Cytotechnology. 1999 Sep;31(1-2):95-102. doi: 10.1023/A:1008024322602.
Alcohol dehydrogenase-I (ADH-I) derived from horse liver stimulated IgM production by human-human hybridoma, HB4C5 cells and lymphocytes. The IPSF activity of ADH-I was suppressed by coexistence of short DNA whose chain length is less than 200 base pairs (bp) and fibrous DNA in a dose-dependent manner. These DNA preparations completely inhibited the IPSF activity at the concentration of 250 mug/ml and 1.0 mg/ml, respectively. DNA sample termed long DNA whose average chain length is 400-7000 bp slightly stimulated IPSF activity at 0.06 mug/ml. However, long DNA suppressed IPSF activity by half at 1.0 mg/ml. The laser confocal microscopic analysis had revealed that ADH-I was incorporated by HB4C5 cells. The uptake of ADH-I was strongly inhibited by short DNA and fibrous DNA. However, long DNA did not suppress the internalization of ADH-I into HB4C5 cells. These findings indicate that short DNA and fibrous DNA depress IPSF activity of ADH-I by inhibiting the internalization of this enzyme. According to the gel-filtration analysis using HPLC, ADH-I did not directly interact with short DNA. It is expected from these findings that short DNA influences HB4C5 cells to suppress the internalization of ADH-I. Moreover, these facts also strongly suggest that ADH-I acts as IPSF after internalization into the cell.
马肝醇脱氢酶-I（ADH-I）可刺激人-人杂交瘤 HB4C5 细胞和淋巴细胞产生 IgM。ADH-I 的 IPSF 活性可被长度小于 200 个碱基对（bp）的短 DNA 与纤维状 DNA 共同存在的方式以剂量依赖的方式抑制。这些 DNA 制剂在 250μg/ml 和 1.0mg/ml 的浓度下完全抑制 IPSF 活性。平均链长为 400-7000bp 的 DNA 样本被称为长 DNA，其在 0.06μg/ml 时轻微刺激 IPSF 活性。然而，长 DNA 在 1.0mg/ml 时将 IPSF 活性抑制了一半。激光共聚焦显微镜分析表明 ADH-I 被 HB4C5 细胞摄取。HB4C5 细胞摄取 ADH-I 强烈地被短 DNA 和纤维状 DNA 抑制。然而，长 DNA 并没有抑制 ADH-I 内化进入 HB4C5 细胞。这些发现表明短 DNA 和纤维状 DNA 通过抑制该酶的内化来降低 ADH-I 的 IPSF 活性。根据使用 HPLC 的凝胶过滤分析，ADH-I 不会直接与短 DNA 相互作用。从这些发现中可以预期，短 DNA 会影响 HB4C5 细胞抑制 ADH-I 的内化。此外，这些事实还强烈表明 ADH-I 在进入细胞后作为 IPSF 发挥作用。
