Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Department of Biochemistry and Molecular Biology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Department of Dermatology, University of Maryland School of Medicine, Baltimore, Maryland, USA; Department of Obstetrics and Gynecology and Reproductive Sciences, University of Maryland School of Medicine, Baltimore, Maryland, USA.
J Invest Dermatol. 2014 May;134(5):1220-1229. doi: 10.1038/jid.2013.533. Epub 2013 Dec 13.
Tazarotene-induced gene 3 (TIG3) is a tumor suppressor protein that has a key role in controlling cell proliferation. TIG3 is observed at reduced levels in epidermal squamous cell carcinoma, and the restoration of expression in skin cancer cells reduces cell survival. TIG3 suppresses cell survival through mechanisms that involve localization at the plasma membrane and at the centrosome. TIG3 interacts at the plasma membrane to activate enzymes involved in keratinocyte terminal differentiation, and at the centrosome to inhibit daughter centrosome separation during mitosis leading to cessation of cell proliferation and induction of apoptosis. An important goal is identifying the motifs required for TIG3 localization at these intracellular sites as a method to understand the function of TIG3 at each location. TIG3 encodes an N-terminal hydrophilic region (amino acids 1-135) and a C-terminal membrane-anchoring domain (amino acids 135-164). We show that the C-terminal hydrophobic domain targets intact TIG3 to the plasma membrane, but when isolated as an independent element localizes at the mitochondria. We further demonstrate that a segment of the N-terminal hydrophilic region targets the centrosome. These studies provide important insights regarding the mechanisms that guide subcellular localization of this keratinocyte survival regulator.
TIG3 是一种抑癌蛋白,可诱导肿瘤(Tazarotene-induced gene 3),在控制细胞增殖方面起着关键作用。在表皮鳞癌细胞中,TIG3 的表达水平降低,而在皮肤癌细胞中恢复表达则会降低细胞存活率。TIG3 通过在质膜和中心体定位的机制抑制细胞存活。TIG3 在质膜上与参与角质形成细胞终末分化的酶相互作用,在中心体上抑制有丝分裂期间子中心体的分离,从而停止细胞增殖并诱导细胞凋亡。一个重要的目标是确定 TIG3 在这些细胞内位置定位所需的基序,作为理解 TIG3 在每个位置功能的一种方法。TIG3 编码一个 N 端亲水区域(氨基酸 1-135)和一个 C 端膜锚定结构域(氨基酸 135-164)。我们表明,C 端疏水区靶向完整的 TIG3 到质膜,但作为一个独立的元素分离时定位在线粒体。我们进一步证明,N 端亲水区域的一个片段靶向中心体。这些研究为指导这种角质形成细胞生存调节剂的细胞内定位的机制提供了重要的见解。