Recombinant human uteroglobin suppresses cellular invasiveness via a novel class of high-affinity cell surface binding site

Gopal C. Kundu; Giuditta Mantile; Lucio Miele

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Recombinant human uteroglobin suppresses cellular invasiveness via a novel class of high-affinity cell surface binding site

机译：重组人子宫珠蛋白通过一类新型的高亲和力细胞表面结合位点抑制细胞侵袭性

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The mechanism(s) that regulates invasion of trophoblasts through the uterine epithelium during embryo implantation and nidation in hemochorial placental mam- als is poorly understood. While limited trophoblast invasion is essential for the establishment of normal pregnancy, dys- rgulation of this process may contribute to the pathogenesis of choriocarcinoma, a highly invasive and lethal form of cancer arising from the trophoblasts.

机译：尚不了解调节血细胞胎盘哺乳动物胚胎着床和消融过程中滋养细胞通过子宫上皮侵入的机制。虽然有限的滋养细胞浸润对于正常妊娠的建立至关重要，但该过程的失调可能会导致绒毛膜癌的发病，绒毛膜滋养细胞是高度浸润性和致死性的癌症。

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《Proceedings of the National Academy of Sciences of the United States of America》 |1996年第7期|p.2915-2919|共5页
作者
Gopal C. Kundu; Giuditta Mantile; Lucio Miele;
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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
原文格式 PDF
正文语种 eng
中图分类自然科学总论;
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2. Inhibition of micro RNA RNA ‐21‐3p suppresses proliferation as well as invasion and induces apoptosis by targeting RNA‐binding protein with multiple splicing through Smad4/extra cellular signal‐regulated protein kinase signalling pathway in human colorectal cancer HCT HCT 116 cells [J] . Hou Nengyi, Guo Zhiyi, Zhao Gaoping, Clinical and experimental pharmacology & physiology . 2018,第7期

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6. Recombinant human uteroglobin suppresses cellular invasiveness via a novel class of high-affinity cell surface binding site. [O] . G C Kundu, G Mantile, L Miele, 1996

机译：重组人子宫珠蛋白通过一类新型的高亲和力细胞表面结合位点抑制细胞侵袭性。
7. Recombinant human uteroglobin suppresses cellular invasiveness via a novel class of high-affinity cell surface binding site. [O] . Kundu, G C, Mantile, G, Miele, L, 1996

机译：重组人子宫珠蛋白通过一类新型的高亲和力细胞表面结合位点抑制细胞侵袭性。
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机译：小鼠神经母细胞瘤细胞中毒蕈碱胆碱能受体的短期脱敏：激动剂低亲和力和哌仑西平高亲和力结合位点的选择性丧失

Recombinant human uteroglobin suppresses cellular invasiveness via a novel class of high-affinity cell surface binding site

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