FABP7 Antibody (AMM10002B)
- Known as:
- FABP7 Antibody (AMM10002B)
- Catalog number:
- amm10002b
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FABP7 Antibody (AMM10002B)
Related genes to: FABP7 Antibody (AMM10002B)
- 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 Antibody (AMM10002B)
Related articles to: FABP7 Antibody (AMM10002B)
- Radial glial (RG) cells serve as both neural progenitors and structural scaffolds for neuronal migration during cortical development. Although FABP7 has long been recognized as a marker of RG cells, its regulatory function has remained poorly defined. Using human fetal brain slices, embryonic mouse model, cerebral organoids, and assembloids, we demonstrate that is essential for maintaining RG scaffold architecture and coordinating neuronal positioning. Single-cell analysis revealed that deficiency induces transcriptional dysregulation, particularly affecting cytoskeletal organization, neural fate specification, and stress responses. Furthermore, transcriptomic features in knockdown organoids exhibit convergence with neurodevelopmental disorders such as autism, alongside recapitulation of scaffold defects observed in idiopathic autism organoids. Mechanistically, loss suppresses the mevalonate (MVA) pathway, resulting in impaired GTPase-mediated cytoskeletal organization and disruption of radial scaffold integrity. These findings identify as a key regulator of cortical development and disease-relevant molecular programs, linking metabolic signaling to neurodevelopmental vulnerability. - Source: PubMed
Publication date: 2026/04/15
Wang YuanhaoZhang XuBa RuZhu YiminYu HanwenWang DaChu ChuZhang XinyueHong YuanWu ShanshanZhu WanyingXu MinCheng QingZhao ChunjieHan XiaoLiu Yan - Oral Submucous Fibrosis (OSMF) is a significant global oral health problem, particularly prevalent in India, with a high risk of progression to Oral Squamous Cell Carcinoma (OSCC). This study investigates the molecular mechanisms involved in the transformation of OSMF to OSCC using transcriptomic profiling. High-throughput RNA sequencing was performed on fresh de novo OSCC samples ( = 8) and OSMF derived OSCC using Illumina-compatible NEXTflex Rapid Directional RNA Sequencing. Normalization and differential gene expression analysis were conducted, and genes exhibiting an absolute log2 fold change of ≥2 with a co-variate-adjusted -value ≤ 0.05 were identified as significant. Upregulated genes were associated with cytokine and immune responses (ABRA, TTTY14, EIF1AY), cellular proliferation and apoptosis (LINC00314, RPS4Y1, SERPINA5, TRIM63, FABP7), and energy metabolism, indicating metabolic adaptations during malignant progression. Pathway analysis showed increased expression of TNNT1, TNNI1, MYL4, and ACTN3, implicating muscle development and embryonic pathways in OSMF transformation. Conversely, genes related to epithelial differentiation and keratinization (FLG, FLG2, HRNR, TCHH, KRT73), immune regulation and tumor suppression (HLA-G, UNC5D), and metabolic signaling were downregulated, reflecting loss of tissue integrity and immune control. OSMF-derived OSCC exhibits a distinct transcriptomic landscape compared with de novo OSCC, characterized by altered epithelial differentiation, immune modulation, and activation of developmental pathways. The observed gene dysregulation findings establish that OSCC developing in the background of OSMF is molecularly distinct from de novo OSCC, underscoring the biological impact of the pre-existing fibrotic milieu on tumor transcriptional architecture. - Source: PubMed
Publication date: 2026/03/10
Prasad KavithaSamudrala Venkatesiah SowmyaAugustine DominicAnand Ananya AnuragKaryala PrashanthiDasharathy SukeerthiRao Roopa SChaki Soma - Fatty acid binding proteins (FABPs) are key regulators of lipid metabolism and are expressed in the stroma of breast cancer. However, their roles in different breast cancer subtypes remain unclear. This study explored the expression patterns of FABPs across breast cancer subtypes and examined their associations with immune cell infiltration and clinical features using large datasets, with validation performed through testing in breast cancer cell lines and human tissue samples. - Source: PubMed
Publication date: 2026/02/25
Ali Eman Taha OsmanMin Eun-JiCho WonkyoungPark Young Mi - Glioblastoma (GBM) is a highly aggressive brain tumor characterized by metabolic plasticity that fuels growth, therapy resistance, and immune evasion. Among its reprogrammed pathways, serine and lipid metabolism play central roles. The serine synthesis pathway (SSP)-via PHGDH, PSAT1, and SHMT2-supports nucleotide biosynthesis, redox balance, and epigenetic regulation, especially under hypoxic and nutrient-deprived conditions. Meanwhile, fatty acid flux, FABP7-mediated PUFA transport, and cholesterol uptake reshape the tumor microenvironment, sustain glioma stemness, and promote immune suppression. Key lipid enzymes and ferroptosis regulators such as MAGL, ACSL4, and xCT modulate tumor survival and therapy response. GBM cells also exhibit high reliance on exogenous cholesterol, with dysregulation of LXR-SREBP pathways and mevalonate flux contributing to autophagy and proliferation. Therapeutic strategies targeting metabolic vulnerabilities-including SSP blockade, cholesterol homeostasis disruption, and ferroptosis induction-show synergistic effects with conventional agents like temozolomide. This review highlights the intertwined metabolic circuits in GBM and explores their translational potential as targets for precision therapy. - Source: PubMed
Publication date: 2026/02/03
Jiang DongxinWang ChuhengZhao YaoLi Yunqian - Breast cancer (BRCA) is the most prevalent malignancy among women and exhibits significant molecular and clinical heterogeneity. To improve risk stratification and identify novel molecular subtypes, we employed integrative analysis on DNA CpG methylation and transcriptomic data to construct a methylation-driven prognostic model for BRCA. Using LASSO, we identified a 10-gene prognostic signature that effectively stratified patients into two groups designated as high-risk and low-risk groups. Kaplan-Mayer survival analysis revealed worse overall survival of the high-risk patients in the TCGA cohort (p < 0.0001). The risk model was independently validated in two external GEO datasets GSE86166 (p = 0.00011) and GSE42568 (p = 0.00013) demonstrating its resilience and clinical relevance. In addition, the risk groups were not associated with any canonical molecular subtypes of breast cancer. Among the 10 genes, FABP7 and CLIC6 were differentially expressed between the risk groups. FABP7 had the highest negative LASSO coefficients followed by CLIC6. In further analysis, FABP7 (R = 0.42, p = 3e-04) and CLIC6 (R = 0.48, P < 0.001) both showed a strong inverse correlation between CpG methylation and expression, with more than two-fold higher expression in low-risk group and linked to improved survival in all three independent cohort. Functional enrichment analysis identified that genes overexpressed in the low-risk subtype were significantly enriched in immune-related pathways. Immunological analysis indicated a more immunogenic tumor microenvironment in the FABP7 and CLIC6 positive, low-risk group, with significantly higher infiltration of CD8 T cells (p = 0.047) and resting NK cells (p = 0.0391), while FABP7 and CLIC6 negative, high-risk tumors had increased M2 macrophages (p = 9.19 × 10) and Tregs (p = 0.0122). To summarize, this integrative model identified a novel methylation-based risk classifier/molecular subtype for BRCA, highlighting FABP7 and CLIC6 as a key prognostic biomarker with potential utility for risk stratification for strategic treatment. These findings require further validation through wet-lab experiments and prospective clinical studies to support clinical translation. - Source: PubMed
Publication date: 2025/12/26
Fahima KanizHosen Md RaiyanMahmud Zimam