FAM120A Peptide
- Known as:
- FAM120A Peptide
- Catalog number:
- zp-5307
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- FAM120A Peptide
Related genes to: FAM120A Peptide
- 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 Peptide
Related articles to: FAM120A Peptide
- Schizophrenia (SCZ) is a highly heritable complex disorder influenced by coding and noncoding genetic variation. Its genetic causes, particularly those involving noncoding variation, are largely unknown. High-throughput CRISPR screens enable dissection of disease-associated loci and identification of noncoding regulatory elements and variants that modulate gene expression. We screened SCZ GWAS loci linked to genes that are also associated in whole-exome sequencing studies to identify regulatory elements and variants impacting expression of disease-relevant genes. We used CRISPRi paired with HCR-FlowFISH to epigenetically silence 333 putative regulatory elements and measure the downstream effects on gene expression of causal SCZ genes, , , and , in iPSCs and iPSC-derived neurons (iNeurons). We identified 78 regulatory elements that significantly alter expression of a SCZ gene, including noncoding enhancers/silencers as well as promoters of genes and lncRNAs. Pooled prime editing screens interrogated noncoding variant influence on gene expression for SCZ-associated variants and uncharacterized common variants from diverse population studies. We find that a common variant in the promoter of , rs112851681:A>G (MAF = 3.56%, 1000 Genomes) enhances transcriptional activity in iPSCs and iNeurons. These findings show distinct noncoding mechanisms that map within GWAS signals, and provide a path forward for interrogating noncoding regulatory elements and variants in disease loci. - Source: PubMed
Publication date: 2026/09/17
Hamilton Marisa CRiley Julia WNelson Alexander CLi BoxunDornbaum Sophie FSafi AlexiasCui XiekuiJones Ian RColey Aaron AHagy Kevin TRai RuhiBarrera AlejandroAllen Andrew SShen YinSherwood Richard ILove Michael ISullivan Patrick FGersbach Charles ACrawford Gregory E - 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