从长期受对硝基酚(para-nitrophenol,PNP)污染的土壤中,分离到一株能够降解对硝基酚并以其作为唯一碳源和氮源生长的菌株,命名为PN-1。经16S r DNA序列分析,初步鉴定该菌株为假单胞菌(Pseudomona)。通过研究其对PNP的降解、重金属以及...从长期受对硝基酚(para-nitrophenol,PNP)污染的土壤中,分离到一株能够降解对硝基酚并以其作为唯一碳源和氮源生长的菌株,命名为PN-1。经16S r DNA序列分析,初步鉴定该菌株为假单胞菌(Pseudomona)。通过研究其对PNP的降解、重金属以及抗生素抗性、植物促生等特性,得到如下结果:该菌株对PNP的最大耐受质量浓度为200 mg/L,具有卡那霉素和氯霉素抗性,对4种重金属Cd2+、Pb2+、Zn2+和Cr6+的最低抑制浓度(minimum inhibitory concentration,MIC)分别为700、500、800和100 mg/L,同时具有产吲哚乙酸(IAA)和铁载体、1-氨基环丙烷-1-羧酸(ACC)脱氨酶活性以及溶磷能力。通过用荧光蛋白标记后能在土壤中正常存活,具有能与植物联合修复PNP污染土壤的潜力,有较好的使用前景。展开更多
Transforming growth factor-β （TGF-β） binds with two transmembrane serine/threonine kinase receptors, type Ⅱ （TβRII） and type Ⅰ receptors （TβRⅠ）, and one accessory receptor, type Ⅲ receptor （TβRⅢ）, to...Transforming growth factor-β （TGF-β） binds with two transmembrane serine/threonine kinase receptors, type Ⅱ （TβRII） and type Ⅰ receptors （TβRⅠ）, and one accessory receptor, type Ⅲ receptor （TβRⅢ）, to transduce signals across cell membranes. Previous biochemical studies suggested that TβRI and TβRIII are preexisted homo-dimers. Using single-molecule microscopy to image green fluorescent protein-labeled membrane proteins, for the first time we have demonstrated that TβRI and TβRⅢ could exist as monomers at a low expression level. Upon TGF-β1 stimu- lation, TβRI follows the general ligand-induced receptor dimerization model for activation, but this process is TβRⅡ- dependent. The monomeric status of the non-kinase receptor TβRⅢ is unchanged in the presence of TGF-β1. With the increase of receptor expression, both TβRI and TβRIII can be assembled into dimers on cell surfaces.展开更多
The bones are the most common sites of breast cancer metastasis. Upon arrival within the bone microenvironment, breast cancer cells coordinate the activities of stromal cells, resulting in an increase in osteoclast ac...The bones are the most common sites of breast cancer metastasis. Upon arrival within the bone microenvironment, breast cancer cells coordinate the activities of stromal cells, resulting in an increase in osteoclast activity and bone matrix degradation. In late stages of bone metastasis, breast cancer cells induce apoptosis in osteoblasts, which further exacerbates bone loss. However, in early stages, breast cancer cells induce osteoblasts to secrete inflammatory cytokines purported to drive tumor progression. To more thoroughly evaluate the role of osteoblasts in early stages of breast cancer metastasis to the bones, we used green fluorescent protein-labeled human breast cancer cell lines MDA-MB-231 and MDA-MB-435, which both induce osteolysis after intra-femoral injection in athymic mice, and the murine pre-osteoblastic cell line MC3T3-E1 to modulate osteoblast populations at the sites of breast cancer metastasis. Breast cancer cells were injected directly into the femur with or without equal numbers of MC3T3-E1 cells. Tumors grew significantly larger when co-injected with breast cancer cells and MC3T3-E1 cells than injected with breast cancer cells alone. Osteolysis was induced in both groups, indicating that MC3T3-E1 cells did not block the ability of breast cancer cells to cause bone destruction. MC3T3-E1 cells promoted tumor growth out of the bone into the extraosseous stroma. These data suggest that breast cancer cells and osteoblasts communicate during early stages of bone metastasis and promote tumor growth.展开更多
基金This work was supported by the National Natural Science Foundation of China （90713024, 20821003, 30921004）, the National Basic Research Program of China （2007CB935601, 2010CB833706） and the Chinese Academy of Sciences.
文摘Transforming growth factor-β （TGF-β） binds with two transmembrane serine/threonine kinase receptors, type Ⅱ （TβRII） and type Ⅰ receptors （TβRⅠ）, and one accessory receptor, type Ⅲ receptor （TβRⅢ）, to transduce signals across cell membranes. Previous biochemical studies suggested that TβRI and TβRIII are preexisted homo-dimers. Using single-molecule microscopy to image green fluorescent protein-labeled membrane proteins, for the first time we have demonstrated that TβRI and TβRⅢ could exist as monomers at a low expression level. Upon TGF-β1 stimu- lation, TβRI follows the general ligand-induced receptor dimerization model for activation, but this process is TβRⅡ- dependent. The monomeric status of the non-kinase receptor TβRⅢ is unchanged in the presence of TGF-β1. With the increase of receptor expression, both TβRI and TβRIII can be assembled into dimers on cell surfaces.
基金supported by U.S. Army Medical Research and Materiel Command grants W81-XWH-07-1-0399 (to D.R. Welch) and W81-XWH-08-1-0779 (to T.M. Bodenstine)partial support from NIH-CA134981 and CA-87728 (D.R. Welch)the National Foundation for Cancer Research Center for Metastasis Research (D.R. Welch) and Susan G. Komen for the Cure (D.R. Welch)
文摘The bones are the most common sites of breast cancer metastasis. Upon arrival within the bone microenvironment, breast cancer cells coordinate the activities of stromal cells, resulting in an increase in osteoclast activity and bone matrix degradation. In late stages of bone metastasis, breast cancer cells induce apoptosis in osteoblasts, which further exacerbates bone loss. However, in early stages, breast cancer cells induce osteoblasts to secrete inflammatory cytokines purported to drive tumor progression. To more thoroughly evaluate the role of osteoblasts in early stages of breast cancer metastasis to the bones, we used green fluorescent protein-labeled human breast cancer cell lines MDA-MB-231 and MDA-MB-435, which both induce osteolysis after intra-femoral injection in athymic mice, and the murine pre-osteoblastic cell line MC3T3-E1 to modulate osteoblast populations at the sites of breast cancer metastasis. Breast cancer cells were injected directly into the femur with or without equal numbers of MC3T3-E1 cells. Tumors grew significantly larger when co-injected with breast cancer cells and MC3T3-E1 cells than injected with breast cancer cells alone. Osteolysis was induced in both groups, indicating that MC3T3-E1 cells did not block the ability of breast cancer cells to cause bone destruction. MC3T3-E1 cells promoted tumor growth out of the bone into the extraosseous stroma. These data suggest that breast cancer cells and osteoblasts communicate during early stages of bone metastasis and promote tumor growth.
