細胞的生長、分化、發育都需要能量。粒腺體為細胞能量的來源。核醣體的生物活性與細胞循環、增生及腫瘤生成有關。有研究指出抑癌基因或原致癌基因會參與調控核醣體成熟與生物活性。抑癌基因p53受到核醣體蛋白或其他蛋白的修飾而引起細胞循環停滯或死亡。粒腺體的rRNA由粒腺體DNA轉錄而來，粒腺體核醣體蛋白的產生則來自細胞核基因。粒腺體核醣體蛋白的功能尚未被釐清而其是受到是轉錄因子嚴格的控制並與粒腺體的功能有關。我們選殖出一基因為老鼠粒腺體核醣體蛋白S36。我們將老鼠粒腺體核醣體蛋白S36送到NIH3T3中，發現老鼠粒腺體核醣體蛋白S36分佈於粒腺體中。老鼠粒腺體核醣體蛋白S36過量表現會造成抑癌基因p53的磷酸化並讓其下游基因p21表現進而引起細胞循環的停滯且影響粒腺體的功能。前胸腺素(ProT)過量表現會促進細胞的增生。前胸腺素是一個轉錄因子，其也可與其他轉錄因子如CBP結合調節基因的表現。我們的研究發現前胸腺素會造成粒腺體核醣體蛋白S36 mRNA的表現量增加。報告基因的研究也顯示出老鼠粒腺體核醣體蛋白S36啟動區段-480到-190 bp可能是前胸腺素的反應區域。在老鼠粒腺體核醣體蛋白S36啟動區段我們發現了可能是前胸腺素結合的片段，而其附近也含有其他其他轉錄因子如CREB的結合片段。我們推測前胸腺素可以透過與其他轉錄因子的作用來調控老鼠粒腺體核醣體蛋白S36的表現。

Most of the energy required for cell growth, differentiation, and development are met by mitochondrial ATP. Ribosomal biogenesis is correlated with cell cycle, cell proliferation, cell growth and tumorigenesis. Some oncogenes and tumor suppressors are involved in regulating the formation of mature ribosome and the ribosomal biogenesis. p53 induced cell cycle arrest when stabilized by ribosomal proteins and MDM2/HDM2 interaction. p53-dependent cycle arrest is primarily mediated by the CDK inhibitor p21. The mitochondrial rRNA are encoded by mtDNA, whereas the ribosomal proteins are encoded in the nuclear genes, they are synthesized on cytoplasmic ribosomes, and imported into the mitochondria. All of the proteins in mammalian mitochondrial ribosomes are products of nuclear genes. The majority of the mammalian MRPs have never been characterised in the laboratory. It is tightly regulated by series of transcription factors for maintain mitochondrial biogenesis and function. In this report, we cloned a gene mitochondrial ribosomal protein S36 (mMRPS36). Overexpression mMRPS36 in cells suppresses cell proliferation and induced cell cycle arrest. mMRPS36 overexpression induced p21 expression through the transcriptional level by p53 mechanism. We discovered that mMRPS36 protein is localized in the mitochondria and affects the mitochondrial function. These results suggest that mMRPS36 plays an important role in mitochondrial ribosomal biogenesis may cause nucleolar stress, leading to cell cycle arrest in a p21-dependent manner. Prothymosin α (ProTα) overexpression promotes cell proliferation and cell cycle. The function of ProTα in transcription activation interacted with co-activator of transcription CBP is a role for this acidic polypeptide in gene expression. In the present study, we found that ProTα increased the expression of mMRPS36 mRNA. Reporter assays revealed that the ProTα response region was in the range of -480 to -190 bp. ProTα is a nuclear protein and suggest that binds DNA in a sequence-specific manner. Potential ProTα binding sites were detected in 5’-flanking region of MRPS36 gene and closed to CREB transcription factor binding site. Taken together, these results suggest that C/EBP and CREB sites in the essential promoter region are critical for ProT response, and CREB showed a functional cooperation with coactivator p300/ CBP in driving the transcriptional regulation of ProT induce mMRPS36 gene expression.

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