Ask about this productRelated genes to: SLC35A5 Blocking Peptide
- Gene:
- SLC35A5 NIH gene
- Name:
- solute carrier family 35 member A5
- Previous symbol:
- -
- Synonyms:
- FLJ20730
- Chromosome:
- 3q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-04
- Date modifiied:
- 2016-10-05
Related products to: SLC35A5 Blocking Peptide
Related articles to: SLC35A5 Blocking Peptide
- Solute carrier (SLC) transporters have been linked to type 2 diabetes (T2D) and play a crucial role in cellular metabolism. Growth and metabolism depend on ornithine decarboxylase 1 (ODC1), a crucial regulator of polyamine production, especially in the pancreas. This study examines the interaction between ODC1 and SLC gene expressions under glucotoxicity conditions, which simulate hyperglycemia. In silico analysis of human pancreatic β-islet tissue datasets from T2D patients identified differentially expressed SLC genes. In vitro studies were conducted using HEK293T cells and COS-7 cell lines. Overexpression and knockdown of ODC1 in HEK293T cells revealed ODC1's influence on the mRNA expression profiles of SLC. In vitro overexpression with and without high glucose also revealed ODC1's influence on SLC genes. Specifically, ODC1 modulated the expression of SLC11A2, SLC30A1, SLC39A6, and other SLCs, including SLC17A6, SLC25A12, SLC26A2, SLC35A5, SLC38A2, SLC9A6, SLC6A8, and SLC20A1. Glucotoxicity mostly suppressed SLC gene expression; however, ODC1 overexpression partially reversed this effect for certain SLCs. This work highlights an unrecognized regulatory network involving ODC1 and SLCs, suggesting a potential role for polyamine pathway modulation in controlling transport dynamics. These findings suggest a novel regulatory network where ODC1 influences SLC gene expression, impacting metabolic pathways and nutrient transport. This study provides preliminary evidence that ODC1 may be a potential regulator of SLC transporters, offering new insights into the metabolic dysregulation of T2D and potential therapeutic targets. - Source: PubMed
Publication date: 2025/06/24
Kaur ManpreetDahiya NehaSingh Varsha - According to statistics 2020, female breast cancer (BRCA) became the most commonly diagnosed malignancy worldwide. Prognosis of BRCA patients is still poor, especially in population with advanced or metastatic. Particular functions of each members of the solute carrier 35A (SLC35A) gene family in human BRCA are still unknown regardless of awareness that they play critical roles in tumorigenesis and progression. Using integrated bioinformatics analyses to identify therapeutic targets for specific cancers based on transcriptomics, proteomics, and high-throughput sequencing, we obtained new information and a better understanding of potential underlying molecular mechanisms. Leveraging BRCA dataset that belongs to The Cancer Genome Atlas (TCGA), which were employed to clarify SLC35A gene expression levels. Then we used a bioinformatics approach to investigate biological processes connected to SLC35A family genes in BRCA development. Beside that, the Kaplan-Meier estimator was leveraged to explore predictive values of SLC35A family genes in BCRA patients. Among individuals of this family gene, expression levels of SLC35A2 were substantially related to poor prognostic values, result from a hazard ratio of 1.3 (with 95 percent confidence interval (95% CI: 1.18-1.44), the for trend (ptrend) is 3.1 × 10). Furthermore, a functional enrichment analysis showed that SLC35A2 was correlated with hypoxia-inducible factor 1A (HIF1A), heat shock protein (HSP), E2 transcription factor (E2F), DNA damage, and cell cycle-related signaling. Infiltration levels observed in specific types of immune cell, especially the cluster of differentiation found on macrophages and neutrophils, were positively linked with SLC35A2 expression in multiple BRCA subclasses (luminal A, luminal B, basal, and human epidermal growth factor receptor 2). Collectively, SLC35A2 expression was associated with a lower recurrence-free survival rate, suggesting that it could be used as a biomarker in treating BRCA. - Source: PubMed
Publication date: 2021/11/30
Ta Hoang Dang KhoaMinh Xuan Do ThiTang Wan-ChunAnuraga GanggaNi Yi-ChunPan Syu-RueiWu Yung-FuFitriani FennyPutri Hermanto Elvira MustikawatiAthoillah MuhammadAndriani VivinAjiningrum Purity SabilaWang Chih-YangLee Kuen-Haur - Solute carrier family 35 member A5 (SLC35A5) is a member of the SLC35A protein subfamily comprising nucleotide sugar transporters. However, the function of SLC35A5 is yet to be experimentally determined. In this study, we inactivated the gene in the HepG2 cell line to study a potential role of this protein in glycosylation. Introduced modification affected neither - nor -glycans. There was also no influence of the gene knock-out on glycolipid synthesis. However, inactivation of the gene caused a slight increase in the level of chondroitin sulfate proteoglycans. Moreover, inactivation of the gene resulted in the decrease of the uridine diphosphate (UDP)-glucuronic acid, UDP--acetylglucosamine, and UDP--acetylgalactosamine Golgi uptake, with no influence on the UDP-galactose transport activity. Further studies demonstrated that SLC35A5 localized exclusively to the Golgi apparatus. Careful insight into the protein sequence revealed that the C-terminus of this protein is extremely acidic and contains distinctive motifs, namely DXEE, DXD, and DXXD. Our studies show that the C-terminus is directed toward the cytosol. We also demonstrated that SLC35A5 formed homomers, as well as heteromers with other members of the SLC35A protein subfamily. In conclusion, the SLC35A5 protein might be a Golgi-resident multiprotein complex member engaged in nucleotide sugar transport. - Source: PubMed
Publication date: 2019/01/11
Sosicka PaulinaBazan BożenaMaszczak-Seneczko DorotaShauchuk YauhenOlczak TeresaOlczak Mariusz - SLC35A4 has been classified in the SLC35A subfamily based on amino acid sequence homology. Most of the proteins belonging to the SLC35 family act as transporters of nucleotide sugars. In this study, the subcellular localization of endogenous SLC35A4 was determined via immunofluorescence staining, and it was demonstrated that SLC35A4 localizes mainly to the Golgi apparatus. In silico topology prediction suggests that SLC35A4 has an uneven number of transmembrane domains and its N-terminus is directed towards the Golgi lumen. However, an experimental assay refuted this prediction: SLC35A4 has an even number of transmembrane regions with both termini facing the cytosol. In vivo interaction analysis using the FLIM-FRET approach revealed that SLC35A4 neither forms homomers nor associates with other members of the SLC35A subfamily except SLC35A5. Additional assays demonstrated that endogenous SLC35A4 is 10 to 40nm proximal to SLC35A2 and SLC35A3. To determine SLC35A4 function SLC35A4 knock-out cells were generated with the CRISPR-Cas9 approach. Although no significant changes in glycosylation were observed, the introduced mutation influenced the subcellular distribution of the SLC35A2/SLC35A3 complexes. Additional FLIM-FRET experiments revealed that overexpression of SLC35A4-BFP together with SLC35A3 and the SLC35A2-Golgi splice variant negatively affects the interaction between the two latter proteins. The results presented here strongly indicate a modulatory role for SLC35A4 in intracellular trafficking of SLC35A2/SLC35A3 complexes. - Source: PubMed
Publication date: 2017/02/03
Sosicka PaulinaMaszczak-Seneczko DorotaBazan BożenaShauchuk YauhenKaczmarek BeataOlczak Mariusz - The clinical use of paclitaxel is limited by variable responses and the potential for significant toxicity. To date, studies of associations between variants in candidate genes and paclitaxel effects have yielded conflicting results. We aimed to evaluate the relationships between global gene expression and paclitaxel sensitivity. - Source: PubMed
Njiaju Uchenna OGamazon Eric RGorsic Lidija KDelaney Shannon MWheeler Heather EIm Hae KyungDolan M Eileen