TAF10（TATA-box binding protein associated factor 10）是转录因子复合物TFIID的重要组成部分，属于TAF基因家族。TAF家族成员（如TAF1-TAF15）的共同特点是它们与TBP（TATA结合蛋白）结合形成TFIID复合物，在RNA聚合酶II介导的基因转录起始中发挥核心作用。TAF10的主要生物学功能是通过与其他TAF蛋白及TBP结合，帮助TFIID识别启动子区域的TATA盒或其他核心启动元件，从而促进转录前起始复合物的组装。TAF10的表达产物是一种保守的核蛋白，广泛存在于真核生物中，其特点是含有组蛋白折叠结构域（histone fold domain），这使得它能与TAF3、TAF8等家族成员形成异源二聚体，稳定TFIID的结构。主要作用位点在细胞核内，参与调控包括细胞周期、发育相关基因在内的多种基因的转录。若TAF10发生功能丧失性突变（loss-of-function mutation），可能导致TFIID复合物组装异常，影响全局基因转录，在小鼠模型中表现为胚胎致死；而某些错义突变（missense mutation）可能与癌症发生相关，例如在结直肠癌中已观察到TAF10的异常表达。TAF10过表达可能破坏TFIID复合物的 stoichiometry（化学计量平衡），导致转录失调，进而影响细胞增殖相关基因（如MYC、CCND1）的表达；反之，其表达降低会削弱TFIID的稳定性，引起p53通路激活或细胞分化障碍。该基因与神经发育疾病和多种肿瘤（如白血病、乳腺癌）存在关联，在肝癌中TAF10高表达常预示不良预后。TAF家族成员均参与转录调控，但各自具有组织特异性，例如TAF7在精子发生中起独特作用，而TAF10则对维持胚胎干细胞多能性至关重要。

由RNA聚合酶II转录起始需要70多个多肽的活动。它协调这些活动的蛋白质是转录因子的IID（TFIID），其结合到核心启动子正确定位聚合酶，作为支架的转录复合物的其余部分的组件，并作为调节信号的信道。 TFIID是由TATA结合蛋白（TBP）和一组被称为TBP相关因子或TAFS进化保守的蛋白质的。 TAFS可能参与基础转录，作为共激活因子，功能的启动子识别或修改一般转录因子（基转移酶），以方便复杂的组装和转录起始。这个基因编码与TFIID复合物的子集相关联TFIID的小亚基中的一个。已经与人类和哺乳动物细胞的研究表明，这种亚单位所需的转录激活的雌激素受体，用于通过细胞周期进程，并且也可能需要对某些细胞分化的程序。 [由RefSeq的，2008年7月提供]

TAF10, encoding a conserved nuclear protein and a critical subunit of the TFIID transcription factor complex, plays a pivotal role in the initiation of RNA polymerase II-mediated gene transcription. As a member of the TATA-box binding protein associated factor (TAF) family, TAF10 utilizes its histone fold domain to form stable heterodimers with other TAFs, such as TAF3 and TAF8, thereby ensuring the structural integrity and stoichiometric balance of the TFIID complex. This complex is essential for recognizing core promoter elements, including the TATA box, and facilitating the assembly of the pre-initiation complex at the start sites of target genes. TAF10 is broadly expressed across eukaryotes and is particularly vital for maintaining the pluripotency of embryonic stem cells, as well as regulating the transcription of genes involved in cell cycle progression and development, such as MYC and CCND1. Disruption of TAF10 function through loss-of-function mutations leads to defective TFIID assembly, resulting in global transcriptional failure and embryonic lethality in murine models, while dysregulation of its expression levels can have profound pathological consequences. Specifically, TAF10 overexpression can perturb the stoichiometry of the TFIID complex, leading to transcriptional dysregulation and aberrant expression of proliferation-associated genes, a phenomenon frequently observed in various malignancies including leukemia, breast cancer, and colorectal cancer. In hepatocellular carcinoma, high TAF10 expression is often associated with poor clinical prognosis, whereas reduced expression may compromise TFIID stability, potentially triggering p53 pathway activation or impairing cellular differentiation. Thus, TAF10 serves as a fundamental regulator of basal transcription, with its precise expression and interaction dynamics being critical for normal cellular homeostasis, embryonic development, and the prevention of tumorigenesis.

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