FAM120A antibody - middle region (ARP55089_P050)
- Known as:
- FAM120A (anti-) - middle region (ARP55089_P050)
- Catalog number:
- arp55089_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FAM120A antibody - middle region (ARP55089_P050)
Related genes to: FAM120A antibody - middle region (ARP55089_P050)
- Gene:
- FAM120A NIH gene
- Name:
- family with sequence similarity 120A
- Previous symbol:
- C9orf10
- Synonyms:
- KIAA0183, OSSA
- Chromosome:
- 9q22.31
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-09
- Date modifiied:
- 2017-07-12
Related products to: FAM120A antibody - middle region (ARP55089_P050)
Related articles to: FAM120A antibody - middle region (ARP55089_P050)
- Bladder cancer (BC) is one of the most deadly diseases in the USA, with 84,530 new cases and 17,870 estimated deaths in 2026. The growth factor progranulin is involved in several human pathologies, including frontotemporal dementia (FTD), immune response, and cancer. We showed that in BC, progranulin and its signaling receptor, EphA2, drive tumor cell motility, invasion, and in vivo tumor formation, making it a critical pathway in tumor establishment. However, the molecular mechanisms of progranulin/EphA2 action are still poorly defined. - Source: PubMed
Publication date: 2026/08/11
Satasiya VrundaMartinelli CanioPascal GabrielDucci GiacomoVentura ElisaWilliams Stephen JBurk Sharon RaffaellaTchamou Manuela NanaShani ShendiKlain MicheleSacco ElenaVanoni MarcoBelfiore AntoninoIozzo Renato VGiordano AntonioMorrione Andrea - Posttraumatic stress disorder (PTSD) occurs following potentially traumatic experiences, but not everyone who experiences trauma develops PTSD. Genetic factors play an important role in shaping how individuals respond to trauma, reflecting gene-environment interaction. An open and important question in PTSD genetics research is the extent to which gene-environment interactions vary across specific traumas. We aimed to compare gene-environment interaction effects across a broad range of self-reported potentially traumatic experiences across the lifespan. We analysed existing data from two large UK cohorts: the UK Biobank and GLAD-EDGI-COPING (N = 144,702). PTSD symptoms were assessed using the six-item abbreviated PTSD Checklist. We examined eleven self-reported trauma exposures, including five childhood traumas and six adulthood traumas. We conducted gene-environment interaction analyses for each trauma at three levels of genetic specificity: polygenic risk scores, specific genes, and specific genetic variants. Childhood traumas showed stronger associations with PTSD symptoms and greater gene-environment interactions than adulthood traumas on average. Childhood emotional and physical neglect also demonstrated greater gene-environment interactions than childhood abuse. Interaction patterns varied across genes and variants, with several leading PTSD-associated genes (e.g. ) having particularly strong interactions with certain traumas. Several genes () demonstrated consistently stronger interactions across all childhood or all adulthood traumas. Differences in gene-environment interactions across traumas were not explained by variation in exposure rates, associations with PTSD symptoms, or gene-environment correlations. Our findings are consistent with differential gene-environment interactions on PTSD across potentially traumatic experiences, with those in childhood exhibiting the strongest interactions. To account for the moderating role of trauma type on genetic associations, genetic research on PTSD should incorporate detailed trauma exposure information, which may improve PTSD risk prediction and support more personalised prevention approaches. - Source: PubMed
Publication date: 2026/09/16
Knyspel JacobKakar SaakshiCarnegie AnnaKalsi GursharanMeldrum LauraSmith IonaBristow ShannonDavies Molly RArmour ChérieBioResource NihrEley Thalia CBreen GeromeWong Chloe C YColeman Jonathan R I - Depression-related liability is frequently accompanied by reduced physical function, yet the shared genetic architecture linking mood-related traits and physical-function decline remains incompletely characterized. We applied genomic structural equation modeling to European-ancestry GWAS summary statistics for five constituent phenotypes: depressive symptoms, depression diagnosis, grip strength, appendicular lean mass, and walking pace. A Depression-Physical Function shared genetic factor was constructed as a cross-trait genetic covariance dimension and evaluated using LDSC-based validation and leave-one-trait-out sensitivity analyses. We then performed factor GWAS, FUMA locus annotation, Bayesian fine-mapping, MAGMA gene-based analysis, transcriptome-wide association analysis, pathway enrichment, CELLECT/MAGMA cell-type specificity analysis, partitioned heritability analysis, and gsMap spatial transcriptomic mapping. The shared factor showed good model fit and retained 755,397 quality-controlled variants for downstream analysis. The factor was positively genetically correlated with depression-related traits and negatively correlated with physical-function-related traits. FUMA identified 245 genome-wide significant SNPs, 44 lead SNPs, and 38 genomic risk loci, with 127 positional mapped genes. Fine-mapping prioritized one high-confidence locus. MAGMA identified 19 Bonferroni-significant genes and 326 FDR-significant genes, while TWAS identified 322 FDR-significant expression-associated genes. Integrating FUMA positional mapping, MAGMA gene-level association and TWAS expression-level association prioritized eight convergent genes: TMEM106B, CENPW, DRD2, LRFN5, NCAPG, DCAF16, SGIP1, and FAM120A. Functional enrichment highlighted postsynaptic structure, neuron spine, synaptic plasticity, and synapse organization. CELLECT/MAGMA prioritized brain non-myeloid neurons and glial populations, with additional endocrine-metabolic and immune-hematopoietic signals. Spatial transcriptomic mapping localized top signals to brain and spinal cord regions in the embryonic neuro-muscle reference. Partitioned heritability analysis showed enrichment in conserved, intronic, promoter, and chromatin-related genomic annotations. These findings support a shared polygenic covariance dimension linking depression-related liability with reduced physical-function-related genetic propensity. Downstream analyses prioritized candidate loci, genes, and biological contexts, with enrichment patterns consistent with neuronal, synaptic, and regulatory genomic processes. - Source: PubMed
Publication date: 2026/07/16
Zeng WenYang XiupengXu Yonggang - Clear cell renal cell carcinoma (ccRCC) is characterized by extensive lipid metabolic reprogramming that drives tumor progression and therapeutic resistance. Although sterol regulatory element-binding protein 1 (SREBP1) is a central regulator of lipogenesis in ccRCC, the upstream mechanisms governing its activation remain poorly defined. Here, we investigated the role of FAM120A in SREBP1-dependent lipid metabolism and evaluated the therapeutic potential of the natural product Soulangianolide A (SA). - Source: PubMed
Publication date: 2026/07/17
Luo WeiSong ZhengLiu ZishuZhang GuangshuaiYan SiPeng RuiBai ZhaofangQin ShuanglinXiao Xiaohe - Amyotrophic lateral sclerosis (ALS) is a disabling and fatal neurological disease, which is characterized by the loss of motor neuron function in the brain and spinal cord. Due to genetic complexity, ALS disease is not well understood. By applying a bioinformatic approach, referred to as convergent analysis, we identified the poorly characterized protein FAM120A as a new candidate gene related to RNA metabolism, a process known to be affected during ALS disease. We studied Fam120A in the context of ALS in vivo and in vitro using an ALS mouse model and a cellular model. We found that Fam120A mRNA levels were decreased in the pre-symptomatic stage in the spinal cord of SOD1G93A mice, while Fam120A protein levels were decreased at the symptomatic stage. Fam120A was expressed mainly in neurons in the spinal cord. Overexpression of FAM120A in a motor neuron cell culture model decreased the levels of SOD1G93A aggregates. In summary, our results warrant further studies of FAM120A in the context of ALS, since it appears to be involved in disease progression and might have a role in proteostasis maintenance. - Source: PubMed
Publication date: 2026/02/10
Vicencio EmilianoGomez LauraBeltran SebastianHernandez FernandaRodriguez LeonardoBravo ConstanzaJofré ThiareGálvez FabiánLabrador LuisRojas-Rivera DiegoCortés Bastián ICortez CristianManque PatricioWoehlbier Ute