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Last update 08 May 2025

SLC6A17

Last update 08 May 2025

Basic Info

Synonyms

NTT4, SLC6A17, Sodium-dependent neurotransmitter transporter NTT4

+ [5]

Introduction

Synaptic vesicle transporter with apparent selectivity for neutral amino acids. The transport is sodium-coupled but chloride-independent, likely driven by the proton electrochemical gradient generated by vacuolar H(+)-ATPase in an overall electrogenic mechanism. May contribute to the synaptic uptake of neurotransmitter precursors in a process coupled in part to vesicle exocytosis.

Drugs associated with SLC6A17

HG-1336

Target

SLC6A17

Mechanism

SLC6A17 modulators

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Nervous System Diseases

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with SLC6A17

100 Translational Medicine associated with SLC6A17

0 Patents (Medical) associated with SLC6A17

Literatures (Medical) associated with SLC6A17

03 Jan 2025·Current Medicinal Chemistry

Unveiling the Role of SLC6A17 in Lung Adenocarcinoma: Prognosis, Pathways, and Therapeutic Implications

Article

Author: Li, Yingjie ; Li, Jingbo ; Wen, JiFan ; Li, Dongbing ; Chen, Ping

Background:The role of solute carrier family 6 member 17 (SLC6A17) in lung adenocarcinoma (LUAD) is unclear.Objectives:To address this gap in knowledge, we employed bioinformatics analysis and experimental validation.Methods:This research aimed to scrutinize the expression patterns of the SLC6A17 gene across a spectrum of cancers and specifically within LUAD, utilizing data extracted from The Cancer Genome Atlas (TCGA). The correlation between SLC6A17 expression and LUAD prognosis was investigated to assess its diagnostic relevance. The study delved into the possible regulatory mechanisms of SLC6A17, focusing on its links to immune cell infiltration and drug response in LUAD. The examination of SLC6A17 expression was extended to single-cell sequencing data in LUAD, alongside an evaluation of the gene's genomic alterations and clinical implications within this disease context. Validation of SLC6A17 expression levels was conducted using datasets from GSE87340 and various cell lines, employing quantitative real-time polymerase chain reaction (qRTPCR) techniques.Results:SLC6A17 exhibited aberrant expression in both pan-cancer and LUAD. Increased expression of SLC6A17 in LUAD patients was significantly associated with poorer overall survival (p = 0.008), progress-free survival (p = 0.019), and disease specific survival (p = 0.030). In LUAD patients, the levels of SLC6A17 expression were found to be a significant standalone indicator of prognosis, with a p-value of 0.031. SLC6A17 exhibited associations with various pathways, including focal adhesion, ECM receptor interaction, cell cycle, linoleic acid metabolism, pathways in cancer, and more. SLC6A17 expression demonstrated correlations with immune infiltration in LUAD. SLC6A17 expression revealed a notably inverse relationship with several substances, including AR-42, T0901317, tubastatin A, SB52334, and amuvatinib, within the context of LUAD. SLC6A17 was found to be significantly positively regulated in LUAD cell lines.Conclusions:These findings suggest that SLC6A17 indicates the potential of a potential prognostic biomarker and immunotherapeutic target for patients with LUAD.

01 Dec 2024·Computational and Structural Biotechnology Journal

In silico structural studies on the vesicular neutral amino acid transporter NTT4 (SLC6A17)

Article

Author: Kukułowicz, Jędrzej ; Bajda, Marek

NTT4 is one of the neutral amino acid transporters that regulate neural concentration of precursors for glutamate biosynthesis. Here, we provide insight into the structure of NTT4 and rationalize substrate selectivity. Furthermore, we demonstrate how the mutations associated with mental disabilities imply malfunction of the transporter at the molecular level. We also compared the structures of NTT4 and B⁰AT2 (SLC6A15), which is a close homolog, sharing 66 % of the common amino acids. Our analyses may be useful in the search for compounds that inhibit substrate transport. Moreover, they allow a better understanding of the function of these transporters.

01 Aug 2024·Brain, Behavior, and Immunity

Social fear extinction susceptibility is associated with Microbiota-Gut-Brain axis alterations

Article

Author: Theune, Nigel ; Moloney, Rachel D ; Hill, Colin ; Draper, Lorraine A ; Slattery, David A ; Brocka, Marta ; Myers, Eibhlís M ; Shkoporov, Andrey N ; Cryan, John F ; Ritz, Nathaniel L ; Moloney, Gerard M ; Cowan, Caitlin S M ; Bastiaanssen, Thomaz F S ; Dinan, Timothy G ; Smith, Linda

Social anxiety disorder is a common psychiatric condition that severely affects quality of life of individuals and is a significant societal burden. Although many risk factors for social anxiety exist, it is currently unknown how social fear sensitivity manifests biologically. Furthermore, since some individuals are resilient and others are susceptible to social fear, it is important to interrogate the mechanisms underpinning individual response to social fear situations. The microbiota-gut-brain axis has been associated with social behaviour, has recently been linked with social anxiety disorder, and may serve as a therapeutic target for modulation. Here, we assess the potential of this axis to be linked with social fear extinction processes in a murine model of social anxiety disorder. To this end, we correlated differential social fear responses with microbiota composition, central gene expression, and immune responses. Our data provide evidence that microbiota variability is strongly correlated with alterations in social fear behaviour. Moreover, we identified altered gene candidates by amygdalar transcriptomics that are linked with social fear sensitivity. These include genes associated with social behaviour (Armcx1, Fam69b, Kcnj9, Maoa, Serinc5, Slc6a17, Spata2, and Syngr1), inflammation and immunity (Cars, Ckmt1, Klf5, Maoa, Map3k12, Pex5, Serinc5, Sidt1, Spata2), and microbe-host interaction (Klf5, Map3k12, Serinc5, Sidt1). Together, these data provide further evidence for a role of the microbiota-gut-brain axis in social fear responses.

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SLC6A17

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