TEAD4（TEA domain transcription factor 4）是TEAD转录因子家族的一员，该家族包括TEAD1-4四个成员，均含保守的TEA结构域（一种DNA结合域），负责识别并结合MCAT（肌肉-心脏-激活因子）等特定DNA序列，调控靶基因表达。TEAD家族共性是与共激活因子YAP/TAZ（Yes-associated protein/Transcriptional coactivator with PDZ-binding motif）结合，激活下游基因参与细胞增殖、分化、器官发育等过程。TEAD4在胚胎发育（如滋养层干细胞维持、胎盘形成）和成体组织（如肌肉、心脏）中发挥关键作用，其表达产物通过调控细胞周期蛋白（如Cyclin D1）和抗凋亡基因（如BIRC5）促进细胞存活与增殖。主要作用位点包括细胞核内靶基因启动子区域，如Hippo信号通路下游效应分子。突变可能导致TEAD4功能异常，例如DNA结合能力丧失或YAP/TAZ相互作用缺陷，与胎儿生长受限、先兆子痫等妊娠疾病相关，在癌症中（如胃癌、卵巢癌）常见TEAD4过表达，通过激活促癌基因驱动肿瘤进展。过表达时，TEAD4增强YAP/TAZ介导的转录活性，促进组织过度生长或纤维化；低表达则可能导致胚胎致死（小鼠模型）或肌肉再生障碍。TEAD4还与代谢疾病相关，如通过调节GLUT4影响葡萄糖摄取。其功能依赖与YAP/TAZ的相互作用，若该通路异常（如Hippo通路失活），TEAD4活性不受抑制，导致病理增生。

该基??因产物是转录增强因子（TEF）家族的转录因子，其含有TEA / ATTS DNA结合域的成员。它是在骨骼肌中优先表达，并结合在肌肉特异性基因启动子指导它们的基因表达发现在M-CAT调控元件。编码不同同种型，其中一些是通过使用非-AUG（UUG）起始密码子的翻译可变剪接转录物，已被用于这个基因说明。 [由RefSeq的，2008年7月提供]

TEAD4, a member of the TEAD family of transcription factors, contains a conserved TEA domain that mediates specific DNA binding to MCAT (muscle- and heart-specific activating factor) sequences, thereby regulating the expression of target genes. This family, which includes TEAD1 through TEAD4, functions primarily by forming complexes with the transcriptional coactivators YAP and TAZ, a partnership that is central to the execution of the Hippo signaling pathway. Through this interaction, TEAD4 drives the transcription of genes involved in cell proliferation, differentiation, and organ development, with key downstream targets including cell cycle regulators such as Cyclin D1 and anti-apoptotic factors like BIRC5, which collectively promote cell survival and growth. TEAD4 is critically expressed in both embryonic and adult tissues, playing essential roles in trophoblast stem cell maintenance, placentation, and the homeostasis of muscle and cardiac tissues, while also influencing metabolic processes such as glucose uptake through the regulation of GLUT4. Dysregulation of TEAD4 function, whether through mutations that impair DNA binding or YAP/TAZ interaction, or through aberrant expression levels, has significant pathological implications; for instance, loss of function can lead to embryonic lethality in mouse models or impaired muscle regeneration, whereas overexpression is frequently observed in cancers such as gastric and ovarian carcinoma, where it drives tumor progression by enhancing YAP/TAZ-mediated transcription of oncogenic genes. Furthermore, defects in the Hippo pathway that fail to properly inhibit TEAD4 activity can result in pathological tissue hyperplasia or fibrosis, and specific TEAD4 abnormalities have been linked to pregnancy complications including fetal growth restriction and preeclampsia, underscoring its vital role in maintaining physiological balance across development and adult life.

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