RAB9A 293T Cell Transient Overexpression Lysate(Denatured)
- Known as:
- RAB9A 293T Cell Transient Overexpression Lysate(Denatured)
- Catalog number:
- H00009367-T02
- Product Quantity:
- 100 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- RAB9A 293T Cell Transient Overexpression Lysate(Denatured)
Related genes to: RAB9A 293T Cell Transient Overexpression Lysate(Denatured)
- Gene:
- RAB9A NIH gene
- Name:
- RAB9A, member RAS oncogene family
- Previous symbol:
- RAB9
- Synonyms:
- -
- Chromosome:
- Xp22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1999-03-24
- Date modifiied:
- 2014-11-18
Related products to: RAB9A 293T Cell Transient Overexpression Lysate(Denatured)
Related articles to: RAB9A 293T Cell Transient Overexpression Lysate(Denatured)
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Publication date: 2026/03/06
Liu JiayingMai YansuiXie YuZhou XiaolingYe YitingJiang DongxuHe LianYe ZhandongLi DanXia ChenglaiSu JiyanHuang Song - : Metabolic dysfunction-associated steatotic liver disease (MASLD) and depression frequently occur together. Identifying the genes that influence both MASLD and depression may facilitate the discovery of biological pathways associated with disease risk. : We recruited 525 participants from Mexican American families living in the Rio Grande Valley of south Texas. We collected clinical data, biometric measurements, hepatic health assessments using Vibration-Controlled Transient Elastography (VCTE), and depression evaluations determined with the Beck Depression Inventory-II. We estimated the heritability (h) of MASLD-related measures, depression status, aspartate aminotransferase (AST), alanine aminotransferase (ALT), the AST/ALT ratio, and Vibration-Controlled Transient Elastography measurements. For each gene, we derived a genetic endophenotype representing its expression level. We then performed functional network and gene ontology enrichment analyses to characterize the underlying protein pathways. : We observed significant associations between the expression of two genes, Thyroid Hormone Receptor-Associated Protein 3 () (h = 0.56 [0.45, 0.67]) and ADAM Metallopeptidase with Thrombospondin Type 1 Motif 7 () (h = 0.66 [0.55, 0.77]), with depression and multiple MASLD-related phenotypes. We identified 351 genes with expression levels significantly correlated with one or more MASLD phenotypes and depression. Among these, five genes-, , , , and -were jointly associated with three phenotypes: AST/ALT, ALT, and Controlled Attenuation Parameter (CAP kPa). Based on the Fisher Combined Test, only ( = 3.0 × 10) and ( = 2 × 10) were jointly significant for depression (BDI-II) and AST, ALT, AST/ALT ratio, FAST, and CAP (kPa). We present a protein-protein interaction network comprising nodes (proteins) and edges (interactions), and a gene ontology enrichment analysis of cellular components. : Our findings highlight pleiotropic genes underlying MASLD and depression. Two genes, and , warrant further investigation as potential targets for therapeutic interventions to manage MASLD and depression among Mexican Americans. These results may improve our understanding of the pathways involved in these two diseases, advance current research, and contribute to improvements in personalized medicine. : We identified possible shared gene expression phenotypes linking MASLD and depression, which may provide insight into a common molecular underpinning. Pathway enrichment and gene analysis were used to help refine networks and enhance our understanding of complex gene-environmental interactions and their implications for precision medicine. - Source: PubMed
Publication date: 2026/03/19
Manusov Eron GDiego Vincent PAlmeida MarcioGalan Jacob AHerklotz KathrynAbrego Iii EdwardoSultana HabibaPena Marquez LuisArriaga Marco ALeandro MarceloPeralta JuanC Leandro AnaHoward Tom ECurran Joanne ELaston SandraBlangero JohnWilliams-Blangero Sarah - Polyethylene terephthalate microplastics (PET-MPs) function as endocrine-disrupting agents that interfere with steroidogenesis and folliculogenesis, potentially contributing to polycystic ovary syndrome (PCOS). This study integrates computational toxicology and machine learning to delineate the mechanisms linking PET-MP exposure to PCOS pathogenesis. We conducted systematic multi-omics analysis by merging PET-MP-associated targets from ChemBL, PubChem, SwissTargetPrediction, SuperPred, and GeneCards with PCOS-related genes from GeneCards and the Comparative Toxicogenomics Database. Differential expression and weighted gene co-expression network analysis (WGCNA) were then applied to ovarian transcriptome datasets (GSE106724 and GSE137684). LASSO regression was used to prioritize hub genes, which underwent validation via diagnostic nomograms, molecular docking, molecular dynamics simulations, single-cell expression analysis, immune microenvironment profiling, and pathway enrichment. The results identified 22 overlapping genes connecting PET-MP exposure to PCOS, with RAB9A and MAOB highlighted as potential diagnostic biomarkers that appear to influence inflammatory responses, disrupt steroid hormone homeostasis, and induce mitochondrial dysfunction. Single-cell analysis revealed hub gene enrichment in ovarian granulosa cells (GCs), indicating targeted impacts on the follicular microenvironment, while immune profiling showed macrophage and γδ T cells as possible mediators of PET-MP-induced PCOS. Molecular docking and dynamics simulations demonstrated stable binding affinities of PET-MPs to RAB9A and MAOB. Overall, these findings position RAB9A and MAOB as environmental susceptibility biomarkers associating PET-MP exposure with PCOS development, providing molecular insights for targeted interventions. - Source: PubMed
Publication date: 2026/03/22
Bai HaiJiang YuxiaoZhu BozhiHuang JingZhang YuLiu XunruiGe LiyingZhang ShanshanShi YueWang Mingming - Phosphatase and tensin homolog (PTEN) is a critical regulator of cell proliferation, differentiation, and inflammatory balance. However, its downstream proteomic effects in periodontal ligament stem cells (PDLSCs) remain poorly understood. This study aimed to elucidate the proteomic alterations induced by PTEN inhibition and identify potential molecular pathways underlying periodontal regeneration. - Source: PubMed
Publication date: 2026/03/20
Phothichailert SuphalakNowwarote NunthawanKornsuthisopon ChatvadeeMurakami ShinyaSrithanyarat Supreda SuphanantachatOsathanon Thanaphum - The small GTPase Rab9 plays a major role in the vesicular trafficking of cation-independent mannose-6-phosphate receptor (CI-M6PR). CI-M6PR trafficking has also been reported to be perturbed by the dysfunction of a ubiquitin ligase necessary for protein quality control (PQC). However, the mechanism underlying the participation of the PQC machinery in CI-M6PR trafficking is poorly understood. In this study, we found an extremely short half-life of GDP-bound Rab9, which is in clear contrast to its phylogenetically closest relative, Rab7. Comparison of the amino acid sequences of these relatives revealed that hydrophobic residues are specifically exposed in the switch I region of Rab9a and that these residues are recognized by the PQC machinery. We defined this exposed hydrophobicity as a conformation-dependent hydrophobic (CDH) degron because its existence determines the instability of Rab proteins in a nucleotide-dependent manner. CDH degron-mediated instability is essential for Rab9a function, given that forced accumulation of CDH degron-mutated Rab9a in cells resulted in the defective localization of CI-M6PR, a similar phenotype observed in PQC dysfunction. Thus, the CDH degron-driven PQC system is necessary for the proper vesicular trafficking of CI-M6PR. We also identified valosin-containing protein/p97 as a CDH degron-dependent PQC factor for GDP-bound Rab9a. - Source: PubMed
Publication date: 2026/01/31
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