Ask about this productRelated genes to: FABP7 protein
- Gene:
- FABP7 NIH gene
- Name:
- fatty acid binding protein 7
- Previous symbol:
- -
- Synonyms:
- B-FABP, BLBP
- Chromosome:
- 6q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-20
- Date modifiied:
- 2016-10-05
Related products to: FABP7 protein
Related articles to: FABP7 protein
- This study examined the effects of the trans-resveratrol (Res) and l-carnitine (l-Car) complex (RC) on mice genetically resistant to obesity. Male DBA/2J mice received low (RCl, 25/300 mg/kg BW) or high (RCh, 50/600 mg/kg BW) doses of the RC for 64 days in a control diet (CD) or a high-fat-high-carbohydrate diet (HFCD). Differential expression (DE) of genes in the liver was analyzed using DNA microarrays. HFCD alone altered 471 genes (1.7%) versus CD. In CD-fed mice, RCl and RCh affected 170 (0.6%) and 321 (1.2%) genes, respectively. In HFCD-fed mice, RCl and RCh affected 109 (0.4%) and 223 (0.8%) genes. Opposite DE changes between HFCD and RC + HFCD occurred in immune recognition and fat-storage genes (, , , , , etc.). Uniform responses to HFCD and RC + CD were seen in , , , , , , , , , , , and . RC effects were consistent with liver morphology. Key RC-targeted pathways included retinoid metabolism, PPAR signaling, and antigen presentation. In HFCD-fed mice, additional pathways were steroid biosynthesis, oxylipin metabolism, and Jak-STAT signaling. DBA/2J mice may exhibit an innate compensatory response involving PPAR signaling, , and , and the contribution of polymorphisms in these genes merits separate investigation in future studies of obesity resistance. - Source: PubMed
Publication date: 2026/08/31
Gmoshinski Ivan VTrusov Nikita VShipelin Vladimir ANikityuk Dmitriy B - Fatty acid-binding proteins (FABPs) are intracellular lipid chaperones that regulate fatty acids and metabolism and signaling. Although Fabp3 and Fabp7 expression has been described in the rodent cochlea, detailed characterization in a primate model has not been performed. This study investigated the spatial and temporal expression patterns of FABP3 and FABP7 in the cochlea of the common marmoset. - Source: PubMed
Publication date: 2026/08/22
Hosoya MakotoSuda SatoshiUeno MasafumiShimanuki Marie NNishiyama TakanoriOishi NaokiOzawa Hiroyuki - Metastasis remains the primary cause of breast cancer mortality. Triple-negative breast cancer (TNBC) is a highly aggressive breast cancer subtype. It lacks targeted therapies and carries a high risk of metastasis. MiRNAs are one of the potential diagnostics and therapeutic biomarkers, given that the regulation of mRNA is critical for tumor growth and metastatic transformation of tumor cells. Identifying the differential expression of the miRNA-mRNA axis at the primary tumor site will provide novel molecular mechanisms for metastasis initiation. In this study, we applied an integrated approach to explore the metastasis-specific miRNA-mRNA regulatory axis in TNBC using TCGA-derived miRNA-seq and RNA-seq data. Differential expression analysis between metastatic and non-metastatic TNBC patient data identified 11 dysregulated miRNAs, of which 8 showed linear expression changes with increasing disease aggressiveness. Among them, hsa-miR-1-1/2, hsa-miR-9, and hsa-miR-1180 displayed strong diagnostic potential (AUC >0.8) and significant associations with overall survival in metastatic TNBC patients. Parallel RNA-seq analysis revealed 36 differentially expressed genes (DEGs). Target prediction highlighted that only hsa-miR-9-5p targeted three of the 36 DEGs-FABP7, GPR26, and UNC5D, where FABP7 demonstrated strong association with cancer pathways. The expression of these genes was also correlated with the overall survival of the TNBC patients. Validation of this axis in various breast cancer cells (metastatic and non-metastatic) was performed, and the results indicated an inverse expression pattern of hsa-miR-9-5p and FABP7, especially in metastatic TNBC cells. These findings propose the hsa-miR-9-FABP7 axis as a promising biomarker signature for predicting metastatic potential from primary TNBC tumors. - Source: PubMed
Publication date: 2026/07/24
Rathore DeepshikhaDheer VasundharaSingh SurbhiPatel ShanayaDesai ChiragDave Heena V - Astrocytes in the mouse hippocampal dentate gyrus (DG) derive, at least in part, from BLBP+ cells, but the mechanism that controls the onset of their differentiation remains poorly understood. To address this, we first characterised the developmental dynamics of BLBP+ cells using Ki67 and the cyclin-dependent kinase inhibitor p57. Ki67+/BLBP+ proliferative progenitors peaked at P1 and declined by P3-P6, when p57+/BLBP+ early-differentiating astrocytes instead accumulated. This temporal switch prompted us to examine what maintains the proliferative pool and restricts premature differentiation. We identified Sox4, a downstream transcription factor of TGFβ signalling, as a selective marker of the undifferentiated astrocytic lineage in the developing DG. At E15-E17, Sox4 was co-expressed with BLBP and pVimentin in basal radial glia (bRG), and at P1-P6 with BLBP, Sox3 and Ki67 in proliferative glial progenitors including the Olig2+/BLBP+ astrocyte progenitors (ASPs) we recently identified. Our data further suggest that Sox4 marks ASPs but not either NeuroD+ neuronal progenitors or p57+/BLBP+ early-differentiating astrocytes. From P14 onwards, Sox4 expression persisted in a subpopulation of BLBP+ radial glia-like cells (RGLs) at the SGZ and in BLBP+ cells in the molecular layer. Together, these data suggest that Sox4 selectively marks BLBP+ glial progenitors (bRG, RGLs and ASPs) but not their differentiated progeny. Consistent with an autocrine TGFβ1-Sox4 pathway described in glioma-initiating cells, TGFβ1 was co-expressed with BLBP in bRG, RGLs and ASPs. Blockade of TGFβ signalling with SB431542 in DG explants depleted Sox4+ progenitors and, in turn, promoted the accumulation of p57+/BLBP+ astrocytes. Our data thus suggest that TGFβ signalling maintains Sox4+ progenitors and thereby restricts the early differentiation of BLBP+ astrocytes in the mouse DG. - Source: PubMed
Publication date: 2026/07/01
Ohyama KyojiOmura ShoichiroTakayama NatsumiTakahashi Tokiharu - Oocyte quality determines fertilization success during the reproductive period of fish and is affected by a key intrinsic factor: the level of lipid deposition in the yolk. In this study, lipidomics was used to characterize lipid profiles of adipose tissue, liver, serum and ovary to clarify divergent hepatic lipid allocation to fat depots versus ovary in Sichuan taimen (). The results showed that glycerophospholipids (GPs) constituted the most diverse lipid class across all four tissues, with phosphatidylcholine (PC) being the most abundant in each tissue. Relative to adipose tissue, liver, and serum, the ovary exhibited significant enrichment of PC and phosphatidylethanolamine (PE) and higher accumulation of docosahexaenoic acid (DHA)- and arachidonic acid (ARA)-containing GPs and triacylglycerols (TGs), as well as enrichment in TGs, diacylglycerols (DGs), and cardiolipin (CL), compared to adipose tissue. The expression levels of , , , , , , , and were higher in the liver, while was highly expressed specifically in the ovary. The results of this study demonstrate that long-chain polyunsaturated fatty acids (LC-PUFAs) exhibited selective enrichment in the ovary, which facilitates yolk lipid deposition and provides structural and energetic support for oocyte development and early embryonic development. From a lipidomic perspective, this study reveals the regulatory characteristics underlying ovarian yolk deposition in , providing important evidence for understanding the mechanisms of egg quality formation as well as a theoretical basis for broodstock management, artificial propagation, and the improvement of egg and larval quality. - Source: PubMed
Publication date: 2026/07/02
Wei QinyaoChen YeyuWang FubinShao WeiRu YongshenYang HuanchaoDu JunSong ZhaobinLai ZhenmingLi Hua