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Last update 23 Jan 2025

GABPA

Last update 23 Jan 2025

Basic Info

Synonyms

E4TF1-60, E4TF1A, GA binding protein transcription factor subunit alpha

+ [8]

Introduction

(Microbial infection) Necessary for the expression of the Adenovirus E4 gene. Transcription factor capable of interacting with purine rich repeats (GA repeats). Positively regulates transcription of transcriptional repressor RHIT/ZNF205 (PubMed:22306510).

Drugs associated with GABPA

C4X-6665

Target

GABPA

Mechanism

GABPA agonists

Active Org.

C4X Discovery Holdings Plc

Originator Org.

C4X Discovery Holdings Plc

Active Indication

Inflammation

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GABPA

100 Translational Medicine associated with GABPA

0 Patents (Medical) associated with GABPA

224

Literatures (Medical) associated with GABPA

01 Jan 2025·Nature Cell Biology

The transcription factor GABPA is a master regulator of naive pluripotency

Article

Author: Wang, Meng ; Zhang, Yi ; Zhou, Chengjie ; Zhang, Chunxia

AbstractThe establishment of naive pluripotency is a continuous process starting with the generation of inner cell mass (ICM) that then differentiates into epiblast (EPI). Recent studies have revealed key transcription factors (TFs) for ICM formation, but which TFs initiate EPI specification remains unknown. Here, using a targeted rapid protein degradation system, we show that GABPA is not only a regulator of major ZGA, but also a master EPI specifier required for naive pluripotency establishment by regulating 47% of EPI genes during E3.5 to E4.5 transition. Chromatin binding dynamics analysis suggests that GABPA controls EPI formation at least partly by binding to the ICM gene promoters occupied by the pluripotency regulators TFAP2C and SOX2 at E3.5 to establish naive pluripotency at E4.5. Our study not only uncovers GABPA as a master pluripotency regulator, but also supports the notion that mammalian pluripotency establishment requires a dynamic and stepwise multi-TF regulatory network.

01 Jan 2025·Science of The Total Environment

Amino modifications exacerbate the developmental abnormalities of polystyrene microplastics via mitochondria-mediated apoptosis pathway in zebrafish larvae

Article

Author: Yang, Wenhui ; Guo, Hongzhi ; Ding, Ping ; Hu, Guocheng ; Li, Xintong ; Yu, Yunjiang ; Zhang, Jiayi ; He, Miao ; Ni, Yuyang

Microplastics (MPs) are ubiquitous in the environment and have been identified as a potential threat to ecosystems. However, the mechanisms of toxicity of modified MPs remain unknown. This study investigated the developmental toxicity of amino-modified polystyrene microplastics (PS-NH₂) with environmentally relevant concentrations ranging from 0.1 to 100 μg/L in the early developmental stages of zebrafish. Adding amino functional groups resulted in significant alterations in the surface morphology and zeta potential of traditional polystyrene microplastics (PS-MPs). Zebrafish larvae exposed to PS-NH₂ exhibited increased developmental toxicity compared to PS-MPs, as indicated by reduced body length, heart rate, and spontaneous movement. The expression of cat1, sod1, gstr1, nrf2a, nrf2b, and HO-1, as well as alterations in ROS, SOD, CAT, and MDA levels, all demonstrated oxidative damage caused by PS-NH₂ exposure. Mitochondrial dysfunction was also induced, as evidenced by changes in the expression of cox4i1, ndufs1, and uqcrc1, as well as changes in the levels of ATP, cytochrome c, NAD, and NADH. Furthermore, PS-NH₂ exposure disrupted apoptosis regulation, increasing apoptotic cells and caspase activity, along with changes in caspase-3 and bcl-2 expression. Molecular docking showed that PS-NH₂ interacts with bcl-2 with high binding energy. This study contributes to understanding the toxic effects and mechanisms of charge-modified MPs in zebrafish.

01 Dec 2024·iScience

miR-450b-5p promotes development of endometriosis by inhibiting the GABPA/HOXD10 axis

Article

Author: Liu, Yongmei ; Li, Ruiyun ; Wang, Yidan ; Huang, Yi ; Yang, Yuan

Despite decades of research, the pathogenesis of endometriosis remains unclear. Recent studies have shown that microRNAs play an important role in this condition. In this study, we found that the expression level of miR-450b-5p was increased in ectopic endometrial tissues and that GA-binding protein A (GABPA) and HOXD10 expression levels were decreased. Overexpression of miR-450b-5p or knockdown of GABPA significantly promoted the proliferation and invasion of hEM15A cells and inhibited apoptosis in vivo and in vitro. Furthermore, GABPA was shown to be a direct target of miR-450b-5p and to bind directly to the promoter of the HOXD10 gene, regulating its transcription. Finally, intraperitoneal injection of HOXD10-overexpressing lentivirus in mice significantly attenuated ectopic endometrial lesions. miR-450b-5p directly targets GABPA, regulates expression of HOXD10, and promotes the growth of ectopic endometriotic lesions. Therefore, the miR-450b-5p/GABPA/HOXD10 signaling pathway may be a potential target for treatment of heterotopic endothelial cell disease.

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GABPA

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