Intracellular trafficking of endogenous fibroblast growth factor‐2
Intracellular trafficking of endogenous fibroblast growth factor‐2
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内源性成纤维细胞生长因子 2 的细胞内运输
DOI：
10.1111/j.1742-4658.2008.06316.x
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发表时间：
2008
期刊：
影响因子：
--
通讯作者：
M. Vittorelli
中科院分区：
文献类型：
--
作者：
S. Taverna;S. Rigogliuso;M. Salamone;M. Vittorelli
我们以前曾报道过成纤维细胞生长因子-2（FGF-2）的释放是如何通过脱落囊泡介导的。在本研究中，我们解决了新合成的FGF-2如何靶向出芽囊泡的问题。考虑到体外培养的Sk-Hep 1肝癌细胞仅在血清存在下培养时释放FGF-2并脱落膜囊泡，我们向饥饿细胞中加入血清并监测生长因子的细胞内运动。 FGF-2靶向细胞周边以及细胞核和核仁。向细胞外周的运动不受影响微管的药物的影响，但被cytocalasin B抑制。 肌动蛋白参与FGF-2向细胞外周的运输得到了免疫共沉淀和免疫定位实验的支持。未观察到FGF-2颗粒移动至细胞外周和FM 4 - 64标记的细胞内脂质的共定位。分析了两种FGF-2释放抑制剂哇巴因和甲胺对FGF-2细胞内定位和囊泡脱落的影响。哇巴因抑制FGF-2向细胞周边移动。因此，脱落囊泡的FGF-2含量降低。甲胺抑制囊泡脱落;在其存在下，FGF-2聚集在细胞周边，但其释放速率降低。靶向细胞核和核仁的FGF-2不受细胞钙蛋白B的影响，而它被改变微管动力学的药物抑制。 哇巴因和甲胺均不干扰FGF-2向细胞核和核仁的转运。因此，FGF-2靶向出芽囊泡以及细胞核和核仁是由根本不同的机制介导的。
We have previously reported how the release of fibroblast growth factor‐2 (FGF‐2) is mediated by shed vesicles. In the present study, we address the question of how newly synthesized FGF‐2 is targeted to the budding vesicles. Considering that in vitro cultured Sk‐Hep1 hepatocarcinoma cells release FGF‐2 and shed membrane vesicles only when cultured in the presence of serum, we added serum to starved cells and monitored intracellular movements of the growth factor. FGF‐2 was targeted both to the cell periphery and to the nucleus and nucleolus. Movements toward the cell periphery were not influenced by drugs affecting microtubules, but were inhibited by cytocalasin B. Involvement of actin in FGF‐2 trafficking toward the cell periphery was supported by coimmunoprecipitation and immune localization experiments. Colocalization of FGF‐2 granules moving to the cell periphery and FM4‐64‐labelled intracellular lipids were not observed. Ouabain and methylamine, two inhibitors of FGF‐2 release, were analyzed for their effects on FGF‐2 intracellular localization and on vesicle shedding. Ouabain inhibited FGF‐2 movements toward the cell periphery. The FGF‐2 content of shed vesicles was therefore reduced. Methylamine inhibited vesicle shedding; in its presence, FGF‐2 clustered at the cell periphery, but the rate of its release decreased. FGF‐2 targeting to the nucleus and nucleolus was not affected by cytocalasin B, whereas it was inhibited by drugs that modify microtubule dynamics. Neither ouabain, nor methylamine interfered with FGF‐2 translocation to the nucleus and nucleolus. FGF‐2 targeting to the budding vesicles and to the nucleus and nucleolus is therefore mediated by fundamentally different mechanisms.
大鼠 H -K -ATP 酶 α2 亚基的新型 N 末端剪接变体。
DOI：
10.1074/jbc.273.5.2543
发表时间：
1998
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Kone,BC;Higham,SC
通讯作者：
Higham,SC
影响因子：
11.2
作者：
V. Dolo;A. Ginestra;Donata Cassarà;S. Violini;G. Lucania;M. Torrisi;H. Nagase;S. Canevari;A. Pavan;M. Vittorelli
通讯作者：
V. Dolo;A. Ginestra;Donata Cassarà;S. Violini;G. Lucania;M. Torrisi;H. Nagase;S. Canevari;A. Pavan;M. Vittorelli
影响因子：
11.2
作者：
V. Abrahams;Shawn Straszewski;M. Kamsteeg;B. Hanczaruk;P. Schwartz;T. Rutherford;G. Mor
通讯作者：
V. Abrahams;Shawn Straszewski;M. Kamsteeg;B. Hanczaruk;P. Schwartz;T. Rutherford;G. Mor