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It is an active transporter presenting a 12-helix trans-membrane helix protein with an internal sequence symmetry.
However, unlike the NTE of ABCC1/MRP1, the NTE of HMT-1 is not sufficient for self-association suggesting that multiple regions of HMT-1 must associate with one another to form an active transporter.
Because MRP4 and MRP5 have structural similarities, Wijnholds et al. [126] investigated if they share similar substrates, and through an assay involving a radiolabeled hydrophobic PMEA precursor, they discovered that MRP5 serves as an active transporter of the drug.
Although sulfide is generated in chloroplasts and mitochondria, it is present predominantly in the charged HS- form due to the basic pH inside both organelles, thus requiring an active transporter, which is yet to be identified, to be released.
NKCC1 is not an active transporter but its operation is driven by ion gradients established by Na+,K+-ATPase activity, making it a secondary active transporter [ 18– 20], which requires ongoing or preceding Na+,K+-ATPase activity in order to function.
While the function of EPOR on brain endothelial cells is not yet fully understood, it has been reported that EPOR acts as an active transporter of erythropoietin (EPO) across the blood brain barrier (Brines et al., 2000) and that EPO inhibits the permeability of the blood brain barrier (Casals‐Pascual et al., 2008).
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Naturally evolution does not provide any active transporter for antibiotics, and a passive diffusion process facilitated by channels must be invoked [ 31].
Taken together, an ABC transporter has the ability to utilize much more energy per transport cycle than a secondary active transporter, allowing the transport of more energy-demanding substrates.
The following sections will describe the application of MD and other modeling techniques to the mechanistic investigation of these five transporter systems, viz., LeuT, vSGLT, GlT, GlpT (all secondary active transporters), and an ABCT (a primary active transporter).
However, if association with embigin rather than basigin decreases the kcat of MCT2/1, then this difference may merely reflect a greater expression of a less active transporter rather than a decrease in inhibitor binding affinity.
It is now over 25 years since the causative gene in cystic fibrosis (CF) was identified as ABCC7 [also known as the CF transmembrane conductance regulator (CFTR)] [ 29] and a huge wealth of information has been obtained for this atypical ABC protein which is not in fact a primary active transporter but an ATP-gated chloride channel.
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