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
- Dysregulation of transfer RNA (tRNA) modification and reprogramming of codon-biased translation are commonly associated with cancer initiation and progression. However, their roles in chemoresistance and tumor recurrence remain poorly understood, especially in glioblastoma (GBM). This study establishes the tRNA-modifying enzyme YrdC N-Threonylcarbamoyltransferase Domain Containing (YRDC) as a key mediator of temozolomide (TMZ) resistance in GBM. YRDC catalyzes the formation of N-threonylcarbamoyladenosine (tA) on ANN-decoding tRNAs (A denotes adenosine, and N denotes any nucleotide). YRDC expression is elevated in TMZ-resistant models and recurrent GBM, correlating with poor patient prognosis. Mechanistically, YRDC drives ANN codon-biased translation of target mRNAs, most notably encoding the fatty acid-binding protein FABP7. Elevated FABP7 induces lipid droplet accumulation, which sequesters TMZ-induced reactive oxygen species to mitigate oxidative stress and confer chemoresistance. Targeting this axis, we developed HY-Q66655, a novel blood-brain-barrier-penetrant YRDC inhibitor identified via virtual screening. HY-Q66655 directly inhibits YRDC, suppresses FABP7 translation, depletes lipid droplets, and acts synergistically with TMZ to inhibit tumor growth in vitro and in patient-derived orthotopic xenografts. The YRDC/FABP7 pathway is clinically associated with GBM recurrence, and HY-Q66655 demonstrates broad-spectrum anti-tumor activity across malignancies, revealing a tRNA modification-dependent mechanism and a potential therapeutic strategy. - Source: PubMed
Publication date: 2026/04/21
Zhang YuchaoYang XuesongLi XixiZheng ChenZeng XuechaoChen JunjuGao MingpuCheng LongXu ZhenyanChen LanjieGao YixinZhong JianHuang NunuLiu XuesongHe KejunZhang NuWu Xujia - Fatty acid-binding protein 7 (FABP7) assists in the intracellular trafficking of endogenous cannabinoids and polyunsaturated fatty acids (PUFAs) and has been implicated for various psychiatric diseases. Rising evidence demonstrates the crosstalk between the endocannabinoid and dopaminergic systems, particularly in response to stress. The present study seeks to examine the role of FABP7 expression under chronic stress conditions and its impact on the dopaminergic system, specifically dopamine D1 receptor (D1R) and dopamine D2 receptor (D2R) levels. Adult male FABP7 and FABP7 mice underwent 28-day treatment of unpredictable chronic mild stress (UCMS) procedure. After the stress paradigm, D1R and D2R levels were measured with in vitro autoradiography using [H] SCH23390 and [H] Spiperone, respectively. Stressed mice, regardless of genotype, exhibited an increase in D1R binding across the entire striatum (dorsal caudate putamen (CPu), dorsolateral CPu, dorsomedial CPu, ventral CPu, ventrolateral CPu, ventromedial CPu, nucleus accumbens core and shell), substantia nigra and olfactory tract. Additionally, an increase in D2R binding induced by UCMS was observed in the olfactory tract and certain regions of the striatum (dorsal CPu and ventral CPu). The UCMS paradigm upregulates D1R and D2R binding independent of FABP7 gene deletion, suggesting a compensatory role of other FABPs in the brain in maintaining dopaminergic homeostasis. This stress-induced shift in D1R: D2R ratio may underlie the pathogenesis of major depressive disorder and substance use disorder, as well as the high comorbidity among these conditions. - Source: PubMed
Publication date: 2026/04/20
Lu HuyRoeder NicoleRichardson BrittanyHamilton JohnLagamjis GeorgeOwada YujiKagawa YoshiteruSharma AbhisheakThanos Panayotis K - 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