Ask about this productRelated genes to: SLC35F2 Blocking Peptide
- Gene:
- SLC35F2 NIH gene
- Name:
- solute carrier family 35 member F2
- Previous symbol:
- -
- Synonyms:
- FLJ13018
- Chromosome:
- 11q22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-25
- Date modifiied:
- 2015-12-04
Related products to: SLC35F2 Blocking Peptide
Related articles to: SLC35F2 Blocking Peptide
- Genetic variants affect baseline health and biomarker values, which in turn may impact both the therapy selected for an individual and the magnitude of change induced by the medication. Here, we propose an approach for complex longitudinal repeated measures biobank data, which separates genetic effects for disease from the genetic effects for medication usage and those for treatment response. For 211,845 individuals, we construct a pre-post study design from 1,420,443 repeated blood pressure (BP) measurements and 1,117,900 prescription records for common BP influencing drugs, using electronic health records. We model these jointly alongside 8,430,446 imputed single nucleotide polymorphism (SNP) markers and 17,852 whole-exome sequence loss-of-function (LoF) variants, all within a single novel graphical modeling framework. We identify pharmacogenetic candidate SNPs and LoF variants in genes , and , which are associated with angiotensin receptor blocker therapy and response after controlling for hypertensive disease status across multiple worldwide biobanks. We additionally detect and replicate established clinically relevant variants for statin treatment across multiple biobanks. We find that genetic variation for BP is predominantly shaped prior to the age of 50, but we identify 127 independent loci associated with age-specific BP changes later in life. Finally, once post-treatment measures are conditioned on pre-treatment measures and therapy, we find evidence for four independent loci influencing BP treatment response, including a variant in which has previously been associated with diuretic and beta-blocker response. Our graphical modeling and pre-post study design provides a robust way of detecting time-, treatment- and treatment response-specific genetic associations within large-scale biobank studies. - Source: PubMed
Publication date: 2026/03/20
Borczyk MalgorzataMachnik NickHajto JacekKrätschmer IlseKonowalska PaulaBaszkiewicz BartoszKorostynski MichalRobinson Matthew R - Human choroid plexus papilloma (HIBCPP) cells derived from choroid plexus papilloma in the lateral ventricle are considered suitable model cells for the blood-cerebrospinal fluid barrier (BCSFB). Therefore, in this study, the transporters expressed in HIBCPP cells were identified, and the functions of representative transporters were evaluated. - Source: PubMed
Publication date: 2025/12/10
Kurosawa ToshikiOhtsuki SumioIshikawa HiroshiSchroten HorstSchwerk ChristianKubo YoshiyukiDeguchi Yoshiharu - The Solute Carrier (SLC) superfamily of integral membrane proteins transport a wide array of small molecules across plasma and organelle membranes, and function as important drug transporters and as viral receptors. They populate different conformational states during the solute transport process, including outward-open, intermediate (occluded), and inward-open conformational states. For some SLC proteins this structural "flipping" corresponds to swapping between conformations of their N-terminal and C-terminal symmetry-related sub-structures. Conventional AlphaFold2, AlphaFold3, or Evolutionary Scale Modeling methods typically generate models for only one of these multiple conformational states of SLC proteins. While several AI-based protocols for modeling multiple conformational states of proteins have been described recently, these methods are often impacted by "memorization" of one of the alternative conformational states, and do not always provide both the inward- and outward-open conformations of SLC proteins. Here we assess the impact of memorization in modeling SLC proteins with AlphaFold2/3, and describe a combined ESM - template-based-modeling process, based on a previously described template-based modeling method that relies on the internal pseudo-symmetry of many SLC proteins, to consistently model the alternate conformational states of SLC proteins. We also demonstrate how the resulting multi-state models can be validated by comparison with sequence-based evolutionary co-variance data (ECs) that encode information about contacts present in the various conformational states adopted by the protein. This simple, rapid, and robust approach for modeling conformational landscapes of pseudo-symmetric SLC proteins is demonstrated for several integral membrane protein transporters, including SLC35F2 the receptor of a feline leukemia virus envelope protein required for viral entry into eukaryotic cells. - Source: PubMed
Publication date: 2025/10/17
Swapna G V TDube NamitaRoth Monica JMontelione Gaetano T - Carrier-mediated uptake of choline is rate-limiting for acetylcholine biosynthesis and various other biological processes. To date, 16 solute carrier (SLC) proteins have been identified that may facilitate choline permeation across the outer cell membrane. However, their biochemical functions have not yet been experimentally compared. We overexpressed 16 SLC proteins with known choline-transporting capacity and compared their choline transport kinetics. Additionally, we evaluated their capacity to transport choline analogues as well as metabolites involved in its biosynthesis and degradation or modulators of cholinergic neurotransmission to gain insight into the biological functions of the SLCs. Furthermore, we investigated whether the transporters could be distinguished by their sensitivity to inhibition by hemicholinium-3 and other substances. Of the 16 SLCs tested, seven (SLC5A7, SLC35F2, SLC35F3, SLC35F4, SLC25F5, SLC35G4, and SLC44A5) exhibited K values for choline transport in the range of 12 to 50 µM, closely aligning with physiological plasma choline concentrations. Among them, SLC5A7 displayed over tenfold higher intrinsic clearance than any of the others. SLC22A1-3 were confirmed as choline transporters, albeit with low affinity. Hemicholinium-3 most strongly inhibited SLC5A7 and also significantly inhibited SLC35F2-5 and SLC35G4. Choline transport by these six transporters was inhibited by about 50 % at 100 µM decynium-22 and verapamil.. In humans, multiple SLCs may contribute to cellular choline uptake, depending on physiologic conditions and their yet incompletely characterized expression patterns. The present data may also enhance our understanding of inherited and environmental modulation of these transporters with possible consequence, for instance, on motor and cognitive functions. - Source: PubMed
Publication date: 2025/09/17
Redeker Kyra-Elisa MariaBrockmöller Jürgen - SLC35F2 has emerged as a potential oncogenic driver in non-small cell lung cancer (NSCLC), yet its mechanistic role in tumor progression remains poorly understood. This study aimed to explore the mechanism of SLC35F2 in mediating non-small cell lung cancer (NSCLC) progression through the cAMP signaling pathway. By analyzing TCGA and GEPIA databases, the present research found that SLC35F2 expression was significantly elevated in NSCLC tissues compared to normal lung tissues, with high SLC35F2 levels correlating with poor patient prognosis (P < 0.05). Functional enrichment analysis using R language revealed significant alterations in multiple pathways, including cAMP signaling, in SLC35F2-high NSCLC. Experimental validation through RT-qPCR and Western blot confirmed upregulated SLC35F2 expression in NSCLC cell lines. Knockdown of SLC35F2 inhibited cell proliferation, migration, and invasion while promoting apoptosis (P < 0.05), as demonstrated by CCK-8, EdU, colony formation, flow cytometry, TUNEL, scratch, and Transwell assays. Mechanistically, SLC35F2 suppression activated the cAMP signaling pathway, particularly through upregulation of the transcription factor CREB1. These findings suggest that SLC35F2 drives NSCLC progression by modulating the cAMP/CREB1 axis, highlighting its potential as a therapeutic target. - Source: PubMed
Publication date: 2025/07/14
Wei DuWenyu GeLing YuHongzhe ChenDongmei WangXinglu Xu