Ask about this productRelated genes to: MTA3 Blocking Peptide
- Gene:
- MTA3 NIH gene
- Name:
- metastasis associated 1 family member 3
- Previous symbol:
- -
- Synonyms:
- KIAA1266
- Chromosome:
- 2p21
- Locus Type:
- gene with protein product
- Date approved:
- 2003-12-15
- Date modifiied:
- 2016-10-05
Related products to: MTA3 Blocking Peptide
Related articles to: MTA3 Blocking Peptide
- Metastasis-associated protein 3 (MTA3), a key member of the MTA family, is an integral component of the nucleosome remodeling and deacetylase complex, with widespread expression across diverse human tissues and organs. By modulating epigenetic modifications, MTA3 is instrumental in regulating vital physiological processes, including cell differentiation, apoptosis, and metabolism. It plays a crucial role in maintaining normal tissue homeostasis and exerts a significant regulatory influence on pathological conditions, notably cancer and other diseases. This review presents a comprehensive evaluation of the molecular structural characteristics and biological functions of MTA3, providing a detailed overview of its mechanistic role in tumorigenesis and disease progression. Its unique tissue-specific expression patterns and dual functional roles as an oncogene or tumor suppressor, depending on the cellular and disease context, are highlighted. Moreover, by integrating recent research advancements, the feasibility and potential clinical translational value of using MTA3 as a diagnostic and prognostic biomarker, as well as a therapeutic target in developing novel disease intervention strategies, are evaluated in this review. This study aimed to establish a robust theoretical foundation and provide novel research perspectives to support future endeavors focused on improving patient outcomes by precisely modulating MTA3 activity. - Source: PubMed
Publication date: 2026/01/09
Tang YanLi Xiao-JiaoAo HuiLiu Qian-GuoZheng Xiao-FuLiao Chang-LiLi JunWu Yong-Kang - Hepatocellular carcinoma (HCC) is a leading global health concern, recognized for its complex pathogenesis and high mortality rates. The metastatic progression of HCC, considered the terminal event in tumor development, plays a pivotal role in determining patient prognosis, with metastasis being a key factor in poor survival outcomes.HDAC11 was found to be highly expressed in HCC tissues, with its elevated expression significantly correlating with poor patient survival. Both in vitro and in vivo experiments demonstrated that silencing HDAC11 led to a marked reduction in HCC cell proliferation. Interestingly, HDAC11 knockdown also resulted in a substantial increase in the metastatic potential of HCC cells. Mass spectrometry analysis revealed that HDAC11 interacts with the NuRD (MTA3) complex. Consistently, immunoprecipitation and GST pull-down assays demonstrated that the N-terminal region of HDAC11 directly binds to MTA3. Moreover, transcriptomic analysis indicated that HDAC11 represses TGFB1 transcription, thereby inhibiting HCC metastasis. The enhanced metastatic phenotype induced by HDAC11 silencing was reversed upon concurrent down-regulation of TGFB1. Moreover, nanoparticles encapsulating both HDAC11 and TGF-β1 inhibitors effectively suppressed HCC cell proliferation and metastasis. This research elucidates the molecular mechanism by which HDAC11 inhibits metastasis and provides an effective strategy to mitigate the side effects associated with HDAC11 inhibition, offering novel insights and approaches for the precision treatment of HCC. - Source: PubMed
Publication date: 2026/01/17
Yang YangWang JiaoliWu QingqingWang YishanMeng HuiZeng LuluQiu TianZhao HaixiaHu QinWeng QiaoyouLiu MeilingChen MinjiangQiu RongfangJi JiansongChen Weiqian - Neurodevelopmental disorders (NDDs) arise from disruptions in brain development, yet the underlying pathways remain incompletely understood. Here we demonstrate that genome-wide CRISPR knockout screens in mouse embryonic stem cells differentiating into neural lineages identify hundreds of essential genes, only a minority of which are currently implicated in NDDs. Dominant NDD genes were enriched for transcriptional regulators, whereas recessive NDD genes were predominantly involved in metabolic processes. Mouse models for eight genes (Eml1, Dusp26, Dynlrb2, Mta3, Peds1, Sgms1, Slitrk4 and Vamp3) revealed marked neuroanatomical abnormalities, including microcephaly in half of the cases. Focusing on PEDS1, a key enzyme in plasmalogen biosynthesis, we identified a bi-allelic variant in individuals with microcephaly, global developmental delay and congenital cataracts. In mice, Peds1 deficiency led to accelerated cell-cycle exit and impaired neuronal differentiation and migration. These pathways required for neural differentiation provide a genetic framework for discovering additional NDD genes. - Source: PubMed
Publication date: 2026/01/05
Amelan AlanaCollins Stephan CDamseh Nadirah SHamada NanakoSalim AhdDvir EladMonderer-Rothkoff GalyaHarel TamarNagata Koh-IchiYalcin BinnazShifman Sagiv - - Source: PubMed
Publication date: 2025/11/24
Zhou HengWen PingLiu YeYe ZhifeiXiong WeiLiu YonghaoDing HanyuDuan XingxiangLuo YuQin QiangLi RuohanHe YanMao ShanpingYe Qingsong - Prolonged periods of ischemia and hypoxia pose significant challenges to exogenous stem cell transplantation, including minimal cell survival, varied differentiation, and poor integration with existing neural networks. Dental pulp stem cells (DPSCs) are an important choice for stem cell treatment for their excellent potential of neural differentiation and easy accessibility. Stable overexpression of miR-138 in DPSCs were injected into MCAO model mice via brain stereotaxic localization to explore the therapeutic effect on stroke and the related mechanisms by trans-synaptic viral tracing, immunostaining, bioinformatics analysis, behavioral tests and electrophysiological assays. DPSCs transfected with miR-138 can treat stroke by reducing neuroinflammation, decreasing neuronal apoptosis, and promoting neural regeneration, resulting in structural and functional repair of post-stroke neural networks. Among them, miR-138 can regenerate nerves because it can break down GATA zinc finger domain-containing protein 2B (GATAD2B), disrupt nucleosome remodeling complex (NuRD), and transfer MTA from nucleus to cytoplasm. The MTA3 was then transferred from the nucleus to the cytoplasm, activating the Wnt signaling pathway, which finally led to the differentiation of DPSCs into GABAergic neurons and the repair of neuronal death caused by stroke. Within this study, we introduce a novel DPSCs reprogramming approach designed to enhance the differentiation of GABAergic neurons and bolster their viability within the ischemic stroke context, and delineate the regulatory mechanism involving miR-138, which initiates GABAergic neuronal differentiation via modulation of the GATAD2B/MTA3/WNTs signaling pathway. - Source: PubMed
Publication date: 2025/08/08
Zhou HengWen PingLiu YeYe ZhifeiXiong WeiLiu YonghaoDing HanyuDuan XingxiangLuo YuQin QiangLi RuohanHe YanMao ShanpingYe Qingsong