Ask about this productRelated genes to: SLC35F1 antibody
- Gene:
- SLC35F1 NIH gene
- Name:
- solute carrier family 35 member F1
- Previous symbol:
- C6orf169
- Synonyms:
- dJ230I3.1
- Chromosome:
- 6q22.2-q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2003-11-26
- Date modifiied:
- 2018-11-19
Related products to: SLC35F1 antibody
Related articles to: SLC35F1 antibody
- Infection with the hepatitis B virus (HBV) is a key risk factor for hepatocellular carcinoma (HCC) development and progression. It is widely recognized that immunopathological mechanisms are pivotal in the development of HBV-associated HCC; nevertheless, the specific underlying mechanisms through which HBV-induced modifications within the tumor microenvironment (TME) contribute to HCC pathogenesis have yet to be fully elucidated. In the present study, single-cell RNA sequencing was utilized to analyze and compare the immune landscapes between HBV-positive and HBV-negative HCC. These experiments revealed that HBV infection significantly modifies the composition and state of immune cells, leading to the suppression and exhaustion of T cells within the TME. Specifically, increases in the proportions of SLC4A10 CD8 T cells and IFITM3 macrophages were observed, along with an upregulation of the gene in various immune cell subtypes. Taken together, these findings have offered valuable insights into the alteration of the immunological microenvironment in HCC that is associated with HBV infection, suggesting possible targets for immunotherapeutic intervention. - Source: PubMed
Publication date: 2025/07/01
Liu KeChen ErbaoLiang JiamingLi YanyanCheng BinghuaShi WenliZhou ZeyuZhou WenjieTian HuiYang DongyeShao XimingLi Hongchang - Cochlear aging causes substantial hearing impairment in older adults, yet primate-specific mechanisms remain poorly characterized. Our comprehensive analysis combining single-cell and histopathological profiling in aging Macaca fascicularis demonstrates progressive cochlear degeneration featuring accelerated sensory hair cell loss, senescent spiral ganglion neurons with elevated neuroinflammation, and marked stria vascularis atrophy. We discovered that downregulation of transmembrane transport proteins, particularly SLC35F1, serves as a critical biomarker of hair cell aging. Functional validation through Slc35f1 knockdown in adult mice successfully recapitulated key aspects of age-related hearing loss, including hair cell degeneration and auditory function decline. Notably, we showed that long-term metformin administration at clinically relevant doses effectively delays cochlear aging in primates. These findings provide fundamental insights into the cellular and molecular basis of primate cochlear aging while establishing a foundation for developing targeted interventions against age-related hearing loss. - Source: PubMed
Publication date: 2025/06/20
Sun GuoqiangFu XiaolongZheng YandongHong GuodongLiu ZiyiLuo BilanLei JinghuiLv DongliangChang MiaoXiao YuGuo SiweiMa ShuaiLu LingZhang WeiqiBelmonte Juan Carlos IzpisuaQu JingWang SiChai RenjieLiu Guang-Hui - Primary membranous nephropathy (pMN) often progresses to end-stage renal disease (ESRD) in the absence of immunosuppressive therapy. The immunological mechanisms driving pMN progression remain insufficiently understood. - Source: PubMed
Tie XuanChen ZhiangYao ShuleiWu BinxinYan BingjuanZhai HuifangQiao XiSu XiaoleWang Lihua - Delay discounting refers to the behavioral tendency to devalue rewards as a function of their delay in receipt. Heightened delay discounting has been associated with substance use disorders and multiple co-occurring psychopathologies. Human and animal genetic studies have established that delay discounting is heritable, but only a few associated genes have been identified. We aimed to identify novel genetic loci associated with delay discounting through a genome-wide association study (GWAS) using Heterogeneous Stock (HS) rats, a genetically diverse outbred population derived from eight inbred founder strains. We assessed delay discounting in 650 male and female HS rats using an adjusting amount procedure in which rats chose between smaller immediate sucrose rewards or a larger reward at various delays. Preference switch points were calculated and both exponential and hyperbolic functions were fitted to these indifference points. Area under the curve (AUC) and the discounting parameter k of both functions were used as delay discounting measures. GWAS for AUC, exponential k, and one indifference point identified significant loci on chromosomes 20 and 14. The gene Slc35f1, which encodes a member of the solute carrier family, was the sole gene within the chromosome 20 locus. That locus also contained an eQTL for Slc35f1, suggesting that heritable differences in the expression might be responsible for the association with behavior. Adgrl3, which encodes a latrophilin subfamily G-protein coupled receptor, was the sole gene within the chromosome 14 locus. These findings implicate novel genes in delay discounting and highlight the need for further exploration. - Source: PubMed
Lara Montana KayChitre Apurva SChen DenghuiJohnson Benjamin BNguyen Khai-MinhCohen Katarina AMuckadam Sakina ALin BonnieZiegler ShaeBeeson AngelaSanches Thiago MSolberg Woods Leah CPolesskaya OksanaPalmer Abraham AMitchell Suzanne H - The SLC35 (Solute Carrier 35) family members acting as nucleotide sugar transporters are typically localized in the endoplasmic reticulum or Golgi apparatus. It is, therefore, intriguing that some reports document the presence of orphan transporters SLC35F1 and SLC35F6 within the endosomal and lysosomal system. Here, we compared the subcellular distribution of these proteins and found that they are concentrated in separate compartments; i.e., recycling endosomes for SLC35F1 and lysosomes for SLC35F6. Swapping the C-terminal tail of these proteins resulted in a switch of localization, with SLC35F1 being trafficked to lysosomes while SLC35F6 remained in endosomes. This suggested the presence of specific sorting signals in these C-terminal regions. Using site-directed mutagenesis, fluorescence microscopy, and cell surface biotinylation assays, we found that the EQERLL signal located in the cytoplasmic tail of human SLC35F6 is involved in its lysosomal sorting (as previously shown for this conserved sequence in mouse SLC35F6), and that SLC35F1 localization in the recycling pathway depends on two YXXΦ-type signals: a YKQF sequence facilitates its internalization from the plasma membrane, while a YTSL motif prevents its transport to lysosomes, likely by promoting SLC35F1 recycling to the cell surface. Taken together, these results support that some SLC35 members may function at different levels of the endosomal and lysosomal system. - Source: PubMed
Publication date: 2024/06/18
Van den Bossche FrançoisTevel VirginieGilis FlorentineGaussin Jean-FrançoisBoonen MarielleJadot Michel