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Last update 08 May 2025

MEF2D

Last update 08 May 2025

Basic Info

Synonyms

MEF2D, myocyte enhancer factor 2D, Myocyte-specific enhancer factor 2D

Introduction

Transcriptional activator which binds specifically to the MEF2 element, 5'-YTA[AT](4)TAR-3', found in numerous muscle-specific, growth factor- and stress-induced genes. Mediates cellular functions not only in skeletal and cardiac muscle development, but also in neuronal differentiation and survival. Plays diverse roles in the control of cell growth, survival and apoptosis via p38 MAPK signaling in muscle-specific and/or growth factor-related transcription. Plays a critical role in the regulation of neuronal apoptosis (By similarity).

Drugs associated with MEF2D

T-006

Target

MEF2D

Mechanism

MEF2D agonists

Active Org.

Guangzhou Magpie Pharmaceuticals Co., Ltd.

Originator Org.

Guangzhou Magpie Pharmaceuticals Co., Ltd.

Active Indication

Parkinson Disease

Inactive Indication-

Drug Highest PhaseIND Application

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with MEF2D

100 Translational Medicine associated with MEF2D

0 Patents (Medical) associated with MEF2D

471

Literatures (Medical) associated with MEF2D

01 Jun 2025·Modern Pathology

The MEF2D::NCOA2 Fusion Defines a Distinct Emerging Vulvovaginal Myxoid Epithelioid Tumor With Smooth Muscle Differentiation

Article

Author: Thamphya, Brice ; Treilleux, Isabelle ; Croce, Sabrina ; Le Loarer, François ; Devouassoux-Shisheboran, Mojgan ; Bataillon, Guillaume ; Descotes, Françoise ; Donzel, Marie ; Pissaloux, Daniel ; Trecourt, Alexis ; Lopez, Jonathan ; Alix, Eudeline

Myocyte-specific enhancer factor 2D gene and nuclear receptor coactivator 2 gene fusion (MEF2D::NCOA2) was recently reported in 2 vulvovaginal myxoid epithelioid smooth muscle tumors. We aimed to perform an integrated approach combining clinical, morphologic, immunohistochemical, and molecular profiling analyses, including targeted RNA sequencing, targeted gene expression analysis profiling with clustering, DNA mutational analysis, and array comparative genomic hybridization in a series of 3 MEF2D::NCOA2 fusion-associated vulvovaginal tumors, to better describe this entity. The median age at diagnosis was 45 years. Tumors were well circumscribed and located deeply within the vulva, vaginal wall, or between the bladder and the vagina (1/3, 33.3% each). The median size of tumors was 2.5 cm. All tumors had a similar morphology, reminiscent of smooth muscle tumor with prominent myxoid stromal changes (3/3, 100%). Tumor cells were haphazardly arranged in short fascicles and were mostly spindle cells. Microcystic spaces lined by epithelioid cells and/or sheets of epithelioid cells were observed in all tumors (3/3, 100%), associated with a myxoid background. Cytologic atypia was none to mild, and the mitotic counts were always low (≤1 mitosis/high-power fields). Immunohistochemistry found smooth muscle actin, desmin, h-caldesmon, estrogen receptors, and CD34 to be intensely and diffusely expressed in all tumors (3/3, 100%). A MEF2D::NCOA2 transcript was observed in all tumors (3/3, 100%), which was the driver of molecular alteration. No pathogenic variants were found, and array comparative genomic hybridization found simple genomic profiles for all tumors (3/3, 100%). On targeted gene expression analysis, MEF2D::NCOA2 fusion-associated tumors clustered distinctly from other gynecologic mimickers and neoplasms with myxoid stromal changes (vulvovaginal leiomyomas, myxoid vulvovaginal leiomyomas, deep angiomyxomas, myxoid leiomyosarcomas, myxoid endometrial stromal sarcomas, and inflammatory myofibroblastic tumors). The signaling pathways involved in this entity included the expression of genes encoding smooth muscle phenotype proteins, favoring a smooth muscle (myoid) differentiation. All patients were alive and free of disease at the last follow-up. To conclude, vulvovaginal MEF2D::NCOA2 fusion-associated tumors are distinct and emerging entities, with a rather indolent behavior.

01 Apr 2025·Science China Life Sciences

Systematical identification of regulatory GPCRs by single-cell trajectory inference reveals the role of ADGRD1 and GPR39 in adipogenesis

Article

Author: Zhao, Dongyu ; Huang, Shaodong ; Gao, Yuhua ; Chen, Weixuan ; Jiang, Changtao ; Sun, Jinpeng ; Wu, Chenyang ; Ye, Chuan ; Lin, Jun ; Rao, Ziyan ; Huang, Ying ; Wang, Xuemei ; Liao, Yunxi ; Guo, Chenghao

Adipogenesis is the healthy expansion of white adipose tissue (WAT), serving as a compensatory response to maintain metabolic homeostasis in the presence of excess energy in the body. Therefore, the identification of novel regulatory molecules in adipogenesis, specifically membrane receptors such as G protein-coupled receptors (GPCRs), holds significant clinical promise. These receptors can serve as viable targets for pharmaceuticals, offering potential for restoring metabolic homeostasis in individuals with obesity. We utilized trajectory inference methods to analyze three distinct single-nucleus sequencing (sNuc-seq) datasets of adipose tissue and systematically identified GPCRs with the potential to regulate adipogenesis. Through verification in primary adipose progenitor cells (APCs) of mice, we discovered that ADGRD1 promoted the differentiation of APCs, while GPR39 inhibits this process. In the obese mouse model induced by a high-fat diet (HFD), both gain-of-function and loss-of-function studies validated that ADGRD1 promoted adipogenesis, thereby improving metabolic homeostasis, while GPR39 inhibited adipogenesis, leading to metabolic dysfunction. Additionally, through the analysis of 2,400 ChIP-seq data and 1,204 bulk RNA-seq data, we found that the transcription factors (TFs) MEF2D and TCF12 regulated the expression of ADGRD1 and GPR39, respectively. Our study revealed the regulatory role of GPCRs in adipogenesis, providing novel targets for clinical intervention of metabolic dysfunction in obese patients.

01 Apr 2025·Biochemical and Biophysical Research Communications

High glucose-induced alternative splicing of MEF2D in macrophages promotes vascular chronic inflammation in type 2 diabetes mellitus by mediating M1 macrophage polarization

Article

Author: Luo, Jie ; He, Yuqi ; Xie, Haitao

OBJECTIVESTo investigate the effects of a high-glucose environment in type 2 diabetes mellitus (T2DM) on Myocyte enhancer factor 2d (MEF2D) selective splicing and its impact on the disease process and mechanism.METHODSHuman monocyte (THP-1) cells were induced into macrophages with phorbol 12-myristate 13-acetate (PMA), and treated with high glucose for 24 h. PCR confirmed MEF2D splicing products. MEF2D or MEF2D-AS overexpression vectors were transfected into macrophages, and ELISA detected inflammatory factors; flow cytometry analyzed MI/M2 phenotypes; and levels of LC3, PI3K, and LAMP2 were measured. Autophagic flux detection; co-immunoprecipitation detected MEF2D and KCNMA1 interaction; WB and RT-qPCR assessed KCNMA1 expression. Macrophages co-cultured with endothelial cells were analyzed by ELISA for vascular inflammation factors MMP-9, Cys-C, and hsCRP.RESULTSHigh glucose-induced alternative splicing of MEF2D at 86-132 aa. MEF2D-AS group showed higher inflammatory factors, increased M1 phenotype, lower autophagy gene expression, and higher vascular inflammation factors compared to MEF2D group. Autophagy activator Rapamycin or KCNMA1 overexpression reversed these effects. MEF2D targeted KCNMA1, and MEF2D-AS overexpression led to decreased KCNMA1, increased inflammatory factors, M1 polarization, autophagy inhibition, and higher vascular inflammation factors.CONCLUSIONHigh glucose induces MEF2D alternative splicing in macrophages, inhibiting autophagy and promoting M1 polarization via KCNMA1 down-regulation, thus promoting chronic inflammation in T2DM vessels.

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MEF2D

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