Ask about this productRelated genes to: FNBP1L antibody
- Gene:
- FNBP1L NIH gene
- Name:
- formin binding protein 1 like
- Previous symbol:
- C1orf39
- Synonyms:
- TOCA1, FLJ20275
- Chromosome:
- 1p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-05-08
- Date modifiied:
- 2016-01-21
Related products to: FNBP1L antibody
Related articles to: FNBP1L antibody
- LPS-induced peritonitis is a prevalent clinical condition with incompletely understood underlying mechanisms. This study aimed to characterize the gene transcriptome and key proteins in the blood of mice with LPS-induced peritonitis. We established a mouse peritonitis model by administering LPS (10 mg/kg, i.p.) and collected blood samples (n = 6 per group) for bulk RNA sequencing. Through various bioinformatics approaches, we identified 290 differentially expressed genes (242 upregulated and 48 downregulated). Functional enrichment revealed the activation of inflammation-related pathways (e.g., NOD-like and Toll-like receptor signaling) and the suppression of adaptive immunity pathways (e.g., Th1/Th2 cell differentiation and T cell receptor signaling). From these, eight hub proteins (LDLR, FNBP1L, SNX18, FAM20C, INPP5F, PACSIN1, ZAP70, and SYNJ2) were identified, and their structural stability was confirmed via 300 ns molecular dynamics simulations. Critically, to validate our findings at the cellular level and in a clinical context, we further integrated four independent public single-cell RNA-sequencing datasets from human sepsis patients. This cross-platform analysis confirmed that the expression patterns of our hub genes are conserved in human patients with high cell-type specificity (e.g., ZAP70 downregulation in T cells and LDLR upregulation in monocytes). Moreover, a module score derived from these genes demonstrated strong clinical relevance, as it significantly distinguished sepsis patients from healthy controls and stratified clinical subtypes of sepsis. In conclusion, by integrating bulk transcriptomics, molecular dynamics, and cross-platform single-cell data, this research provides multi-scale insights into the systemic inflammatory mechanisms of peritonitis. It identifies therapeutic targets with clinical translational potential. - Source: PubMed
Publication date: 2025/10/30
Li HuijuanZhang JianfengSun Yulong - The damage of ferroptosis is related to the pathogenesis of intervertebral disc degeneration (IDD). N6-methyladenosine (m6A) modification accounts for more than 80% of RNA modifications in eukaryotic cells. However, the key role of m6A related ferroptosis-related genes (FRGs) in IDD remain explorable. Firstly, batch correction between datasets was performed. Weighted gene co-expression network analysis (WGCNA) was then conducted to acquire the most relevant module genes. Differentially expressed genes (DEGs) between the IDD and Normal Group were obtained by differential analysis subsequently. Next, according to the Pearson correlation and the intersection of m6A and FRGs related genes, m6A-FRGs related genes were selected. Additionally, we intersected module genes, DEGs and m6A-FRGs related genes to obtain DEGs of m6A-FRGs related module genes (m6A-FRGs-DEGs). Least absolute shrinkage and selection operator (LASSO) was applied to get HUBgenes. After, we conducted gene set enrichment analysis (GSEA) to gain function items and related pathways of HUBgenes. Single sample gene set enrichment analysis (ssGSEA) and wilcox.test were proceeded to analyse differences in relative abundance of immune cells between the IDD and Normal Groups, and a nomogram was constructed based on significantly different HUBgenes. The Comparative Toxicogenomics Database (CTDbase) was then applied to predict potential drugs or molecular compounds that could modulate HUBgenes. Last but not least, we performed the quantitative real-time fluorescence PCR (qRT-PCR) to verify HUBgenes. 181 m6A-FRGs-DEGs were acquired by the intersection of key module genes (from MEtan, MEsalmon, MEbrown and MEgreen), 362 DEGs and 15,678 m6A-FRGs related genes. Subsequent analysis showed that HUBgenes (ZNF595, PLXDC1, FNBP1L, KLRB1, NRCAM, PPCDC, C9orf139, SIGLEC17P, RRAS2 and DPRXP4) significantly participated in positive regulation of cytokine production, mitochondrial inner membrane and organellar ribosome. Besides, the relative abundance of neutrophils was found significantly different between IDD and normal groups. A nomogram was constructed based on ZNF595 and RRAS2, and there were 11 drugs targeted on ZNF595, while 118 drugs predicted based on RRAS2 such as Tetrachlorodibenzodioxin, Bisphenol A and Benzo(a)pyrene. Lastly, ZNF595 and RRAS2 were both obviously up-regulated in IDD according to the qRT-PCR. Our research suggested 10 HUBgenes were significantly associated with IDD, providing more evidence about the vital role of HUBgenes in IDD. - Source: PubMed
Publication date: 2025/09/29
Che ZhenChen RuibingLi MingLiao ZhuangyaoWang KunYao DengboLiang YuweiLi YuxiWen GuomingXing TongSu KaihuiLiang ChangchunHuang LinZhao Qun - HIV-1 infects several types of CD4+ cells. Among these, dendritic cells (DCs) are considered one of the first to encounter the virus upon sexual transmission. Expression of several restriction factors, of which SAMHD1 is well known, limits productive infection. Still, DCs are essential players in shaping adaptive immune responses that contribute heavily to the pathogenesis of HIV. Here, we set out to identify other factors that potentially contribute to the resistance of dendritic cells to HIV infection. Since endocytosis and the cytoskeleton impact HIV infection, we have put special emphasis on proteins implied in these pathways. In a selective, shRNA-mediated knockdown screen in primary monocyte-derived dendritic cells (MDDCs) infected with HIV in the presence of SAMHD1-disactivating Vpx containing virus-like particles, three proteins hampering HIV-1 infection were identified: FNBP1L, ARHGAP24, and ATP6V1B1. Findings of our research indicate that upon blocking of factors involved in endocytosis, increased viral entry is observed providing supportive evidence for endocytosis mostly being a dead-end entry pathway for HIV infection of MDDCs. Additional experiments show that changes in the cytoskeleton and endosomal pH that lead to impaired fluid-phase endocytosis and phagocytosis are responsible for these shifts in the phenotype observed.IMPORTANCEUnderstanding how HIV-1 interacts with dendritic cells (DCs) is pivotal in deciphering early viral transmission and immune evasion but is subject to a long-standing controversy in HIV virology. Therefore, the identification of endocytosis-related host factors as barriers to productive infection in DCs emphasizes the role of endocytosis as a restrictive pathway for viral entry. By disrupting these processes, we highlight a shift in the cellular environment that could influence viral entry and transmission. These findings challenge existing models of HIV-1 entry into DCs. New insights into how cellular pathways limit viral spread have implications for the development of strategies aimed to curb viral dissemination and reservoir formation. Whether the knockdown of the proteins described simply augments the efficiency of infection via existing pathways or opens additional routes for HIV-1 entry remains to be investigated. - Source: PubMed
Publication date: 2025/03/03
Janevska MarijaWitkowski WojciechVermeire JolienBorowicz MarekNaessens EvelienVanderstraeten HanneNauwynck HansFavoreel HermanVerhasselt Bruno - Autoimmune polyglandular syndrome 1 (APS1) is an autosomal recessive disorder due to biallelic pathogenic variants in the autoimmune regulator () gene that manifests with chronic mucocutaneous candidiasis, primary hypoparathyroidism, and adrenal insufficiency. We report a 39-year-old woman with APS1 who developed partial lipodystrophy during adulthood. She presented with diaper rashes, oral thrush, and tetany during infancy due to candidiasis and hypoparathyroidism. During childhood, she developed hypothyroidism, primary adrenal insufficiency, and ovarian insufficiency. At age 14, she received a sibling-matched allogenic bone marrow transplant due to multiple antibiotic-refractory fungal infections. At age 35, her serum triglycerides were 914 mg/dL (10.32 mmol/L) and she had loss of subcutaneous fat from the upper and lower extremities and hips. A whole-body dual-energy x-ray absorptiometry revealed lower-extremity fat at less than the first percentile. Whole-exome sequencing on DNA extracted from saliva revealed pathogenic variants, p.Leu28Pro and p.Arg257* in but none in the known lipodystrophy genes. Phage-immunoprecipitation-sequencing revealed the presence of autoantibodies to MAGEB1, MAGEB4, and RFX6, which have been previously reported in APS1. Our case suggests that patients with APS1 may develop partial lipodystrophy due to autoantibodies against novel adipocyte-expressed proteins. A causal relationship of high levels of autoantibodies in our patient to adipose tissue-expressed ODC1, NUCKS1, or FNBP1L and lipodystrophy remains uncertain. - Source: PubMed
Publication date: 2024/09/24
Agarwal ShubhamBodansky AaronXing ChaoAnderson Mark SGarg Abhimanyu - Pre-eclampsia is a pregnancy-related disorder characterized by hypertension and proteinuria, severely affecting the health and quality of life of patients. However, the molecular mechanism of macrophages in pre-eclampsia is not well understood. - Source: PubMed
Publication date: 2024/05/23
Cao JinfengJiang WenxinYin ZheLi NaTong ChaoQi Hongbo