EBF2

Last update 08 May 2025

Basic Info

Synonyms

COE2, Early B-cell factor 2, EBF transcription factor 2

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Introduction

Transcription factor that, in osteoblasts, activates the decoy receptor for RANKL, TNFRSF11B, which in turn regulates osteoclast differentiation. Acts in synergy with the Wnt-responsive LEF1/CTNNB1 pathway. Recognizes variations of the palindromic sequence 5'-ATTCCCNNGGGAATT-3' (By similarity).

100 Clinical Results associated with EBF2

100 Translational Medicine associated with EBF2

0 Patents (Medical) associated with EBF2

146

Literatures (Medical) associated with EBF2

01 Jun 2025·Molecular Metabolism

Deubiquitinating enzyme USP2 regulates brown adipose tissue thermogenesis via controlling EBF2 stabilization

Article

Author: Pan, Jiemin ; Chen, Ying ; Bai, Ningning ; Yang, Ying ; Ye, Yafen ; Liu, Caizhi ; Hu, Cheng ; Zhang, Rong ; Su, Yingying ; Xu, Yuejie

OBJECTIVEThe activation of brown adipose tissue (BAT) promotes energy expenditure is recognized as a promising therapeutic strategy for combating obesity. The deubiquitinating enzyme family members are widely involved in the process of energy metabolism. However, the specific deubiquitinating enzyme member that affects the BAT thermogenesis remains largely unexplored.METHODSAdeno-associated virus, lentivirus and small molecule inhibitor were applied to generate USP2 gain- or loss-of-function both in vivo and in vitro. OxyMax comprehensive laboratory animal monitoring system, seahorse and transmission electron microscopy were used to determine the energy metabolism. Quantitative proteomics, immunofluorescence staining and co-immunoprecipitation were performed to reveal the potential substrates of USP2.RESULTSUSP2 is upregulated upon thermogenic activation in adipose, and has a close correlation with UCP1 mRNA levels in human adipose tissue. BAT-specific Usp2 knockdown or systemic USP2 inhibition resulted in impaired thermogenic programs both in vivo and in vitro. Conversely, overexpression of Usp2 in BAT conferred protection against high-fat diet-induced obesity and associated metabolic disorders. Proteome-wide analysis identified EBF2 as the substrate of USP2 that mediates the thermogenic function of USP2 in BAT.CONCLUSIONSOur data demonstrated the vital role of USP2 in regulating BAT activation and systemic energy homeostasis. Activation of USP2-EBF2 interaction could be a potential therapeutic strategy against obesity.

27 Mar 2025·Stem cells (Dayton, Ohio)

ZIC1 transcription factor overexpression in segmental bone defects is associated with brown adipogenic and osteogenic differentiation.

Article

Author: Li, Zhao ; Archer, Mary ; Zhu, Manyu ; Zhou, Myles ; Broderick, Kristen ; Pèault, Bruno ; James, Aaron W ; Cherief, Masnsen ; Arondekar, Shreya ; Qin, Qizhi ; Xing, Xin ; Lee, Min ; Thottappillil, Neelima

Transcriptional factor regulation is central to the lineage commitment of stem/ progenitor cells. ZIC1 (ZIC family member 1) is a C2H2-type zinc finger transcription factor expressed during development, brown fat, and certain cancers. Previously, we observed that overexpression of ZIC1 induces osteogenic differentiation at the expense of white adipogenic differentiation. In the present study, the feasibility of ZIC1 overexpressed human progenitor cells in critical sized bone defect was studied. To achieve this, human adipose stem/stromal cells with other without lentiviral ZIC1 overexpression were implanted in a femoral segmental defect model in NOD-SCIDγmice. Results showed that ZIC1 overexpressed cells induced osteogenic differentiation by protein markers in a critical sized femoral segment defect compared to empty lentiviral control, although bone union was not observed. Immunohistochemical evaluation showed that implantation of ZIC1 overexpression cells led to an increase in osteoblast antigen expression (RUNX2, OCN), activation of Hedgehog signaling (Patched1) and an increase in brown adipogenesis markers (ZIC1, EBF2). In contrast, no change in bone defect-associated vasculature was observed (CD31, Endomucin). Together, these data suggest that overexpression of the ZIC1 transcription factor in progenitor cells is associated with differentiation towards osteoblastic and brown adipogenic cell fates.

01 Mar 2025·Cell Death & Differentiation

SOX4 facilitates brown fat development and maintenance through EBF2-mediated thermogenic gene program in mice

Article

Author: Ren, Kexin ; Luo, Ya ; Wang, Shuai ; Wang, Peng ; Xie, Wenlong ; Guo, Huiling ; Zhu, Yu ; Hou, Lingfeng ; Shen, Huanming ; Li, Weihua ; Wei, Yixin ; Huang, Zhengrong ; Hu, Jie ; Fu, Tong ; He, Ting ; Li, Qiyuan ; Li, Boan

AbstractBrown adipose tissue (BAT) is critical for non-shivering thermogenesis making it a promising therapeutic strategy to combat obesity and metabolic disease. However, the regulatory mechanisms underlying brown fat formation remain incompletely understood. Here, we found SOX4 is required for BAT development and thermogenic program. Depletion of SOX4 in BAT progenitors (Sox4-MKO) or brown adipocytes (Sox4-BKO) resulted in whitened BAT and hypothermia upon acute cold exposure. The reduced thermogenic capacity of Sox4-MKO mice increases their susceptibility to diet-induced obesity. Conversely, overexpression of SOX4 in BAT enhances thermogenesis counteracting diet-induced obesity. Mechanistically, SOX4 activates the transcription of EBF2, which determines brown fat fate. Moreover, phosphorylation of SOX4 at S235 by PKA facilitates its nuclear translocation and EBF2 transcription. Further, SOX4 cooperates with EBF2 to activate transcriptional programs governing thermogenic gene expression. These results demonstrate that SOX4 serves as an upstream regulator of EBF2, providing valuable insights into BAT development and thermogenic function maintenance.

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EBF2

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