Johansson M W, Larsson E, Lüning B, Pasquale E B, Ruoslahti E
La Jolla Cancer Research Foundation, California 92037.
J Cell Biol. 1994 Sep;126(5):1299-309. doi: 10.1083/jcb.126.5.1299.
We describe a novel approach to study tyrosine-phosphorylated (PY) integrins in cells transformed by virally encoded tyrosine kinases. We have synthesized a peptide (PY beta 1 peptide) that represents a portion of the cytoplasmic domain of the beta 1 integrin subunit and is phosphorylated on the tyrosine residue known to be the target of oncogenic tyrosine kinases. Antibodies prepared against the PY beta 1 peptide, after removal of cross-reacting antibodies by absorption and affinity purification, recognized the PY beta 1 peptide and the tyrosine-phosphorylated form of the intact beta 1 subunit, but did not bind the nonphosphorylated beta 1 peptide, the nonphosphorylated beta 1 subunit or other unrelated tyrosine-phosphorylated proteins. The anti-PY beta 1 antibodies labeled the podosomes of Rous sarcoma virus-transformed fibroblasts, but did not detectably stain nontransformed fibroblasts. The localization of the tyrosine phosphorylated beta 1 subunits appeared distinct from that of the beta 1 subunit. Adhesion plaques were stained by the anti-beta 1 subunit antibodies in Rous sarcoma virus-transformed fibroblasts plated on fibronectin, whereas neither podosomes nor adhesion plaques were labeled on vitronectin or on uncoated plates. Anti-phosphotyrosine antibodies labeled podosomes, adhesion plaques and cell-cell boundaries regardless of the substratum. One of the SH2 domains of the p85 subunit of phosphatidylinositol-3-kinase bound to the PY beta 1 peptide, but not to the non-phosphorylated beta 1 cytoplasmic peptide. Other SH2 domains did not bind to the PY beta 1 peptide. These results show that the phosphorylated form of the beta 1 integrin subunit is detected in a different subcellular localization than the nonphosphorylated form and suggest that the phosphorylation on tyrosine of the beta 1 subunit cytoplasmic domain may affect cellular signaling pathways.
我们描述了一种新方法,用于研究由病毒编码的酪氨酸激酶转化的细胞中的酪氨酸磷酸化(PY)整合素。我们合成了一种肽(PYβ1肽),它代表β1整合素亚基细胞质结构域的一部分,并且在已知是致癌酪氨酸激酶作用靶点的酪氨酸残基上被磷酸化。针对PYβ1肽制备的抗体,在通过吸收和亲和纯化去除交叉反应抗体后,能够识别PYβ1肽和完整β1亚基的酪氨酸磷酸化形式,但不与非磷酸化的β1肽、非磷酸化的β1亚基或其他不相关的酪氨酸磷酸化蛋白结合。抗PYβ1抗体标记了劳氏肉瘤病毒转化的成纤维细胞的足体,但未检测到对未转化成纤维细胞的染色。酪氨酸磷酸化的β1亚基的定位似乎与β1亚基的定位不同。在铺有纤连蛋白的劳氏肉瘤病毒转化的成纤维细胞中,粘着斑被抗β1亚基抗体染色,而在玻连蛋白或未包被的平板上,足体和粘着斑均未被标记。抗磷酸酪氨酸抗体标记足体、粘着斑和细胞 - 细胞边界,而与底物无关。磷脂酰肌醇 - 3 - 激酶p85亚基的一个SH2结构域与PYβ1肽结合,但不与非磷酸化的β1细胞质肽结合。其他SH2结构域不与PYβ1肽结合。这些结果表明,β1整合素亚基的磷酸化形式在与非磷酸化形式不同的亚细胞定位中被检测到,并表明β1亚基细胞质结构域的酪氨酸磷酸化可能影响细胞信号通路。