The SLC19A3 Polyclonal Antibody (PACO12246) is a valuable tool for researchers studying SLC19A3, a member of the SLC19 family of transporters involved in the cellular uptake of folate and thiamine. This antibody, raised in rabbits, exhibits high reactivity with human samples and has been validated for use in Western blot applications.SLC19A3 plays a crucial role in folate and thiamine homeostasis, making it a key player in cellular metabolism and nutrient transport. Dysregulation of SLC19A3 has been implicated in various diseases, such as neurological disorders and metabolic syndromes. By targeting SLC19A3 with this antibody, researchers can investigate its expression, localization, and function in different cell types, providing insights into its involvement in disease processes.
With its specificity and reliability in Western blotting, the SLC19A3 Polyclonal Antibody is an essential tool for studies in molecular biology, metabolism, and disease mechanisms. By enabling the detection and analysis of SLC19A3 protein levels, this antibody opens up possibilities for advancing our understanding of nutrient transport pathways and developing targeted therapies for related disorders.
solute carrier family 19, member 3;SLC19A3;THTR2 ;
UniProt Protein Function:
Mediates high affinity thiamine uptake, probably via a proton anti-port mechanism. Has no folate transport activity.
NCBI Summary:
This gene encodes a ubiquitously expressed transmembrane thiamine transporter that lacks folate transport activity. Mutations in this gene cause biotin-responsive basal ganglia disease (BBGD); a recessive disorder manifested in childhood that progresses to chronic encephalopathy, dystonia, quadriparesis, and death if untreated. Patients with BBGD have bilateral necrosis in the head of the caudate nucleus and in the putamen. Administration of high doses of biotin in the early progression of the disorder eliminates pathological symptoms while delayed treatment results in residual paraparesis, mild cognitive disability, or dystonia. Administration of thiamine is ineffective in the treatment of this disorder. Experiments have failed to show that this protein can transport biotin. Mutations in this gene also cause a Wernicke's-like encephalopathy.[provided by RefSeq, Jan 2010]
