Co-overexpression of CD36 and FABPpm increases fatty acid transport additively, not synergistically, within muscle

CD36 脂肪酸 生物化学 脂肪酸结合蛋白 肌膜 化学 生物 受体 基因
作者
Graham P. Holloway,James G. Nickerson,James Lally,Heather L. Petrick,Kaitlyn M. J. H. Dennis,Swati Jain,Hakam Alkhateeb,Arend Bonen
出处
期刊:American Journal of Physiology-cell Physiology [American Physical Society]
卷期号:322 (3): C546-C553 被引量:2
标识
DOI:10.1152/ajpcell.00435.2021
摘要

We aimed to determine the combined effects of overexpressing plasma membrane fatty acid binding protein (FABPpm) and fatty acid translocase (CD36) on skeletal muscle fatty acid transport to establish if these transport proteins function collaboratively. Electrotransfection with either FABPpm or CD36 increased their protein content at the plasma membrane (+75% and +64%), increased fatty acid transport rates by +24% for FABPpm and +62% for CD36, resulting in a calculated transport efficiency of ∼0.019 and ∼0.053 per unit protein change for FABPpm and CD36, respectively. We subsequently used these data to determine if increasing both proteins additively or synergistically increased fatty acid transport. Cotransfection of FABPpm and CD36 simultaneously increased protein content in whole muscle (FABPpm, +46%; CD36, +45%) and at the sarcolemma (FABPpm, +41%; CD36, +42%), as well as fatty acid transport rates (+50%). Since the relative effects of changing FABPpm and CD36 content had been independently determined, we were able to a predict a change in fatty acid transport based on the overexpression of plasmalemmal transporters in the cotransfection experiments. This prediction yielded an increase in fatty acid transport of +0.984 and +1.722 pmol/mg prot/15 s for FABPpm and CD36, respectively, for a total increase of +2.96 pmol/mg prot/15 s. This calculated determination was remarkably consistent with the measured change in transport, namely +2.89 pmol/mg prot/15 s. Altogether, these data indicate that increasing CD36 and FABPpm alters fatty acid transport rates additively, but not synergistically, suggesting an independent mechanism of action within muscle for each transporter. This conclusion was further supported by the observation that plasmalemmal CD36 and FABPpm did not coimmunoprecipitate.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
mkzws发布了新的文献求助10
刚刚
sclslc完成签到,获得积分10
刚刚
刚刚
开朗的夜阑完成签到,获得积分10
刚刚
song完成签到 ,获得积分10
1秒前
淡水痕发布了新的文献求助10
1秒前
小何尖尖角完成签到,获得积分10
1秒前
英俊延恶发布了新的文献求助10
1秒前
123456完成签到,获得积分20
2秒前
3秒前
田超完成签到,获得积分10
3秒前
猪猪hero应助Prime采纳,获得10
3秒前
3秒前
一朵云发布了新的文献求助10
3秒前
sclslc发布了新的文献求助10
3秒前
kuzzi完成签到,获得积分10
4秒前
不是省油的灯完成签到,获得积分10
4秒前
车 干完成签到 ,获得积分10
4秒前
NSS完成签到 ,获得积分10
4秒前
脑洞疼应助宇称yu采纳,获得10
4秒前
绿洲完成签到,获得积分10
4秒前
kajimi完成签到,获得积分10
4秒前
4秒前
瀚泛完成签到,获得积分10
4秒前
4秒前
GedeWang完成签到,获得积分10
5秒前
明理迎曼完成签到,获得积分10
5秒前
idemipere完成签到,获得积分10
6秒前
Lucas应助fbwg采纳,获得30
6秒前
little佳完成签到 ,获得积分10
6秒前
三七二一完成签到,获得积分10
7秒前
7秒前
桃子完成签到,获得积分10
7秒前
尔尔完成签到,获得积分10
8秒前
Ljc发布了新的文献求助10
8秒前
勤劳飞松完成签到,获得积分10
9秒前
沉淀发布了新的文献求助10
9秒前
生动哈密完成签到,获得积分20
9秒前
9秒前
Junanne完成签到,获得积分10
10秒前
高分求助中
ФОРМИРОВАНИЕ АО "МЕЖДУНАРОДНАЯ КНИГА" КАК ВАЖНЕЙШЕЙ СИСТЕМЫ ОТЕЧЕСТВЕННОГО КНИГОРАСПРОСТРАНЕНИЯ 3000
Les Mantodea de Guyane: Insecta, Polyneoptera [The Mantids of French Guiana] 2500
Electron microscopy study of magnesium hydride (MgH2) for Hydrogen Storage 1000
生物降解型栓塞微球市场(按产品类型、应用和最终用户)- 2030 年全球预测 500
Quantum Computing for Quantum Chemistry 500
Thermal Expansion of Solids (CINDAS Data Series on Material Properties, v. I-4) 470
Assessing organizational change : A guide to methods, measures, and practices 400
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3904112
求助须知:如何正确求助?哪些是违规求助? 3449121
关于积分的说明 10856279
捐赠科研通 3174487
什么是DOI,文献DOI怎么找? 1753815
邀请新用户注册赠送积分活动 848047
科研通“疑难数据库(出版商)”最低求助积分说明 790634