Laherty C D, Billin A N, Lavinsky R M, Yochum G S, Bush A C, Sun J M, Mullen T M, Davie J R, Rose D W, Glass C K, Rosenfeld M G, Ayer D E, Eisenman R N
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104, USA.
Mol Cell. 1998 Jul;2(1):33-42. doi: 10.1016/s1097-2765(00)80111-2.
The transcriptional corepressor mSin3 is found in a large multiprotein complex containing the histone deacetylases HDAC1 and HDAC2, in addition to at least five tightly associated polypeptides. We have cloned and characterized a novel component of the mSin3 complex, SAP30, SAP30 binds to mSin3 and is capable of mediating transcriptional repression via histone deacetylases. SAP30 also binds the N-CoR corepressor and is required for N-CoR-mediated repression by antagonist-bound estrogen receptor and the homeodomain protein Rpx, as well as N-CoR suppression of transactivation by the POU domain protein Pit-1. However, SAP30 is not required for N-CoR-mediated repression by unliganded retinoic acid receptor or thyroid hormone receptor, suggesting that SAP30 is involved in the functional recruitment of the mSin3-histone deacetylase complex to a specific subset of N-CoR corepressor complexes.
转录共抑制因子mSin3存在于一个大型多蛋白复合物中,该复合物除了至少有五个紧密相关的多肽外,还包含组蛋白去乙酰化酶HDAC1和HDAC2。我们克隆并鉴定了mSin3复合物的一个新组分SAP30,SAP30与mSin3结合,并能够通过组蛋白去乙酰化酶介导转录抑制。SAP30还与N-CoR共抑制因子结合,并且是拮抗剂结合的雌激素受体和同源结构域蛋白Rpx介导的N-CoR抑制作用以及POU结构域蛋白Pit-1介导的N-CoR对反式激活的抑制作用所必需的。然而,未结合配体的视黄酸受体或甲状腺激素受体介导的N-CoR抑制作用并不需要SAP30,这表明SAP30参与了mSin3-组蛋白去乙酰化酶复合物向N-CoR共抑制因子复合物的特定亚群的功能性募集。