Spike蛋白成熟
中文名称
通路描述
该COVID-19通路是通过结合SARS-CoV-1数据的计算推断和手动校核创建的，具体描述见整体SARS-CoV-2感染通路摘要。SARS-CoV-1的Spike蛋白受N-糖基化和棕榈酰化修饰，辅助折叠的伴侣蛋白为calnexin。最终产物为同源三聚体（Nal et al, 2005）。在SARS-CoV-2中，Spike糖基化模式已广泛表征，包含约20个氨基酸上的N-糖基化和O-糖基化（综述：PetroviÄ et al, 2021; Gong et al, 2021; Shajahan et al, 2021）。尽管没有理由认为宿主糖基化酶的行为与其他宿主或非宿主蛋白不同，但尚未显示宿主酶和伴侣蛋白直接参与SARS-CoV-2 Spike糖基化。间接证据来自抑制实验（Reyes et al, 2021; Franco et al, 2022），但受同时抑制ACE2受体糖基化等蛋白糖基化的干扰。
英文描述
Defective SLC16A1 causes symptomatic deficiency in lactate transport (SDLT) Four members of the SLC16A gene family encode classical monocarboxylate transporters MCT1-4. Widely expressed, they all function as proton-dependent transporters of monocarboxylic acids such as lactate and pyruvate and ketone bodies such as acetacetate and beta-hydroxybutyrate. These processes are crucial in the regulation of energy metabolism and acid-base homeostasis.
SLC16A1 encodes MCT1, a ubiquitiously expressed protein. Heterozygous defects in SLC16A1 were found in patients with symptomatic deficiency in lactate transport (SDLT aka erythrocyte lactate transporter defect; MIM:245340), resulting in an acidic intracellular environment and muscle degeneration with the release of myoglobin and creatine kinase (Merezhinskaya et al. 2000). This defect could compromise extreme performance in otherwise healthy individuals.
SLC16A1 is essential for lactate transport in muscle cells. It is also highly enriched in astrocytes and oligodendroglia, neuroglia that support, insulate and provide energy metabolites to axons. Oligodendroglia dysfunction can lead to axon degeneration in several diseases. The cause is unknown but disruption of SLC16A1 transporter produces axon damage and neuron loss in animal and cell culture models. In humans, this transporter is reduced in patients with amyotrophic lateral sclerosis (Lee et al. 2012).
In cancer cells, a common change is the upregulation of glycolysis. The anti-cancer drug candidate 3-bromopyruvate (3-BrPA) can inhibit glycolysis through its uptake into cancer cells via SLC16A1 so it is the main determinant of 3-BrPA sensitivity in these cells (Birsoy et al. 2013).
SLC16A1 encodes MCT1, a ubiquitiously expressed protein. Heterozygous defects in SLC16A1 were found in patients with symptomatic deficiency in lactate transport (SDLT aka erythrocyte lactate transporter defect; MIM:245340), resulting in an acidic intracellular environment and muscle degeneration with the release of myoglobin and creatine kinase (Merezhinskaya et al. 2000). This defect could compromise extreme performance in otherwise healthy individuals.
SLC16A1 is essential for lactate transport in muscle cells. It is also highly enriched in astrocytes and oligodendroglia, neuroglia that support, insulate and provide energy metabolites to axons. Oligodendroglia dysfunction can lead to axon degeneration in several diseases. The cause is unknown but disruption of SLC16A1 transporter produces axon damage and neuron loss in animal and cell culture models. In humans, this transporter is reduced in patients with amyotrophic lateral sclerosis (Lee et al. 2012).
In cancer cells, a common change is the upregulation of glycolysis. The anti-cancer drug candidate 3-bromopyruvate (3-BrPA) can inhibit glycolysis through its uptake into cancer cells via SLC16A1 so it is the main determinant of 3-BrPA sensitivity in these cells (Birsoy et al. 2013).
所含基因
1 个基因