SLCO1C1, the official full name is solute carrier organic anion transporter family member 1C1. SLCO1C1 is also known as solute carrier family 21 member 14 (SLC21A14). It is encoded by the SLCO1C1 gene in humans and belongs to SLC21A family of solute carriers. This gene is conserved in chimpanzee, cow, rat, dog, frog, and zebrafish. It has been documented that 153 organisms have orthologs with this gene. SLCO1C1 is shown to be widely expressed in brain, fat and 3 other tissues, and is involved in the uptake of organic anions.
|Basic Information of SLCO1C1|
|Protein Name||Solute carrier organic anion transporter family member 1C1|
|Aliases||OATP14, OATP1C1, OATPF, SLC21A14|
|Organism||Homo sapiens (Human)|
SLCO1C1 is a member of the sodium-independent organic anion transporter family and mediates cellular uptake of organic anions. This transmembrane transporter is involved in sodium-independent uptake of thyroid hormones in brain tissues. The affinity of SLCO1C1 for thyroid hormones thyroxine, tri-iodothyronine is particularly high. In addition, the gene polymorphisms are associated with fatigue and depression in patients with hyperthyroidism. Multiple transcript variants can be generated due to alternative splicing. Moreover, SLCO1C1 is regulated in a parallel manner with MCT8 during inflammation at the blood-brain barrier (BBB) and they are essential for thyroid hormone access to the brain. SLCO1C1 is able to control skeletal muscle regeneration in satellite cell activation, and it shows that finely tuned thyroid hormone signaling is very important during myogenesis. Furthermore, PDE3A-SLCO1C1 genetic variant has no relationship with an anti-TNF response in UK patients with rheumatoid arthritis cohort.
Fig.1 Rat SLCO1C1 membrane topology. (Westholm, 2010)
This article indicates that the SLCO1C1 is able to control skeletal muscle regeneration in satellite cell activation, also it shows that finely tuned thyroid hormone signaling is very important during myogenesis.
This article shows an increased SLCO1C1 mRNA expression with 2.62-fold in gadoxetate disodium-treated cells.
This article indicates that L-thyroxin can block SR101 transport into astrocytes through competitive inhibition of the SLCO1C1 transporter, and this can significantly reduce oligodendrocyte labeling.
This article shows that PDE3A-SLCO1C1 genetic variant has no relationship with an anti-TNF response in UK patients with rheumatoid arthritis cohort.
This article demonstrates that SLCO1C1 is regulated in a parallel manner with MCT8 during inflammation at BBB and it is essential for thyroid hormone access to the brain.
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