prevalent malignancy often diagnosed in advanced stages. Despite advancements in therapy, it retains a high mortality rate and significant recurrence risk. This study utilizes single-cell sequencing (scRNA-seq) to unravel HNSCC's complexity, identify therapeutic targets, and refine prognostic models.METHODSPseudotime trajectory and stemness analyses were performed on HNSCC tumor subpopulations, focusing on the C2 MALAT1+ Tumors subpopulation, which had the lowest CytoTRACE Score and represented the Lineage 2 endpoint in Slingshot analysis. The study examined programmed death and metabolic pathways in each subpopulation and developed a novel prognostic model using LASSO regression.RESULTSThe C2 MALAT1+ Tumors subpopulation exhibited reduced expression of programmed death pathways (e.g., Entotic cell death, Apoptosis, Pyroptosis) and metabolic pathways (e.g., Riboflavin metabolism, Glycolysis/Gluconeogenesis). Key transcription factors included LEF1, RFX3, CREM, MZF1, and ZNF202. Prognostic models based on the MALAT1 Tumors Risk Score (MTRS) revealed worse survival and higher tumor purity in the high MTRS group. Risk genes included ADM, RPL31, EIF5B, and TAF7. Additionally, activated CD4 memory T cells were enriched in the high MTRS group, which also showed greater sensitivity to Cisplatin, Docetaxel, and Paclitaxel.CONCLUSIONSScRNA-seq revealed the heterogeneity of HNSCC subpopulations, highlighting the unique features of the C2 MALAT1+ Tumors subpopulation. This study identified novel prognostic markers and therapeutic targets, offering insights into HNSCC progression, drug resistance, and potential treatments.

2025-03-01·Biochemical and Biophysical Research Communications

Discovery of myeloid zinc finger (MZF) 1 nuclear bodies

Article

作者: Calderwood, Stuart K ; Eguchi, Takanori

Myeloid zinc finger 1 (MZF1) is a multifaceted transcription factor that can act either as a transcriptional activator or a gene repressor. We examined its production of nuclear bodies (NBs) and subcellular localization. Proteomic and protein-protein interaction analysis were used to identify its cofactors and interactions. These revealed the presence of MZF1-NBs (intranuclear oligomers containing MZF1). MZF-NBs are similar to some other nuclear bodies, notably promyelocytic leukemia (PML) -NBs in terms of size and morphology. However the two structures appear to be different. MZF-NBs and PML-NBs were found to associate in the nucleus. Both MZF1 and PML are SUMO1-SUMOylated in PC-3 cells. Sumoylated MZF1 can interact with proteins containing SUMO-interaction motifs (SIM) through SUMO-SIM interaction. Interactome analysis revealed that its NBs participate in the stress response (TPR and UBAP2L), protein folding (CALR and ANKRD40), transcription, post-translational modification (TRIM33, ACOT7, CAMK2D, and CAMK2G), and RNA binding (ALURBP and CPSF5).

项与 MZF1 相关的新闻（医药）

2023-03-15

·生物谷

科学家揭示了吉非替尼/奥希替尼(GR/OR)的获得性耐药新机制

非小细胞肺癌（NSCLC）是最常见的癌症组织学类型，约占癌症患者的85%。表皮生长因子受体（EGFR）突变作为NSCLC中的重要致癌驱动因素，为晚期疾病患者的生物标志物导向治疗模型拉开了帷幕。非小细胞肺癌（NSCLC）是最常见的癌症组织学类型，约占癌症患者的85%。表皮生长因子受体（EGFR）突变作为NSCLC中的重要致癌驱动因素，为晚期疾病患者的生物标志物导向治疗模型拉开了帷幕。许多EGFR酪氨酸激酶抑制剂（TKIs）已经开发出来，包括常用的第一代TKIs吉非替尼和高效的第三代TKIs奥希替尼。尽管这些药物在治疗患者方面疗效显著，但对这些药物的耐药性仍然是一个有待解决的根本挑战。图片来源：https://pubmed.ncbi.nlm.nih.gov/36778111/ 近日，来自首都医科大学的研究者们在Int J Biol Sci.杂志上发表了题为“Acquired resistance to EGFR-TKIs in NSCLC mediates epigenetic downregulation of MUC17 by facilitating NF-κB activity via UHRF1/DNMT1 complex”的文章，该研究表明吉非替尼/奥希替尼(GR/OR)的获得性耐药性促进UHRF1/DNMT1复合物抑制粘蛋白17（MUC17）的表达。GR/OR细胞中的MUC17可作为表观遗传传感器，用于生物监测对EGFR TKI的耐药性。 EGFR TKIs治疗给EGFR突变的非小细胞肺癌患者带来了显著益处。然而，大多数患者在治疗后最终产生获得性抵抗。本研究研究了MUC17在EGFR TKI获得性耐药细胞中的表观遗传效应。研究者们发现，GR/OR细胞增强全基因组DNA超甲基化，主要是在与多种致癌途径相关的5-UTR中，其中GR/OR细胞通过以剂量和时间依赖的方式下调MUC17表达而发挥促癌作用。 GR/OR通过促进DNMT1/UHRF1复合物依赖性启动子甲基化，从而激活NF-κB活性，从而获得耐药性介导的MUC17下调。MUC17通过促进MZF1的表达，增加IκB-α的生成并抑制NF-κB活性。体内结果还表明，DNMT1抑制剂（5-Aza）与吉非替尼/奥西美替尼联合使用可恢复对OR/GR细胞的敏感性。 MUC17在耐药细胞中的分子机制示意图。图片来源：https://pubmed.ncbi.nlm.nih.gov/36778111/ 综上所述，长期接触吉非替尼/奥希替尼可通过UHRF1/DNMT1介导的MUC17表观遗传沉默增强全基因组甲基化，并促进肺癌细胞的耐药性。该结果表明，MUC17通过上调吉非替尼/奥希替尼耐药细胞中的MZF1表达和抑制NF-κB活性来促进药物敏感性。因此，MUC17可以作为一种表观遗传传感器，用于对EGFR TKI的耐药性进行生物监测。（生物谷 Bioon.com）参考文献 Shuye Lin et al. Acquired resistance to EGFR-TKIs in NSCLC mediates epigenetic downregulation of MUC17 by facilitating NF-κB activity via UHRF1/DNMT1 complex. Int J Biol Sci. 2023 Jan 9;19(3):832-851. doi: 10.7150/ijbs.75963.