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2-羟基肉豆蔻酸对G蛋白Gi1α的肉豆蔻酰化进行化学抑制，不会干扰其棕榈酰化或与膜的结合。有证据表明，是棕榈酰化而非肉豆蔻酰化调节膜附着。

Chemical inhibition of myristoylation of the G-protein Gi1 alpha by 2-hydroxymyristate does not interfere with its palmitoylation or membrane association. Evidence that palmitoylation, but not myristoylation, regulates membrane attachment.

作者信息

Galbiati F, Guzzi F, Magee A I, Milligan G, Parenti M

机构信息

Dipartimento di Farmacologia, Università di Milano, Italy.

出版信息

Biochem J. 1996 Feb 1;313 ( Pt 3)(Pt 3):717-20. doi: 10.1042/bj3130717.

DOI:10.1042/bj3130717
PMID:8611146
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1216969/
Abstract

The alpha-subunit of the G-protein Gi1 alpha is normally dually acylated at its N-terminus with the saturated fatty acids myristate and palmitate. Inhibition of protein myristoylation by treatment with 2-hydroxymyristate prevented neither the incorporation of [3H]palmitate nor the membrane association of this protein when expressed in the COS cells. Construction of a mutant of Gi1 alpha in which serine-6 was replaced by aspartic acid prevented both myristoylation and palmitoylation, and the expressed protein was found primarily in the cytoplasmic fraction. These data indicate the myristoylation is not an absolute requirement for palmitoylation of Gi1 alpha and that palmitoylation, but not myristoylation, plays a key role in membrane association of this G-protein alpha-subunit.

摘要

G蛋白Gi1α的α亚基通常在其N端被饱和脂肪酸肉豆蔻酸和棕榈酸进行双重酰化。用2-羟基肉豆蔻酸处理抑制蛋白质肉豆蔻酰化，在COS细胞中表达时，既不阻止[3H]棕榈酸的掺入，也不阻止该蛋白与膜的结合。构建一个将丝氨酸-6替换为天冬氨酸的Gi1α突变体，可同时阻止肉豆蔻酰化和棕榈酰化，并且发现表达的蛋白主要存在于细胞质部分。这些数据表明，肉豆蔻酰化不是Gi1α棕榈酰化的绝对必要条件，并且棕榈酰化而非肉豆蔻酰化在该G蛋白α亚基的膜结合中起关键作用。

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Chemical inhibition of myristoylation of the G-protein Gi1 alpha by 2-hydroxymyristate does not interfere with its palmitoylation or membrane association. Evidence that palmitoylation, but not myristoylation, regulates membrane attachment.2-羟基肉豆蔻酸对G蛋白Gi1α的肉豆蔻酰化进行化学抑制，不会干扰其棕榈酰化或与膜的结合。有证据表明，是棕榈酰化而非肉豆蔻酰化调节膜附着。
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本文引用的文献

1
Binding of acylated peptides and fatty acids to phospholipid vesicles: pertinence to myristoylated proteins.酰化肽和脂肪酸与磷脂囊泡的结合：与肉豆蔻酰化蛋白的相关性。
Biochemistry. 1993 Oct 5;32(39):10436-43. doi: 10.1021/bi00090a020.
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Mutagenesis of the amino-terminal glycine to alanine in Gs alpha subunit alters beta gamma-dependent properties and decreases adenylylcyclase activation.将Gsα亚基氨基末端的甘氨酸突变为丙氨酸会改变βγ依赖性特性，并降低腺苷酸环化酶的激活。
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Failure to myristoylate the alpha subunit of Gz is correlated with an inhibition of palmitoylation and membrane attachment, but has no affect on phosphorylation by protein kinase C.Gzα亚基肉豆蔻酰化失败与棕榈酰化及膜附着的抑制相关，但对蛋白激酶C的磷酸化没有影响。
J Biol Chem. 1994 Feb 11;269(6):4571-6.
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Receptor regulation of G-protein palmitoylation.
Proc Natl Acad Sci U S A. 1994 Mar 29;91(7):2800-4. doi: 10.1073/pnas.91.7.2800.
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Treatment of T cells with 2-hydroxymyristic acid inhibits the myristoylation and alters the stability of p56lck.用2-羟基肉豆蔻酸处理T细胞可抑制肉豆蔻酰化并改变p56lck的稳定性。
Biochemistry. 1993 Sep 7;32(35):9250-5. doi: 10.1021/bi00086a034.
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Signals determining protein tyrosine kinase and glycosyl-phosphatidylinositol-anchored protein targeting to a glycolipid-enriched membrane fraction.决定蛋白酪氨酸激酶和糖基磷脂酰肌醇锚定蛋白靶向富含糖脂膜组分的信号。
Mol Cell Biol. 1994 Aug;14(8):5384-91. doi: 10.1128/mcb.14.8.5384-5391.1994.
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Palmitoylation of a G protein alpha i subunit requires membrane localization not myristoylation.G蛋白αi亚基的棕榈酰化需要膜定位而非肉豆蔻酰化。
J Biol Chem. 1994 Dec 9;269(49):30898-903.
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Palmitoylation of multiple Src-family kinases at a homologous N-terminal motif.多个Src家族激酶在同源N端基序处的棕榈酰化修饰。
Biochem J. 1994 Nov 1;303 ( Pt 3)(Pt 3):749-53. doi: 10.1042/bj3030749.
10
N-terminal fatty acylation of the alpha-subunit of the G-protein Gi1: only the myristoylated protein is a substrate for palmitoylation.G蛋白Gi1的α亚基的N端脂肪酰化：只有肉豆蔻酰化的蛋白是棕榈酰化的底物。
Biochem J. 1994 Nov 1;303 ( Pt 3)(Pt 3):697-700. doi: 10.1042/bj3030697.