TAF1C（TATA-box binding protein associated factor 1C）是RNA聚合酶II转录起始复合物TFIID的一个亚基，属于TAF（TBP-associated factors）基因家族。TAF家族成员是TFIID复合物的核心组成部分，它们与TBP（TATA-box结合蛋白）结合，共同参与识别核心启动子并调控基因转录起始。TAF1C在核糖体RNA（rRNA）的转录中起关键作用，它通过与RNA聚合酶I相互作用，调控核糖体生物合成，从而影响细胞生长和增殖。TAF1C的主要作用位点是核仁，这是细胞核内负责rRNA合成和加工的区域。TAF1C的突变可能导致其功能异常，影响rRNA的转录，进而干扰核糖体生成，最终导致细胞增殖受阻或凋亡。研究表明，TAF1C的异常表达与某些癌症相关，例如在肝癌和乳腺癌中TAF1C的表达水平显著升高，可能通过促进肿瘤细胞的快速增殖和存活来驱动癌症进展。如果TAF1C过表达，可能会增强rRNA的合成，导致核糖体数量增加，从而加速蛋白质合成和细胞生长，这可能在某些情况下促进肿瘤发生。相反，TAF1C表达降低可能导致rRNA合成减少，核糖体不足，进而抑制细胞增殖，甚至引发细胞凋亡。TAF1C属于TAF基因家族，该家族的共性是与TBP结合形成TFIID复合物，参与调控RNA聚合酶II介导的mRNA转录，但TAF1C独特之处在于它还参与RNA聚合酶I介导的rRNA转录。TAF家族成员通常具有保守的结构域，如组蛋白折叠结构域（histone fold domain），这有助于它们与其他转录因子相互作用。TAF1C的功能异常不仅影响rRNA合成，还可能通过间接调控其他基因的表达（如细胞周期相关基因）来影响整体细胞功能。目前关于TAF1C的研究仍在深入，其在疾病中的作用机制和潜在治疗靶点值得进一步探索。

由RNA聚合酶I转录的启动需要的TATA结合蛋白组成复合物的形成（TBP）和三个特异于RNA聚合酶I这种复杂的，被称为SL1，绑定TBP相关因子（TAFS）到的核糖体RNA基因的核心启动子，以正确地定位聚合酶和充当调节信号的信道。该基因ENCO德最大的特异SL1-TAF。编码不同亚型多重选择性剪接转录变异体已经确定。 [由RefSeq的，2011年7月提供]

TAF1C, a member of the TATA-box binding protein-associated factor (TAF) gene family, functions as a critical subunit of the general transcription factor TFIID, which is essential for the initiation of eukaryotic transcription. While TAF family members typically share conserved histone fold domains that facilitate interactions with the TATA-box binding protein (TBP) to form the TFIID complex for RNA polymerase II-mediated mRNA synthesis, TAF1C exhibits a distinct dual role by also engaging with RNA polymerase I. This unique interaction allows TAF1C to regulate the transcription of ribosomal RNA (rRNA) within the nucleolus, thereby directly influencing ribosome biogenesis and the cell's capacity for protein synthesis. By modulating the production of ribosomes, TAF1C plays a pivotal role in controlling cell growth and proliferation; consequently, its dysregulation can have profound cellular consequences. Loss of TAF1C function or reduced expression leads to impaired rRNA synthesis and a deficit in ribosome production, which can suppress cell proliferation and potentially trigger apoptosis. Conversely, the overexpression of TAF1C, as observed in various malignancies including hepatocellular carcinoma and breast cancer, enhances rRNA synthesis and increases ribosome abundance, thereby accelerating protein synthesis and promoting tumor cell survival and rapid proliferation. Beyond its direct role in rRNA transcription, TAF1C may indirectly influence the expression of other genes, such as those involved in cell cycle regulation, suggesting a broader impact on overall cellular homeostasis. The aberrant expression of TAF1C in cancer contexts highlights its potential as a driver of tumorigenesis and a promising target for therapeutic intervention, although further research is required to fully elucidate its mechanistic contributions to disease progression.

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