FAM129A (phospho-Ser602) Antibody
- Known as:
- FAM129A (phosphorilated-Ser602) Antibody
- Catalog number:
- abx000398
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- FAM129A (phospho-Ser602) Antibody
Related genes to: FAM129A (phospho-Ser602) Antibody
- Gene:
- NIBAN1 NIH gene
- Name:
- niban apoptosis regulator 1
- Previous symbol:
- C1orf24, FAM129A
- Synonyms:
- NIBAN, GIG39
- Chromosome:
- 1q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-08
- Date modifiied:
- 2019-04-18
Related products to: FAM129A (phospho-Ser602) Antibody
Related articles to: FAM129A (phospho-Ser602) Antibody
- Type 2 diabetes (T2DM) is clinically heterogeneous. A subgroup with markedly reduced C-peptide has poorer glycemic stability and different therapeutic needs, but the associated peripheral immune features and practical non-invasive markers are not well defined. We investigated whether T2DM with low C-peptide (T2DM-LowC) is associated with a distinct peripheral immune profile. - Source: PubMed
Publication date: 2026/07/08
Xu YajingLi YitingZeng XiyingChen LijunLin HongliXie WenxinWang ZitongJiang ZhengrongDuan HonghongHuang Huibin - Cellular stress response pathways support cell survival under stress and are often leveraged by cancer cells to gain advantageous traits. How cells respond to Golgi stress is incompletely understood, limiting insights into the role of Golgi stress in cancer. Here, we combined small-molecule stress models and proteomic analyses to elucidate stress-induced changes at the Golgi. Our data establish the depletion of Golgi transport proteins as a common response to different Golgi stressors, including ionophores and oxysterol-binding protein (OSBP) inhibitors. Ionophores further induce de novo expression of the stress response protein FAM129A (also known as NIBAN1), which localizes to the remodeled secretory pathway. In a group of melanoma cells, displaying a dedifferentiated epithelial-to-mesenchymal-transition (EMT)-like phenotype, FAM129A is constitutively expressed. In these cells, stress-induced localization of FAM129A to the secretory pathway is achieved by relocalization from the plasma membrane. Collectively, our data highlight the Golgi-endosome interface as a critical hub of the cellular response to Golgi stress and reveal cancer cell-specific effects of this response. - Source: PubMed
Publication date: 2026/05/11
Simon GinaAbraham Pol SavinaDendusic MelisaSchulze NinaStupia SimoneKoci MichelleBuzuk LanaThier BeatriceSteinbach PhilineTrinh HaiSchillinger JasminNinck SabrinaKaschani FarnuschKaiser MarkusEhrmann MichaelPaschen AnnetteHellerschmied Doris - Recent evidence increasingly supports a potential role of Perivascular Macrophages (PVMs), a unique subpopulation of brain immune cells, in the pathogenesis of Alzheimer's disease (AD). Strategically positioned at the brain-vasculature interface, PVMs sense the redox status, modulate immunity, and potentially influence ferroptosis-an iron-dependent form of regulated cell death increasingly implicated in AD. However, whether the involvement of PVMs in AD pathology specifically entails mechanisms related to the crosstalk between immunometabolism and ferroptosis, and the precise molecular pathways linking PVMs, immunometabolism, and ferroptosis to AD, remains unclear. - Source: PubMed
Publication date: 2025/09/18
Miao XiaoleiYue WeiWang JinxuChen JiahuiQiu LeiPaerhati HalisaZhou QinLi PengyiWu AnshiZhang Minhao - The development of bladder cancer (BLCA) is associated with mitochondrial dysfunction and neutrophil extracellular traps (NETs); however, the relationship between mitochondrial function and NET formation in BLCA remains poorly understood. In this study, BLCA datasets, along with mitochondria- and NET-related genes, were retrieved from public databases and existing literature. Differential expression analysis, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction (PPI) networks were applied to identify prognostic genes. A prognostic model incorporating six key genes (CCDC80, NIBAN1, CSPG4, PDGFRA, MAP1A, and PCOLCE2) was established through machine learning methods and univariate Cox regression analysis. This model demonstrated strong prognostic accuracy for BLCA, further validated by a nomogram exhibiting excellent predictive performance. Using the established prognostic model, patient samples were stratified into high-risk (HRG) and low-risk groups (LRG). Significant differences in immune cell infiltration-including eosinophils and 24 other immune cell types-were observed between these groups. The risk scores strongly correlated with multiple immune cells, notably natural killer cells. Furthermore, immune checkpoint analysis revealed significant upregulation of only three checkpoint genes (TNFRSF14, TNFRSF25, and VEGFA) in the LRG. Additionally, fibroblasts were identified as key cells through analysis of the GSE222315 dataset, with prognostic gene expression varying significantly during fibroblast differentiation. Experimental validation via reverse transcription-quantitative polymerase chain reaction (RT-qPCR) confirmed that all six prognostic genes were significantly downregulated in BLCA clinical samples collected for this study. Overall, the study highlights six novel prognostic biomarkers and presents a robust predictive model, providing new insights into BLCA prognosis. - Source: PubMed
Publication date: 2025/07/04
Huang WenlinXu YongLiu JinGeCheng TianleTang Cheng - Acute myeloid leukemia (AML) is an aggressive blood cancer characterized by poor survival outcomes. Further, due to the extreme molecular heterogeneity of the disease, drug treatment response varies from patient to patient. The variability of drug response can cause unnecessary treatment in more than half of the patients with no or partial therapy responses leading to severe side effects, monetary as well as time loss. Understanding the genetic risk factors underlying the drug response in AML can help with improved prediction of treatment responses and identification of biomarkers in addition to mechanistic insights to monitor treatment response. Here, we report the results of the first Exome-Wide Association Study (EWAS) of ex-vivo drug response performed to date with 175 AML cases and 47 drugs. We used information from 55,423 germline exonic SNPs to perform the analysis. We identified exome-wide significant (p < 9.02 × 10) associations for rs113985677 in CCIN with tamoxifen response, rs115400838 in TRMT5 with idelalisib response, rs11878277 in HDGFL2 with entinostat, and rs2229092 in LTA associated with vorinostat response. Further, using multivariate genome-wide association analysis, we identified the association of rs11556165 in ATRAID, and rs11236938 in TSKU with the combined response of all 47 drugs and 29 nonchemotherapy drugs at the genome-wide significance level (p < 5 × 10). Additionally, a significant association of rs35704242 in NIBAN1 was associated with the combined response for nonchemotherapy medicines (p = 2.51 × 10), and BI.2536, gefitinib, and belinostat were identified as the central traits. Our study represents the first EWAS to date on ex-vivo drug response in AML and reports 7 new associated loci that help to understand the anticancer drug response in AML patients. - Source: PubMed
Publication date: 2025/04/04
Giri Anil KLin JakeKyriakidis KonstantinosTripathi GarimaAlmusa Henrikki