FATP4 deficiency causes ichthyosis premature syndrome in mice and humans associated with suppression of polar lipids but an increase in neutral lipids including triglycerides (TGs). Such a shift has been extensively characterized in enterocyte-, hepatocyte-, and adipocyte-specific Fatp4-deficient mice.

2019年9月13日 · Fatty acid transport protein 4 (FATP4) is an acyl-CoA synthetase that is required for normal permeability barrier in mammalian skin. FATP4 (SLC27A4) mutations cause...

Long-chain fatty acid transport protein 4 is a protein that in humans is encoded by the SLC27A4 gene. [5][6] This membrane protein is also called FATP4 or ACSVL5 (very long chain fatty acyl-CoA synthetase 5).

FATP2/5也涉及胆酸的合成（蓝色箭 头），从ER开始，Cy通过M、Per，最后 分泌到胆小管（BC）。 胆汁的肝肠循环 需要FATP5的BACS活性重新活化。 FATP2在胆囊、胆管细胞中都有表达。

使用 rna 干扰 (sirna)，我们敲低了 neuro2a 细胞中 fatp4（提议名称：acsvl5）的表达。当 fatp4 耗尽时，长链 (c16:0) 和极长链脂肪酸 (c24:0) 的激活都会降低。尽管酶活性降低，但当 fatp4 耗尽时，[14c]c16:0 的初始摄取率并未受到影响。

2001年5月30日 · FATP4 (SLC27A4) is a member of the fatty acid transport protein (FATP) family, a group of evolutionarily conserved proteins that are involved in cellular uptake and metabolism of long and very long chain fatty acids. We cloned and …

Fatty acid transport protein 4 (FATP4), encoded by SLC27A4, is a major fatty acid CoA synthase for ULC fatty acid production [15]. By the action of FATP4, ULC fatty acid CoA is synthesized in the epidermis. Reduced ULC fatty acid CoA synthesis activity due to FATP4 mutations causes ichthyosis prematurity syndrome [16].

2001年5月30日 · FATP4 (SLC27A4) is a member of the fatty acid transport protein (FATP) family, a group of evolutionarily conserved proteins that are involved in cellular uptake and metabolism of long and very long chain fatty acids. We cloned and …

心肌细胞分泌的血管内皮生长因子 b (vegf-b) 或骨骼肌产生的 3-羟基异丁酸可调节相邻 ecs 中 fatp3 和 fatp4 的表达。 同样，FATP4 和 FATP5 主要由心脏、骨骼肌和脂肪组织的毛细血管和微静脉表达。

2022年6月30日 · The widely distributed FATP4 is not a direct FA transporter but plays a predominant function as an ACS. FATP4 deficiency causes ichthyosis premature syndrome in mice and humans associated with suppression of polar lipids but an increase in neutral lipids including triglycerides (TGs).