FABPH_HUMAN M-FABP ELISA tesk kit
- Known as:
- FABPH_HUMAN M-FABP Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen16035
- Product Quantity:
- 1
- Category:
- Peptides
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- Other suppliers
- Gene target:
- FABPH_HUMAN M-FABP ELISA tesk kit
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- The peripheral myelin protein P2 (also known as PMP2/FABP8) has two basic functions in vivo: the transport of fatty acids within the cell to the target compartments and the adhesion of lipid bilayers in the peripheral nervous system myelin to each other. In this work, we focus on the membrane-binding properties of P2 and its Charcot-Marie-Tooth disease variants. Experiments were carried out on lipid monolayers at the air-water interface as a membrane model system, with the lipid composition of the cytoplasmic leaflet of myelin. Our study provides quantitative data on the membrane affinity of P2 and its disease-linked or structure-based missense variants toward the native lipid membrane and shows affinity differences due to single P2 point mutations. Phospholipid monolayer surface pressure measurements are supported by epifluorescence microscopy, which not only shows the adhesive property of all P2 variants but also the complex cross-linking property of the wild-type P2. An analysis of transcriptomics databases confirms expression of P2 in human, but not mouse, central nervous system nonneuronal cells. Taken together, our work further confirms the role of P2 in binding myelin-like lipid membranes as well as its direct effects on lipid membrane properties. - Source: PubMed
Schöffmann Florian ArndtImran Md Abdus ShukurSchwieger ChristianHetland ØysteinJerschabek VanessaRaasakka ArneKursula PetriHinderberger Dariush - Suicide remains a critical global public health issue, accounting for nearly one million deaths annually and imposing profound societal and economic burdens. Despite its urgency, the lack of diagnostic and predictive biomarkers continues to hinder the development of effective prevention and treatment strategies. This study presents a comprehensive meta-analysis that integrates publicly available postmortem brain transcriptomic datasets and a domestic cohort, encompassing 16 cohorts. The transcriptomic data, sourced from the Gene Expression Omnibus repository, were generated using various techniques, including traditional RNA sequencing, microarray methods, and single-cell RNA sequencing. Differential expression analyses were performed across multiple brain regions, with meta-analyses stratified by cortical regions, the dorsolateral prefrontal cortex (DLPFC), and combined. We further analyzed whether covariates may affect the identified genes. Three meta-analytic approaches were employed, complemented by pathway and cell-set enrichment analyses. The unadjusted meta-analysis consistently identified several genes with altered expression, including upregulated P2RY12, CX3CR1, and GPR34, and downregulated SOX9 and PMP2, all at nominal significance. Additionally, multiple genes encoding long non-coding RNAs (lncRNAs) exhibited nominally altered expression in suicide, including RP5-837J1.4, AC159540.14, DNM1P47, AC004158.2, EEF1A1P30, and RP11-339B21.8. Several alternative strategies to run meta-analysis were performed and moderators were investigated. Cell-type-specific expression deconvolution and meta-analysis identified several genes overlapping with bulk expression meta-analysis, and genes were attributed to neuronal lineages. These findings highlight plausible molecular targets for future validation studies, suggesting the involvement of microglia (P2RY12 and CX3CR1), astrocytes (SOX9), immune responses (GPR34), myelin regulation (PMP2), and epigenetic modulation via lncRNAs. This research advances the understanding of the molecular architecture of suicide and provides a foundation for future studies focused on targeted prevention and therapeutic interventions. - Source: PubMed
Publication date: 2026/03/31
Sokolov Aleksandr VLafta Muataz SJokinen JussiSchiöth Helgi B - Hilar cholangiocarcinoma (HC) is a highly aggressive malignancy with a poor prognosis, highlighting the urgent need to elucidate its molecular drivers. This study aimed to systematically identify and functionally validate key genes and pathways driving HC pathogenesis. RNA sequencing (RNA-seq) was performed on paired primary HC tumors and matched adjacent non-tumorous tissues to identify differentially expressed genes (DEGs). Subsequent bioinformatic analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and protein-protein interaction (PPI) network construction, were conducted to characterize the functional landscape and identify hub genes. Transwell assays and orthotopic metastatic models were used to investigate the functions of Contactin-1 (CNTN1) in HC invasion in vitro and metastasis in vivo. RNA-seq analysis identified 35 DEGs in HC, mainly involved in cell adhesion, cytoskeletal regulation, and axon development. PPI network analysis identified six hub genes, including , , , , , and . Furthermore, we demonstrated that CNTN1, a neuronal membrane glycoprotein, was markedly up-regulated in HC at both mRNA and protein levels, and its elevated expression correlated with poor prognosis. Gain- and loss-of-function studies demonstrated that promotes HC cell invasion in vitro and metastasis in vivo. Mechanistically, exerts its pro-invasive effects by activating the PI3K-AKT signaling pathway and inducing epithelial-mesenchymal transition (EMT). Our integrated analysis identifies as a critical oncogenic driver in HC, promoting metastasis through PI3K-AKT-mediated EMT. These findings nominate as a potential prognostic biomarker and therapeutic target in HC. - Source: PubMed
Publication date: 2026/03/11
Ding XiangmingCai ChiyuLu YuanxiangWang ZipengHou JunjingXue YushuZhang LuyunXie MengLi Dongxiao - 8q21.11 microdeletion syndrome is a rare chromosomal disorder characterized by a highly variable phenotype, including mild to moderate intellectual disability, distinctive facial dysmorphisms, and congenital anomalies such as ocular defects, cardiac malformations, and limb abnormalities. The deletion size in 8q21.11 microdeletion syndrome ranges from 0.12 to 13.15 Mb, with a critical small region of overlap (SRO) of 539.77 Kb. The gene in this region is implicated in neurodevelopmental disorders and ocular anomalies. Other genes, including PEX2 and PMP2, contribute to the complex clinical presentation by affecting metabolic and immune functions. Here, we present a prenatal diagnosis of 8q21.11 microdeletion syndrome in a fetus with increased nuchal translucency detected via ultrasound. This case underscores the importance of high-resolution genomic testing and genetic counseling in the management of 8q21.11 microdeletion syndrome, providing valuable insights into prenatal assessment of this rare condition. - Source: PubMed
Publication date: 2026/02/17
Libotte FrancescoMargiotti KatiaFabiani MarcoMesoraca AlvaroGiorlandino Claudio - Due to a lack of information related to molecular changes in heroin use, we aimed to examine heroin-dependent alterations in different regions of the post-mortem human brain. Tissues were obtained from males (n = 24 heroin users, n = 24 controls) through the Turkish Forensic Medicine Institute after structured verbal interviews with the relatives of the deceased to gather history of substance use. Following toxicological confirmation of heroin use, the hippocampus, putamen, and caudate nucleus were dissected from the left hemispheres. Proteomic analyses were performed using a high-resolution liquid chromatography-electrospray ionization-tandem mass spectrometry (LC-ESI-MS/MS) system. Label-free quantitative analysis revealed significant differential expression of 87 proteins in the hippocampus, 121 proteins in the putamen, and 80 proteins in the caudate nucleus compared to controls. These differentially expressed proteins (DEPs) were subsequently used to construct protein-protein interaction (PPI) networks using the STRING database, revealing significantly enriched and highly interconnected interaction networks in all three regions. Gene Ontology (GO) enrichment analysis of DEPs consistently identified extracellular exosome, extracellular space, and vesicle as the top three cellular components. Molecular function enrichment further indicated alterations in signaling, binding, and stress-related processes. The expression of TST, RYR2, ACTBL2, and RPS27 decreased, whereas the expression of COL4A2, OGN, PMP2, and MAP2K6 increased in the hippocampus. In the putamen, the most prominent increases were observed in DNM2 and MADD expression. In the caudate nucleus, the expressions of RPS6KA2, TMED10, and NBEA proteins decreased, whereas HPX protein expression increased. Overall, these alterations promote oxidative stress and molecular changes linked to neurodegeneration, which likely contribute to impaired neuronal function and synaptic plasticity. - Source: PubMed
Publication date: 2026/02/21
Sürmen Mustafa GaniPence SadrettinSürmen SaimeBuyuk YalcinKuras SibelElibol BirsenPence Halime Hanim