Ask about this productRelated genes to: SLC38A4 Blocking Peptide
- Gene:
- SLC38A4 NIH gene
- Name:
- solute carrier family 38 member 4
- Previous symbol:
- -
- Synonyms:
- PAAT, NAT3, ATA3
- Chromosome:
- 12q13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2002-01-25
- Date modifiied:
- 2017-03-22
Related products to: SLC38A4 Blocking Peptide
Related articles to: SLC38A4 Blocking Peptide
- Metastasis is the main cause of cancer-related death. The liver is an organ with high metastatic tropism for various malignancies. Hepatic-resident macrophage Kupffer cells are the major non-parenchymal cells in the liver that phagocytize disseminated tumor cells to restrict liver metastasis. However, the critical molecules that modulate phagocytosis of tumor cells by Kupffer cells are still largely unknown. Here, we identified SLC38A4 expressed on tumor cells as a critical suppressor during tumor liver metastasis. SLC38A4 enhances the phagocytosis of various tumor cells by Kupffer cells, leading to a reduction in liver metastasis. Mechanistically, SLC38A4 downregulates the expression of "don't eat me" molecule CD24, which mediates the roles of SLC38A4 in Kupffer cells phagocytosis and tumor liver metastasis. MYC directly binds to CD24 promoter and activates CD24 transcription. Through downregulating MYC, SLC38A4 suppresses the expression of CD24. Patients with low SLC38A4 expression in tumors have more liver metastases. This study demonstrates that SLC38A4 promotes Kupffer cell phagocytosis and restricts tumor liver metastasis by suppressing CD24. The SLC38A4/MYC/CD24 axis represents a novel phagocytosis checkpoint for Kupffer cells and a potential therapeutic target for liver metastasis. - Source: PubMed
Publication date: 2026/05/01
Li JieLiu Yong-DaWang RenjieLin Xing-YiZhu Yi-QingLu Wan-PengTang Yan-FangGuo Xing-PengAi Yu-HanXu Ting-TingLin SenHuang MeiWang JinghanZhu Xiao-TingYuan Ji-Hang - Medication overuse headache (MOH) causes substantial disability in suffering patients, significantly reducing the quality of life. It may lead to structural and functional brain changes detectable by neuroimaging. Successful and effective treatments can alleviate headache burden, reduce consumption of abused drugs and reverse the biological alterations. Therefore, improvement of therapeutic strategies and optimization of patient stratification to match the individuals who can benefit with certain approaches, is essential. This study investigates DNA methylation (DNAm) associated with response to MOH treatment. - Source: PubMed
Publication date: 2026/04/02
Kwiatkowska Katarzyna MalgorzataFavoni ValentinaFerraresi FrancescaPirazzini ChiaraRavaioli FrancescoBacalini Maria GiuliaDall'Olio DanieleSala ClaudiaCastellani GastoneCalzari LucianoGentilini DavideTerlizzi RossanaPierangeli GiuliaCortelli PietroMascarella DavideGaragnani PaoloCevoli Sabina - Developmental dysplasia of the hip (DDH), a morphological abnormality of the hip joint, is a well-recognized risk factor for hip osteoarthritis (OA). Much remains unknown about the genetic factors of DDH and its subtypes. To further understand its genetic basis, we conducted genome-wide association studies (GWASs) using a total of 1 085 Japanese DDH cases (including 788 hip dysplasia cases without dislocation and 297 cases with dislocated hip) and 24 000 controls. Additionally, we meta-analyzed with United Kingdom (UK) DDH GWAS and the largest hip OA GWAS to date. We identified three genome-wide significant novel loci, COL11A2, CALN1 and TRPM7, associated with hip dysplasia without dislocation. None of these signals were significant in dislocated hips, and additionally two of the signals had an opposite direction of association, suggesting distinct genetic architectures between the subtypes. The Japanese DDH GWAS identified five associated loci (VEGF-C, FOXC1, SMC2, SLC38A4, and TRPM7), and the trans-ancestry meta-analysis with UK revealed two loci (COL11A1 and GDF5) supported by strong trans-ancestry genetic correlation (r = 1.0). In total, nine loci were identified for DDH and its subtypes, with hip dysplasia without dislocation showing distinct genetic signals from hip dislocation. The meta-analysis of DDH and hip OA identified five novel signals for hip OA. Susceptibility loci and heritability enrichment analyses implicated pathways involving bone formation, collagen type XI trimer, and chondrocyte development, as well as their gene regulation, in DDH. These findings enhance understanding of the genetic architecture and biological pathways underlying DDH, providing new insights into its relationship with OA. - Source: PubMed
Publication date: 2026/03/31
Yoshino SoichiroChen ShiboYamaguchi RyosukeKurakazu TaishiHatzikotoulas KonstantinosKoike YoshinaoInoue DaisukeKohno YusukeSasaki KanChoe HyonminBaba ShojiHara ToshihikoIto JujiOkuzu YaichiroShiomoto KyoheiNakamura TomoyukiKoyano GakuShimizu TomohiroKinoshita KoichiTakahashi EijiUtsunomiya TakeshiHara DaisukeSato TaishiKawahara ShinyaKaneuji AyumiYamamoto TakuakiTakahashi DaisukeJinno TetsuyaKawano TsutomuGoto KojiTakagi MichiakiMawatari TaroInaba YutakaNakamura TetsuroKabata TamonHamai SatoshiMotomura GoroSoutham LorraineWilkinson J MarkZeggini EleftheriaIkegawa ShiroNakashima YasuharuTerao Chikashi - Placental enlargement in somatic cell nuclear transfer-derived mice is attributed to biallelic expression of noncanonical (H3K27me3-dependent) imprinted genes owing to loss of imprinting (LOI). Here, we investigated whether a similar mechanism underlies placental enlargement in intersubspecific hybrids between BDF1 (Mus musculus domesticus) and HMI (M. m. castaneus) mice. Quantitative and allelic expression analyses revealed gene-specific LOI in (BDF1 × HMI)F1 placentas: Jade1 (Phf17) and Slc38a4 showed LOI in all placentas regardless of expression levels, whereas Gab1 and Sfmbt2 exhibited LOI only when expression levels were elevated. Notably, Jade1 and Slc38a4 also showed biallelic expression at lower levels in normal-sized (BDF1 × JF1 [M. m. molossinus])F1 placentas. Maternal knockout of Jade1, Slc38a4, Sfmbt2, or the Sfmbt2 miRNA cluster restored monoallelic expression and significantly reduced the weight of (BDF1 × HMI)F1 placentas, indicating that these genes were collectively responsible for placental enlargement in intersubspecific hybrid placentas. Transcriptomic analysis revealed that LOI of noncanonical imprinted genes occurred after implantation. These findings suggest that placental enlargement in (BDF1 × HMI)F1 hybrids is driven by overexpression of multiple noncanonical imprinted genes, resulting from LOI after implantation and additional hybrid-specific, yet unidentified, upregulation mechanisms. - Source: PubMed
Tokita SyunWatanabe NaomiHasegawa AyumiFunaya SatoshiMiura KentoMatoba ShogoOgura AtsuoInoue Kimiko - Gestational diabetes mellitus (GDM) is associated with adverse pregnancy outcomes. When the infant is large for gestational age, placental nutrient transport capacity is often increased. We hypothesized that GDM alters placental nutrient transporter abundance irrespective of infant size. - Source: PubMed
Publication date: 2025/10/25
Mahindra PradhikiHillman Sara LSiassakos DimitriosVaughan Owen R