Trimming of TAP-translocated peptides in the endoplasmic reticulum and in the cytosol during recycling

机译：回收期间内质网和细胞质中TAP易位肽的修饰

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摘要

Cytosolic peptides are translocated to the endoplasmic reticulum (ER) lumen by the transporters associated with antigen processing (TAP), where major histocompatibility complex (MHC) class I molecules associate with peptides of about 8-10 amino acids. TAP translocates peptides of 9-13 amino acids with the highest relative affinity but also longer and shorter peptides. The fate of the peptides that fail to associate with class I molecules because of incorrect sequence or length, is unknown. Here we show that the bulk of the translocated peptides are rapidly released from the ER by a mechanism that requires adenosine triphosphate (ATP) and that could not be inhibited by GTP gamma S. TAP does not appear to be involved in this process. Whereas free peptides are slowly trimmed in the ER lumen, they are rapidly degraded in the cytosol. A fraction of the peptides released from the ER escapes complete degradation in the cytosol and recycles back to the ER in a TAP-dependent fashion. These results suggest that peptides that are too long for binding to class I molecules in the ER can be trimmed further in the ER lumen or, alternatively, can be transported back to the cytosol where a fraction of the peptides is trimmed to a size suitable for association to MHC class I molecules and recycles back to the ER.

机译：胞质肽通过与抗原加工（TAP）相关的转运蛋白转运到内质网（ER）内腔，其中主要的组织相容性复合物（MHC）I类分子与约8-10个氨基酸的肽缔合。 TAP使具有最高相对亲和力的9-13个氨基酸的肽移位，但肽段的长度也越来越短。由于序列或长度不正确而无法与I类分子缔合的肽的命运是未知的。在这里，我们显示了大部分易位肽通过需要三磷酸腺苷（ATP）的机制快速从ER释放，并且不能被GTPγS抑制。TAP似乎没有参与这一过程。游离肽在ER内腔中缓慢修整，而它们在细胞质中迅速降解。从ER释放的一部分肽逃脱了胞浆中的完全降解，并以TAP依赖性方式循环回到ER。这些结果表明，对于结合到ER中的I类分子而言太长的肽可以在ER腔中进一步修剪，或者可以转运回细胞质，在那里一部分肽被修剪至适合于与MHC I类分子缔合，并循环回ER。

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期刊名称 The Journal of Experimental Medicine
作者

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年(卷),期 1994(180),5
年度 1994
页码 1591–1597
总页数 7
原文格式 PDF
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中图分类免疫学;医学史;
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专利

1. Trimming of TAP-translocated peptides in the endoplasmic reticulum and in the cytosol during recycling. [J] . J Roelse, M Grommé, F Momburg, The Journal of Experomental Medicine . 1994,第5期

机译：回收期间内质网和细胞质中TAP易位肽的修饰。
2. The protease inhibitor, N-acetyl-L-leucyl-L-leucyl-leucyl-L-norleucinal, decreases the pool of major histocompatibility complex class I-binding peptides and inhibits peptide trimming in the endoplasmic reticulum. [J] . E A Hughes, B Ortmann, M Surman, The Journal of Experomental Medicine . 1996,第4期

机译：蛋白酶抑制剂，N-乙酰基-L-亮氨酰-L-亮氨酰-亮氨酰-L-净核糖核酸，可减少主要组织相容性复合物I类结合肽的汇集，并抑制内质网中的肽修整。
3. The protease inhibitor, N-acetyl-L-leucyl-L-leucyl-leucyl-L-norleucinal, decreases the pool of major histocompatibility complex class I-binding peptides and inhibits peptide trimming in the endoplasmic reticulum. [J] . E A Hughes, B Ortmann, M Surman, The Journal of Experomental Medicine . 1996,第4期

机译：蛋白酶抑制剂，N-乙酰基-L-亮氨酰-L-亮氨酰-亮氨酰-L-净核糖核酸，可减少主要组织相容性复合物I类结合肽的汇集，并抑制内质网中的肽修整。
4. Microdosimetric Realistic Model of a Cell with Endoplasmic Reticulum [C] . A. De Angelis, A. Denzi, C. Merla, Annual International Conference of the IEEE Engineering in Medicine and Biology Society . 2019

机译：内质网细胞的微剂量现实模型
5. Protein quality control in the endoplasmic reticulum and cytosol. [D] . Metzger, Meredith Boyle. 2009

机译：内质网和细胞质中的蛋白质质量控制。
6. The protease inhibitor N-acetyl-L-leucyl-L-leucyl-leucyl-L- norleucinal decreases the pool of major histocompatibility complex class I-binding peptides and inhibits peptide trimming in the endoplasmic reticulum [O] . 1996

机译：蛋白酶抑制剂N-乙酰基-L-亮氨酰-L-亮氨酰-亮氨酰-L-正亮氨酸减少主要组织相容性复合物I类结合肽的聚集并抑制内质网中的肽修整
7. Trimming of TAP-translocated peptides in the endoplasmic reticulum and in the cytosol during recycling [O] . 1994

机译：回收期间内质网和细胞质中TAP易位肽的修饰

Trimming of TAP-translocated peptides in the endoplasmic reticulum and in the cytosol during recycling

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