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由游离脂肪酸对表面受体帽化的抑制作用推导得出的帽化模型。

Model for capping derived from inhibition of surface receptor capping by free fatty acids.

作者信息

Klausner R D, Bhalla D K, Dragsten P, Hoover R L, Karnovsky M J

出版信息

Proc Natl Acad Sci U S A. 1980 Jan;77(1):437-41. doi: 10.1073/pnas.77.1.437.

Abstract

When low concentrations (2-5 mole %) of cis unsaturated free fatty acids (group A) are intercalated into lymphocyte plasma membrane, capping is inhibited. No effect is seen with trans unsaturated or saturated fatty acids (group B). The capping inhibition is reversible with increasing doses of extracellular calcium. Fluorescence photobleaching recovery has shown that the group A free fatty acids do not inhibit the receptor immobilization associated with patch formation, but inhibit the final energy-dependent movement of the patched receptors into a cap. We have also shown that the group A free fatty acids cause a shift in membrane-bound calcium to the lipid phase from probable protein-associated sites. We have incorporated these findings into a model for capping and membrane-cytoskeletal interactions.

摘要

当低浓度(2 - 5摩尔%)的顺式不饱和游离脂肪酸(A组)插入淋巴细胞质膜时,帽化受到抑制。反式不饱和脂肪酸或饱和脂肪酸(B组)则无此作用。随着细胞外钙剂量增加,帽化抑制作用是可逆的。荧光光漂白恢复实验表明,A组游离脂肪酸并不抑制与斑块形成相关的受体固定,但抑制斑块化受体最终依赖能量的向帽的移动。我们还表明,A组游离脂肪酸会使膜结合钙从可能与蛋白质相关的位点转移到脂质相。我们已将这些发现纳入帽化和膜 - 细胞骨架相互作用的模型中。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/603f/348286/f109b344c350/pnas00664-0476-a.jpg

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