ReviewIUBMB life2009
The role of the neutral amino acid transporter B0AT1 (SLC6A19) in Hartnup disorder and protein nutrition.
Review in IUBMB life, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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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
48 citing papers in PubMed, 104 citations in OpenAlex.
- Emerging roles of SLC6A14 in digestive system diseases: from amino acid transport to therapeutic targeting.Molecular biology reports · 2026Review
- Structure-guided development of a potent human BCommunications biology · 2026Article
- Inhibitors of the Neutral Amino Acid Transporter SLC6A19 May Treat Diseases or Disorders Associated with Abnormal Amino Acid Metabolism, Epithelial Amino Acid Transport, and/or Amino Acid Levels.ACS medicinal chemistry letters · 2026Article
- Functional maturation of preterm intestinal epithelium through CFTR activation.Communications biology · 2025Article
- Long-term leucine supplementation increases body weight in goats by controlling appetite and muscle protein synthesis under protein-restricted conditions.Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2025Article
- Identification of a novel prognostic and therapeutic prediction model in clear cell renal carcinoma based on Renin-angiotensin system related genes.Frontiers in endocrinology · 2025Article
- Mechanisms involved in aminoacidurias: impacts of genetic and environmental factors.Current research in physiology · 2025Review
- Structural Dynamics of Neutral Amino Acid Transporter SLC6A19 in Simple and Complex Lipid Bilayers.Journal of cellular biochemistry · 2025Article
- Hartnup disease-causing SLC6A19 mutations lead to B0AT1 aberrant trafficking and ACE2 mis-localisation implicating the endoplasmic reticulum protein quality control.Frontiers in cell and developmental biology · 2025Article
- SLC6A19 inhibition facilitates urinary neutral amino acid excretion and lowers plasma phenylalanine.JCI insight · 2024Article
- Transport of Neutral Amino Acids in the Jejunum of Pigs with Special Consideration of L-Methionine.Nutrients · 2024Article
- Neurological sequelae of long COVID: a comprehensive review of diagnostic imaging, underlying mechanisms, and potential therapeutics.Frontiers in neurology · 2024Review
- Article
- Nutrition and Gut Health: Recent Advances and Implications for Development of Functional Foods.International journal of molecular sciences · 2023Article
- New aspects for the brain in Hartnup disease based on mining of high-resolution cellular mRNA expression data for SLC6A19.IBRO neuroscience reports · 2023Review
- Maternal heterozygosity of Slc6a19 causes metabolic perturbation and congenital NAD deficiency disorder in mice.Disease models & mechanisms · 2023Article
- Aristolochic acid-induced nephropathy is attenuated in mice lacking the neutral amino acid transporter BAmerican journal of physiology. Renal physiology · 2022Article
- Unconventional Functions of Amino Acid Transporters: Role in Macropinocytosis (SLC38A5/SLC38A3) and Diet-Induced Obesity/Metabolic Syndrome (SLC6A19/SLC6A14/SLC6A6).Biomolecules · 2022Review
- Radiosensitivity in patients affected by ARPC1B deficiency: a new disease trait?Frontiers in immunology · 2022Article
- Deficient synthesis of melatonin in COVID-19 can impair the resistance of coronavirus patients to mucormycosis.Medical hypotheses · 2021Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hartnup disorder (OMIM 234500) is an autosomal recessive disorder, which was first described in 1956 as an aminoaciduria of neutral amino acids accompanied by a variety of symptoms, such as a photo-sensitive skin-rash and cerebellar ataxia. The disorder is caused by mutations in the neutral amino acid transporter B(0)AT1 (SLC6A19). To date 21 mutations have been identified in more than twenty families. SLC6A19 requires either collectrin or angiotensin-converting enzyme 2 for surface expression in the kidney and intestine, respectively. This ties SLC6A19 together with more complex functions such as blood-pressure control, glomerular structure, and exocytosis.
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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.