Ask about this productRelated genes to: FAM20A antibody
- Gene:
- FAM20A NIH gene
- Name:
- FAM20A golgi associated secretory pathway pseudokinase
- Previous symbol:
- -
- Synonyms:
- DKFZp434F2322
- Chromosome:
- 17q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-03
- Date modifiied:
- 2019-01-25
Related products to: FAM20A antibody
Related articles to: FAM20A antibody
- Vaso-occlusive episodes (VOEs) or acute pain events, involving complex interactions between sickle erythrocytes and other blood cells, are a hallmark of sickle cell disease (SCD). In this study, we analyzed changes in peripheral blood transcriptomes between steady state and VOEs in individuals with SCD. We followed a cohort of 174 individuals with SCD with or without chronic pain and collected peripheral blood at clinic visits (steady state) and during hospitalizations (VOEs). We performed RNA-Seq profiling of CD45+ leukocytes and CD71+ erythroid cells. Pathways linked to complement activation, coagulation, and IL-6/JAK/STAT3 signaling were enriched during VOEs in the CD45+ cells. Contrastingly, the CD71+ cells showed an enrichment of pathways related to the cell cycle, such as mTORC1 signaling and the G2M checkpoint during VOEs. We then analyzed the expression changes of genes in patients with longitudinal data to determine potential biomarkers for VOEs. Expression of 4 genes - FAM20A, IL1B, MS4A4A, and SERPINB2 - was elevated during VOEs compared with steady state in the majority of patients. Furthermore, our results indicate that patients experiencing chronic pain exhibited 44% increased enrichment of significant pathways during VOEs when compared with patients without chronic pain. - Source: PubMed
Publication date: 2026/03/09
Bhat VarshaYoo Justin JPonna SrijaPotdar Alka APatel Ashwin PYu G KarenGibson GregSheehan Vivien A - - Source: PubMed
Publication date: 2026/01/19
Koç Neriman Sıla - Enamel Renal Syndrome (ERS) is a rare disorder characterized by a combination of dental and renal abnormalities, including stones and hypophosphatemia. ERS is genetically heterogeneous. - Source: PubMed
Publication date: 2026/02/05
Eid Marie-Thérèsede Mul AurélieMuresan-Vintila LaureDerain Dubourg LaurenceBertholet-Thomas AuréliaMolin ArnaudThivichon-Prince BéatriceBacchetta Justine - It has been demonstrated that infants and young children exhibit immune tolerance as a consequence of immature immune systems, which are characterized by a natural Th2 bias. RSV infection has been reported to result in acute lower respiratory infection (ALRI), while formalin-inactivated vaccination has been observed to exacerbate Th2 responses, consequently leading to enhanced respiratory disease (ERD). Transcriptomic data from three independent cohorts of RSV-infected infants were analyzed (GSE246622 served as the discovery and train set; GSE105450 and GSE188427 were used as validation sets). Immune infiltration analysis revealed immunological characteristics, which were then used to perform unsupervised clustering using feature-related genes. WGCNA was used to identify co-expressed gene modules, while Mfuzz and TCseq were employed to analyze temporal expression patterns. Machine learning models were developed using a refined panel of candidate genes. Severe symptoms of RSV infection exhibited a strong correlation with age, with younger infants demonstrating more intense inflammatory responses from neutrophils, macrophages, mast cells and dendritic cells. A predictive model was constructed using ten co-expressed genes: The following genes were identified: MCEMP1, FCGR1B, ANXA3, FAM20A, CYSTM1, GYG1, ARG1, SLPI, BMX and SMPDL3A. It was observed that infants of a younger demographic demonstrated a heightened degree of immunosuppression and pronounced innate immune activation in patients of severe symptoms with RSV infection. However, eosinophils exhibited minimal involvement in these processes. These gene models pertaining to the neutrophil, macrophage or mast cell was found to be a relatively effective predictor in patients of severe symptoms. - Source: PubMed
Publication date: 2025/12/29
Ren KaiSun HonggangRen TianMa KailunChen Jizheng - Unnecessary antibiotic use is a major driver of antimicrobial resistance, an urgent public health threat. Acute respiratory infection (ARI) is a leading cause of inappropriate antibiotic use, creating an unmet need for improved diagnostics to identify bacterial etiology in ARI. In this work we show a 4-gene signature defining the absence of bacterial ARI which may be useful for managing antibiotics in ARI. Hospitalized adults with ARI underwent comprehensive microbiologic testing and those with definitive viral (n = 280), bacterial (n = 129), or mixed viral-bacterial infection (n = 95) had whole blood RNA sequencing. A hard-thresholded, mostly relaxed, LASSO-constrained logistic regression model is used to select a parsimonious gene set (ITGB4, ITGA7, IFI27, FAM20A) highly capable of discriminating any bacterial from nonbacterial infection (cross-validated AUC = 0.90). The 4-gene signature is validated in five independent adult RNAseq cohorts (AUC = 0.89-0.98), two adult microarray cohorts (AUC = 0.73-0.90), and one pediatric pneumonia RNAseq cohort (AUC 0.74). Thresholding the 4-gene risk score to yield 90% sensitivity to detect bacterial infection results in 71% specificity and 91% negative predictive value. - Source: PubMed
Publication date: 2025/11/24
Falsey Ann RPeterson Derick RWalsh Edward EBhattacharya SoumyaroopBaran Andrea MChu ChinyiBranche Angela RCroft Daniel PPeasley MichaelCorbett Anthony MAshton JohnMariani Thomas J