Ask about this productRelated genes to: MEF2C Blocking Peptide
- Gene:
- MEF2C NIH gene
- Name:
- myocyte enhancer factor 2C
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5q14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-02-08
- Date modifiied:
- 2015-08-25
Related products to: MEF2C Blocking Peptide
Related articles to: MEF2C Blocking Peptide
- The myocyte enhancer factor 2 (MEF2) transcription factor family plays crucial roles in differentiation, lineage specification, stress responses, and tissue homeostasis. Recent investigations have shown that the dysregulation of MEF2A, MEF2B, MEF2C, and MEF2D is associated with tumorigenesis, tumor progression, and adverse clinicopathological features in several cancers. MEF2B has a particularly important role in B-cell malignancies, where recurrent mutations deregulate BCL6 and promote lymphoma progression. MEF2A, MEF2C, and MEF2D also regulate malignant phenotypes, including proliferation, migration, invasion, apoptosis, drug resistance, angiogenesis, inflammation, and immune evasion, by the mechanism of regulating cell-cycle regulators, apoptosis-related genes, EMT-related genes, and other transcriptional programs. This review summarizes the mechanisms by which MEF2 family members contribute to tumor initiation and progression, with added emphasis on mutations and fusions. We also discuss clinical associations with overall survival and recurrence in solid tumors and hematologic malignancies. Because MEF2 proteins are transcription factors with broad physiological functions, we evaluate therapeutic strategies: RNA interference, genetic perturbation, small molecules that alter MEF2-dependent transcription, and PROTAC or oligonucleotide-PROTAC. These platforms remain promising but require MEF2-specific validation, tumor-selective delivery, and careful toxicity assessment. - Source: PubMed
Publication date: 2026/07/28
Chen YanyanZhu JingniQian JinghangLi ShengYang Liu - RNA-binding proteins are critical regulators of gene expression in both normal physiology and cancer. Here we set out to systematically annotate the functions of RNA-associated proteins across multiple cancer types via domain-focused CRISPR screens targeting RNA-modifying enzymes and RNA-binding proteins. We utilized 3182 sgRNAs targeting 527 RNA-enzymatic and binding domains in 341 RNA-associated proteins and identified multiple RNA-binding proteins as dependencies in acute myeloid leukemia (AML), including the RNA splicing factor PTBP1 and the N6-methyladenosine reader RBM15, with a bias toward the aggressive KMT2A-rearranged (KMT2A-r) subtype of AML. Genetic and cellular validation confirmed all four RNA-binding domains of PTBP1 as required for KMT2A-r AML proliferation. In contrast to the lack of requirement for PTBP1 in myelopoiesis, PTBP1 suppression in AML caused cell cycle arrest, apoptosis, and induction of myeloid differentiation programs. Transcriptomic analysis revealed that PTBP1 loss disrupted the KMT2A-r-essential transcriptional program and caused widespread dysregulation of splicing. CLIP-seq analysis further identified that PTBP1 preferentially binds to a subset of transcripts critical for KMT2A-r AML proliferation, including IKZF1, MEF2C, EZH2, SIK3, and PBX3. Collectively, these findings demonstrate that PTBP1 supports AML proliferation by fine-tuning the expression and splicing of AML-essential genes, providing a workflow for systematically annotating RNA-associated protein dependencies in cancer. - Source: PubMed
Publication date: 2026/08/24
Cao ZhendongMcCannell Kurtis NYu SixiangBudinich Krista AKim Won JunJing YuqingWang Michelle YTittley StevenWen ZhuoyuLiu Kathy FangeShi JunweiAbdel-Wahab Omar - Acute myeloid leukemia (AML) is a hematologic malignancy caused by the malignant proliferation and differentiation block of immature myeloid cells (blasts) in the bone marrow. The pathogenesis, diagnostic classification, treatment, and prognosis of AML are fundamentally linked to the accumulation of genetic variants, fusion gene formation, and chromosomal karyotype abnormalities. Using mRNA sequencing (next-generation sequencing, NGS), we identified and validated two novel fusion genes, and , in a case of AML-M2a. This patient also harbored six single nucleotide variants (SNV) (, , , , , and ) and complex karyotype (CK). The chromosomes exhibited extreme instability and high variability, with tumor cells containing multiple clones and showing continuous karyotype evolution as the disease progressed. The patient was treated with three chemotherapy regimens (VMA, VHAA, and Decitabine-Venetoclax), but none achieved remission. We propose that the combination of these novel fusion genes, multiple SNVs, and the complex karyotype collectively contributed to the patient's multidrug resistance. - Source: PubMed
Publication date: 2026/08/18
Tu JifangWang YunguiGao XiangliWang HuanpingWang HuafengJin JieTong Hongyan - The metabolic importance of brown adipose tissue (BAT) has been recognized, but its origins, particularly supraclavicular BAT (scBAT), remain unclear. Here, we traced scBAT to Mef2c-anterior heart field (AHF)-marked cells. Mef2c-AHF-marked cells isolated from scBAT can spontaneously differentiate into brown adipocytes, express mesenchymal stem cell markers, and can be isolated from the stromal-vascular fraction (SVF) of wild-type scBAT as [CD31CD45Sca-1CD29CD34CD24] (CD34) cells. Mef2c-AHF-marked cells substantially overlap with Prrx1-marked cells in scBAT, which also contribute to beige adipocytes in inguinal white adipose tissue (iWAT). Similarly, CD34 cells isolated from the SVF of iWAT can spontaneously differentiate into beige adipocytes in vitro. Intersectional lineage tracing shows that common progenitors of Mef2c-AHF- and Prrx1-marked cells in scBAT emerge from the developing heart. Thus, these studies reveal a common origin for scBAT and cardiac tissue and suggest that scBAT and iWAT beige adipocytes arise from progenitor populations with overlapping lineage origins and molecular characteristics. - Source: PubMed
Publication date: 2026/08/14
Ran YaliZhang KaiShen Yi-TingMo QianxingWang ZiyiYalamanchili Hari KrishnaJohn SharonKogiso MariGao XiaWang ChunmeiSinha TanviBlack Brian LChen Miao-Hsueh - Attention-Deficit/Hyperactivity Disorder (ADHD) is a highly heritable neurodevelopmental disorder; however, its genetic architecture remains poorly explored in Indigenous populations. This study aimed to analyze and characterize genetic variation in 11 genes (ADGRL3, CDH8, DCC, DUSP6, FOXP1, FOXP2, MEF2C, PCDH7, SEMA6D, SORCS3, and ST3GAL3) previously implicated in ADHD, in an indigenous sample, comparing them with reference populations from the 1000 Genomes Project. Exome data from 64 individuals representing 12 Indigenous groups from the Brazilian Amazon were analyzed. Among the identified, 99 met the inclusion criteria. Four previously unreported variants in the developed reference datasets were identified in ADGRL3, DCC, and FOXP2. Significant differences in allele frequencies were observed for 56 variants compared with continental populations. Multidimensional scaling analysis indicated genetic differentiation of the Indigenous group in relation to other populations. This study highlights the distinct genetic profile of Amazonian Indigenous populations, likely shaped by demographic and evolutionary processes such as genetic drift and founder effects. The identification of exclusive variants and marked allele frequency differences reinforces the importance of including historically underrepresented populations in genomic studies related to ADHD and neurodevelopment, contributing to a broader understanding of human genetic diversity. - Source: PubMed
Publication date: 2026/08/11
de Matos Hirlesson PaixãoMonte NatashaAguiar Kaio Evandro Cardosode Cássia Calderaro RitaSantos Aline PasquiniRodrigues Juliana Carla GomesRibeiro-Dos-Santos André MaurícioDe Souza Sandro JoséRibeiro-Dos-Santos ÂndreaGuerreiro João FariasSantos Sidney Emanuel Batista DosSantos Ney Pereira Carneiro Dos