Ask about this productRelated genes to: FAM98A antibody
- Gene:
- FAM98A NIH gene
- Name:
- family with sequence similarity 98 member A
- Previous symbol:
- -
- Synonyms:
- DKFZP564F0522
- Chromosome:
- 2p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 2005-11-03
- Date modifiied:
- 2018-02-28
Related products to: FAM98A antibody
Related articles to: FAM98A antibody
- Profiling molecular panorama from massive omics data identifies regulatory networks in cells but requires mechanistic interpretation and experimental follow up. Here we combine deep learning and large language model reasoning to develop a hybrid workflow for omics interpretation, called LyMOI. LyMOI incorporates GPT-3.5 for biological knowledge reasoning and a large graph model with graph convolutional networks (GCNs). The large graph model integrates evolutionarily conserved protein interactions and uses hierarchical fine-tuning to predict context-specific molecular regulators from multi-omics data. GPT-3.5 then generates machine chain-of-thought (CoT) to mechanistically interpret their roles in biological systems. Focusing on autophagy, LyMOI mechanistically interprets 1.3 TB transcriptomic, proteomic and phosphoproteomic data and expands the knowledge of autophagy regulators. We also show that LyMOI highlights two human oncoproteins, CTSL and FAM98A, for enhancing autophagy upon treatment with disulfiram (DSF), an antitumour agent. Silencing these genes in vitro attenuates DSF-mediated autophagy and suppresses cancer cell proliferation. Strikingly, DSF treatment with Z-FY-CHO, a CTSL-specific inhibitor previously used for preventing SARS-CoV-2 infection, potently inhibits tumour growth in vivo. - Source: PubMed
Publication date: 2026/01/08
Tang DachaoZhang ChiZhang WeizhiLu FunianXiao LemingHuang XinheShao JiangyiLiu DanFu ShanshanZhao MiaoyingZhang LuoyingJia DaShen Han-MingSun ChaoyangChen GangLiu BinPeng DiXue Yu - Ewing sarcoma (ES) is a highly aggressive pediatric bone cancer with limited treatment options for metastatic or recurrent cases. This study investigated the antitumor effects of kaempferol, a natural flavonoid, on ES and its underlying molecular mechanisms. In vitro experiments demonstrated that kaempferol significantly inhibited the proliferation, migration, and invasion of SK-ES-1 cells in a dose- and time-dependent manner. Mechanistically, kaempferol upregulated miR-26b-5p, which directly targeted and suppressed FAM98A, a pro-oncogenic protein. This regulation led to the inhibition of the EGFR/PI3K/AKT/NF-κB signaling pathway, reducing tumor growth and metastasis. In vivo studies further confirmed that kaempferol suppressed ES tumor growth in a xenograft mouse model, while miR-26b-5p knockdown partially reversed this effect. Our findings suggest that kaempferol exerts its antitumor activity in ES by modulating the miR-26b-5p/FAM98A axis and downstream signaling pathways, highlighting its potential as a novel therapeutic agent for ES treatment. - Source: PubMed
Publication date: 2025/10/16
Ji YiquanGao TianXu ZehuaChen BaoLi Kai - Genome-wide CRISPR screening has emerged as a powerful tool for identifying novel host factors involved in viral infections. In recent years, host factors for several Alpha- and Beta-coronaviruses have been systematically screened and characterized. However, knowledge regarding Gamma- and Delta-coronavirus infections remains limited. In this study, we conducted genome-scale CRISPR knockout (KO) screening in Huh7 cells infected with infectious bronchitis virus (IBV), a Gamma-coronavirus, and porcine deltacoronavirus (PDCoV), a Delta-coronavirus. We identified known host factors for PDCoV, including APN and TMEM41B. We confirmed that human APN does not serve as a critical host factor for IBV. Notably, SPPL3 was identified as a key factor involved in viral particle entry and S protein-induced syncytium formation through the modulation of cellular N-glycosylation. Furthermore, we performed a meta-analysis integrating all Huh7 cell-based genome-wide CRISPR screens across the four genera of coronaviruses (Alpha-, Beta-, Gamma-, and Delta-coronaviruses). Our analysis highlighted conserved host pathways, particularly those related to proteoglycans, glycoproteins, and vesicle trafficking. TMEM41B, SCAP, and FAM98A emerged as the most frequently targeted host genes. These findings provide valuable insights into the life cycles of IBV and PDCoV infections and facilitate the development of host-directed therapeutic strategies. - Source: PubMed
Publication date: 2025/02/05
Li HaoSong CailiangLi YuqingZhang TiejunYang XinWang Hongning - Medulloblastoma (MB) is the most common malignant brain tumor in children, typically arising during infancy and childhood. Despite multimodal therapies achieving a response rate of 70% in children older than 3 years, treatment remains challenging. Ferroptosis, a form of regulated cell death, can be induced in medulloblastoma cells in vitro using erastin or RSL3. Using two independent medulloblastoma RNA-sequencing cohorts (MB-PBTA and MTAB-10767), we investigated the expression of ferroptosis-related molecules through multiple approaches, including Weighted Gene Co-Expression Network Analysis (WGCNA), molecular subtype stratification, protein-protein interaction (PPI) networks, and univariable and multivariable overall survival analyses. A prognostic expression score was computed based on a cross-validated ferroptosis signature. In training and validation cohorts, the regulation of the ferroptosis transcriptional program distinguished the four molecular subtypes of medulloblastoma. WGCNA identified nine gene modules in the MB tumor transcriptome; five correlated with molecular subtypes, implicating pathways related to oxidative stress, hypoxia, and trans-synaptic signaling. One module, associated with disease recurrence, included epigenetic regulators and nucleosome organizers. Univariable survival analyses identified a 45-gene ferroptosis prognostic signature associated with nutrient sensing, cysteine and methionine metabolism, and trans-sulfuration within a one-carbon metabolism. The top ten unfavorable ferroptosis genes included , , , , , , , , , and . Patients with a high ferroptosis score showed a worse prognosis, particularly in the G3 and SHH subtypes. The PPI network highlighted IL6 and CBS as unfavorable hub genes. In a multivariable overall survival model, which included gender, age, and the molecular subtype classification, the ferroptosis expression score was validated as an independent adverse prognostic marker (hazard ratio: 5.8; -value = 1.04 × 10). This study demonstrates that the regulation of the ferroptosis transcriptional program is linked to medulloblastoma molecular subtypes and patient prognosis. A cross-validated ferroptosis signature was identified in two independent RNA-sequencing cohorts, and the ferroptosis score was confirmed as an independent and adverse prognostic factor in medulloblastoma. - Source: PubMed
Publication date: 2025/01/15
Desterke ChristopheFu YuanjiBonifacio-Mundaca JennyMonge ClaudiaPineau PascalMata-Garrido JorgeFrancés Raquel - There are three FAM98 family proteins (FAM98A/B/C) in humans and mice. Their physiological functions remain largely unknown. We have previously reported that Fam98a interacts with Plekhm1 in murine osteoclasts and functions in lysosome trafficking/secretion and bone resorption in osteoclasts in vitro. In this study, we found that all three genes were expressed in precursor and mature osteoclasts. While the knockdown of Fam98c by a specific short-hairpin RNA (shRNA) in osteoclast precursors attenuated osteoclastogenesis, depletion of Fam98b by an shRNA specifically disrupted osteoclast lysosome trafficking and bone resorption with phenotypes similar to Fam98a shRNA-knockdown in our previous study. Loss of Fam98a in myeloid osteoclast precursors was dispensable for trabecular and cortical bone mass in mice, as well as osteoclastogenesis/bone resorption in vitro, possibly due to compensation by increased Fam98b expression in Fam98a-null osteoclasts. These findings indicate that the three Fam98 proteins play distinct roles in osteoclastogenesis and osteoclast function and need further investigation in future studies. - Source: PubMed
Publication date: 2025/01/09
Wang LeiMinocha TarunDas Bhaba KKunika Mikaela DKannan AarthiGao LingMohan SubburamanXing WeirongVarughese Kottayil IZhao Haibo