ReviewSub-cellular biochemistry2025
Urea Transporters and Their Gene Mutations in Diseases.
Review in Sub-cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Urea Transporters in Cancer: Emerging Roles and Their Clinical Implications.Biomedicines · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Urea transporters (UTs) UT-As (encoded by Slc14A2) and UT-B (encoded by Slc14A1), are important members of the solute carrier family. They are a group of membrane channel proteins that are selectively permeable to urea. Slc14A1 is considered the key gene determining the Kidd blood group system, and its variants can lead to the loss of Jk antigens, resulting in transfusion-related complications. Additionally, studies have shown that Slc14A1 is closely associated with cancer development and progression, with its expression level and promoter methylation status potentially serving as biomarkers for cancer progression and prognosis. Recent research suggests that UT-B functional deficiency may cause neurodegenerative diseases by accumulating urea in the brain, thereby affecting neuronal function and viability. Mutations of Slc14A2 are linked to hypertension and metabolic syndrome, due to its essential role in maintaining urea homeostasis. This chapter aims to introduce the clinical significance of UT-B and UT-A and highlight their potential roles as diagnostic and therapeutic targets.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.