SLC16A6 Antibody (Center)
- Known as:
- SLC16A6 Antibody (Center)
- Catalog number:
- AP11941c-ev20
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- SLC16A6 Antibody (Center)
Related genes to: SLC16A6 Antibody (Center)
- Gene:
- SLC16A6 NIH gene
- Name:
- solute carrier family 16 member 6
- Previous symbol:
- -
- Synonyms:
- MCT6, MCT7
- Chromosome:
- 17q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-10
- Date modifiied:
- 2015-12-04
Related products to: SLC16A6 Antibody (Center)
Related articles to: SLC16A6 Antibody (Center)
- Solute carrier (SLC) family genes govern transmembrane transport and cellular metabolism, yet their systematic roles from Helicobacter pylori infection to gastric cancer (GC) remain undefined. By integrating multiple GEO datasets with weighted gene co-expression network analysis, differential expression, and machine learning algorithms, we identified seven core SLC genes (SLC9A9, SLC43A2, SLC16A6, SLC7A14, SLC28A3, SLC4A11, SLC5A2) for H. pylori infection and nine (SLC1A3, SLC2A3, SLC15A3, SLC19A3, SLC2A12, SLC16A4, SLC25A4, SLC9A7, SLC28A3) for GC. Logistic regression models achieved high diagnostic accuracy (AUC = 0.976 and 0.874, respectively). Immune infiltration analysis revealed distinct correlation patterns: SLC4A11 and SLC5A2 associated with activated mast cells, neutrophils, and M2 macrophages in infection, while SLC1A3 and SLC2A3 correlated broadly with M1/M2 macrophages and activated CD4 T cells in GC. Enrichment analyses confirmed involvement in transmembrane transport, immune-related pathways, and cancer signaling. Transcription factor prediction identified CEBPB, RELB, and STAT5A as key upstream regulators. Molecular docking demonstrated strong binding affinities between SLC proteins and repurposable compounds (3'-azido-3'-deoxythymidine, CHEMBL1182312, quinine). This study provides the first systematic characterization of SLC family expression across the H. pylori-GC continuum, identifying potential diagnostic biomarkers and therapeutic targets that warrant further experimental validation. - Source: PubMed
Publication date: 2026/07/25
Lv NuonanHe XueCai TingXu YingtingXie JieZhao XuelinYang BinfangLiu XuemeiZhang Minglin - Cells enable specialized metabolism by compartmentalizing metabolic pathways into distinct organelles, which requires the membrane transport of metabolites. In melanocytes, the amino acid tyrosine is imported into developing melanosomes for the synthesis of the UV-protective pigment melanin. In spite of extensive biochemical characterization, the identity of the melanosomal tyrosine transporter remains unknown. Here, we identify SLC16A6 as an orphan melanosome-localized metabolite transporter. Genetic screens reveal that expression is driven by the SOX10-MITF axis, the well-characterized master regulatory program governing melanogenesis and melanosomal homeostasis. By redirecting SLC16A6 to the plasma membrane with an S240A mutation, we demonstrate that SLC16A6 transports tyrosine, a process competitively inhibited by other bulky amino acids. We further determine that SLC16A6 is sufficient for melanosomal tyrosine uptake. Genetic depletion of triggered loss of melanosome biogenesis and function as well as depletion of most melanosomal components. Collectively, these findings establish SLC16A6 as a melanosomal tyrosine transporter that is essential for melanosome biogenesis. - Source: PubMed
Publication date: 2026/07/07
Cunningham Corey NBott Alex JAdelmann Charles HShields MatthewHeyden Katarina EVan Vranken Jonathan GNarbona-Pérez Álvaro JesúsCantres-Vélez Juan AAdelmant GuillaumeKrah Nathan MGygi Steven PSabatini David MRutter Jared - Ulcerative colitis (UC) is an immune-mediated chronic inflammatory bowel disease, and with the rising global incidence and the risk of malignant transformation, the treatment of UC is challenged by heterogeneous progression and limited targeted therapies, and its underlying pathogenesis remains unclear. This study aims to identify novel therapeutic targets for UC, elucidate the genetic factors associated with UC development, and advance precision medicine strategies for UC. - Source: PubMed
Publication date: 2025/12/08
Zhu XiangYang YujieZhu Yi - Evidence for the microbiome's role in human health and disease has been piling up ever since the human microbiome project. The composition of one's microbiome can have a major effect on one's risk of developing cancer and the nature of how cancer develops. Several estimates suggest the percentage of cancer cases that can be attributed to microorganisms at around 15%. In addition, researchers are still trying to figure out how the microbiota, and the gut microbiota in particular, affects how a patient responds to chemotherapy, immunotherapy, and radiotherapy. In this light, we conducted an in-depth bioinformatics analysis of the gut microbiota- RCCstem cells axis, utilizing python-based programme and enrichment databases to analyses data from many sources, including clinical data, transcription factors, kinases and gene expression profile of RCCstem cells. Five genes, including SLC16A6, CPNE5, AFAP1L1, SCARF1, and NOTCH4, were shown to be shared by the hub gut microbiota and extracellular proteins. Patients with RCCstem cells had a disproportionately high number of certain types of bacteria. In patients expression profile have high CPNE5, AFAP1L1, SCARF1, and NOTCH4 expression. RCCsurvival rates are reduced by roughly 50% due to all of the genes involved. Also, the Actinobacteria and Gammaproteobacteria possible role in renal cancer development via relation to cancer stem cells. The gut microbiota and its components were considered for their possible relevance in the development of RCC. - Source: PubMed
Publication date: 2025/12/09
Alimoradi EhsanHashemnejad Mohammad AminEtemad SarehArabi MaryamBereimipour Ahmad - Acute myeloid leukemia (AML) is a heterogeneous disorder marked by irregular expansion and maturation, giving rise to the aggregation of immature myeloid precursor cells. Although most patients achieve remission with initial treatment, the majority of relapses lead to poorer overall survival. The bone marrow (BM) immune microenvironment has been proven to significantly affect the progression of AML. However, the mechanisms that cause the imbalance of immune cell subsets and phenotypes remain partially obscure. Therefore, this research sought to explore the immune-regulatory genes and to determine their role in AML. - Source: PubMed
Publication date: 2025/09/16
Pan YueyuanWu GuocaiLiu ChenchenChen MingguiXia TianMa YonghuaYang ZhigangWen Ruiting