ArticleExperimental hematology2017
Sustained enhancement of OCTN1 transporter expression in association with hydroxyurea induced γ-globin expression in erythroid progenitors.
Article in Experimental hematology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Organic cation transporter novel 1 (OCTN1): beyond an ergothioneine transporter.Cell communication and signaling : CCS · 2026Review
- Sickle Cell Anemia: Variants in theFrontiers in pharmacology · 2020Article
- Hydroxyurea in the management of sickle cell disease: pharmacogenomics and enzymatic metabolism.The pharmacogenomics journal · 2018Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The clinical benefits of hydroxyurea (HU) treatment in patients with sickle cell disease (SCD) are due largely to increased γ-globin expression. However, mechanisms that control γ-globin expression by HU in erythroid progenitors are incompletely understood. Here, we investigated the role of two HU transporters, urea transporter B (UTB) and organic cation/carnitine transporter 1 (OCTN1), in this process. Endogenous expression of both transporters peaked toward the end of erythroid differentiation. However, unlike UTB, HU-induced OCTN1 expression correlated positively with γ-globin level and was sustained throughout the period of induction. These results highlight a potential major role for OCTN1 in promoting the efficacy of HU.
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