Ask about this productRelated genes to: FLOT1 antibody
- Gene:
- FLOT1 NIH gene
- Name:
- flotillin 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6p21.33
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-30
- Date modifiied:
- 2016-10-05
Related products to: FLOT1 antibody
Related articles to: FLOT1 antibody
- L. Zhang, Y. Mao, Q. Mao, W. Fan, L. Xu, Y. Chen, L. Xu and J. Wang, "FLOT1 promotes tumor development, induces epithelial-mesenchymal transition, and modulates the cell cycle by regulating the Erk/Akt signaling pathway in lung adenocarcinoma," Thoracic Cancer 10, no. 4 (2019): 909-917, https://doi.org/10.1111/1759-7714.13027. The above article, published online on 05 March 2019 in Wiley Online Library (wileyonlinelibrary.com), and its correction, (https://doi.org/10.1111/1759-7714.14990), has been retracted by agreement between the journal Editor-in-Chief, Tateaki Naito; and John Wiley & Sons Australia, Ltd. The retraction has been agreed upon following concerns raised by a third party. An investigation identified duplication between the OEFLOT1_NC flow cytometry plot presented in Figure 2f of this article and a plot published previously by a different author group. The authors were contacted for comment and supporting data, but did not respond. In light of these findings, the editors consider the results and conclusions to be unreliable. The authors did not respond to our notice of retraction. - Source: PubMed
- Extracellular vesicles (EVs) play a vital role in ovarian carcinoma (OvCa) metastasis, yet the mechanisms regulating EV biogenesis remain unclear. Here, we identify CBX2 as a key driver of omental metastasis, with elevated expression in metastatic lesions and association with poor prognosis. CBX2 promotes tumor cell migration, invasion, and metastasis by enhancing EV secretion and pro-metastatic cargo loading through remodeling lipid rafts, cholesterol-rich membrane microdomains essential for EV formation. Deletion of the intrinsically disordered region abolishes lipid raft remodeling and multivesicular body redistribution, indicating dependence on liquid-liquid phase separation (LLPS). CBX2 also transcriptionally upregulates FLOT1 in an LLPS-dependent manner. Disruption of lipid rafts or inhibition of CBX2 phase separation markedly reduces EV production and metastatic potential. These findings reveal an LLPS-dependent mechanism linking CBX2 to lipid raft-mediated EV biogenesis and OvCa metastasis. - Source: PubMed
Publication date: 2026/05/04
Wu QiuleiXu XiaohanLiu XiaoliLi WenhanLi GuoqingGong LanqingHuang LinLiu PanYing FeiquanLiu TongLi YuanyuanZhang WentingWu XinyiGao YisuSun SiWang ZehuaCai JingGuo JianfengLiu LinYang Ping - Neuropsychiatric disorders exhibit complex polygenic architectures, yet the cell-type-specific mechanisms underlying most risk loci remain unclear. Here, we integrate single-cell expression quantitative trait locus (sc-eQTL) data from brain and blood tissues with genome-wide association studies (GWAS) of six neuropsychiatric disorders (schizophrenia (SCZ), Parkinson's disease (PD), bipolar disorder (BP), major depressive disorder (MDD), attention-deficit/hyperactivity disorder (ADHD), and autism spectrum disorder (ASD)) to systematically identify putative causal genes at cellular resolution. Employing summary-data-based Mendelian randomization (SMR) across diverse neuronal and immune cell types, we discovered 345 cell-type-specific risk genes for various diseases, including both replicated candidates (such as MAPT in astrocytes for SCZ and PD and FLOT1 in excitatory neurons and inhibitory neurons for SCZ, BP and MDD) and novel associations (such as APTX in microglia for SCZ). Cross-disorder analyses revealed shared pathways in synaptic function and immune regulation. In contrast, disease-specific and tissue-specific patterns were observed across different disorders. Strikingly, we found that brain-derived risk genes exhibited significantly higher cell-type specificity than those identified in blood, underscoring the more focused cellular context of genetic effects in the central nervous system. Our findings suggest that neuropsychiatric disorders arise from a combination of neuronal dysfunction and immune system dysregulation. The study demonstrates how cell-type-specific mapping uncovers etiological mechanisms obscured in bulk-tissue analyses, proving novel information for clarifying the biological mechanism of gene expression implicated in the development of the six neuropsychiatric disorders. - Source: PubMed
Publication date: 2026/04/22
Wang XinyueLuo LingxueChang SuhuaYang Li - The SPFH-domain containing proteins are widely conserved membrane-associated factors proposed to organise membrane microdomains and thereby regulate key cellular processes. In Pseudomonas aeruginosa PA14, we identified nine such proteins (HflK, HflC and PaFlo3-PaFlo9) that display remarkable sequence divergence, genomic variability and limited phylogenetic conservation. Functional analyses of single and multiple SPFH mutants showed that these proteins are not essential for growth, biofilm formation, swimming and swarming motility, oxidative stress resistance or virulence in the Galleria mellonella infection model, although distinct slight phenotypic effects were observed in specific genetic backgrounds. Phylogenetic comparisons showed that none of the PaFlo proteins cluster with canonical bacterial flotillins such as FloA or FloT from Bacillus subtilis or FloA from Staphylococcus aureus, ruling out specific orthology. Moreover, most PaFlo proteins appear to not have clear orthologs in other γ-Proteobacteria, indicating that they may be narrowly distributed in these bacterial genomes. The absence of conserved genomic context and operon organization further supports functional diversification rather than redundancy. These findings indicate that SPFH proteins are largely dispensable for P. aeruginosa viability and virulence under laboratory conditions and likely fulfil context-dependent or niche-specific roles. - Source: PubMed
García-Maldonado Víctor ManuelRodríguez-Rangel ClaudiaGeorgellis DimitrisAlvarez Adrián F - - Source: PubMed
Publication date: 2026/03/30