Ask about this productRelated genes to: FCHO1 Blocking Peptide
- Gene:
- FCHO1 NIH gene
- Name:
- FCH domain only 1
- Previous symbol:
- -
- Synonyms:
- KIAA0290
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-08
- Date modifiied:
- 2019-02-20
Related products to: FCHO1 Blocking Peptide
Related articles to: FCHO1 Blocking Peptide
- Endocrine-disrupting chemicals (EDCs) are linked to coronary heart disease (CHD), but underlying mechanisms remain unclear. We aimed to identify EDC-related genes and evaluate their causal roles in CHD. - Source: PubMed
Publication date: 2026/08/05
Yao TaoLin Yun-LuFang Luo-XiangWang Yu-TianZhou Lan-FengZhang NingChen Gang - We applied transcriptome tomography to create a whole-brain model of early-stage Huntington's disease (HD) in R6/2 mice, which ubiquitously express truncated human mutant HTT containing approximately 150 CAG repeats. Medium spiny neuron (MSN)-related genes showed abnormal expression in the HD brain, in terms of expression similarity to wild-type Htt. Bdnf was the most probable upstream regulator of these genes. Smarca4, the Bdnf-regulator, was similarly expressed to wild-type Htt in the control brain; however, this was not observed in HD, implying a possible involvement of Smarca4 in glutamate excitotoxicity in HD. Lhx6, a master gene for MSN-related pathway development ordinarily conserved postnatally and in adulthood, was lost in the HD co-expression network. And a network hub node, Fcho1, was lost in connection involving Lhx6 and mitochondrial gene clusters. Loss of Smarca4, Lhx6, and Fcho1 in co-expression may contribute to spatiotemporally specific neuronal loss in HD. - Source: PubMed
Publication date: 2026/06/30
Okamura-Oho YukoShimokawa KazuroOota SatoshiYoshiki AtsushiMorita MasahikoNishimura MasaomiNakamura SakikoTsujimura YukiIshikawa ShumpeiYokota Hideo - Synaptic vesicle (SV) recycling is critical for sustaining neurotransmission. Although FCHO1, a protein containing both an F-BAR domain and a μ-homology (μ-HD) domain, is recognized as a nucleator of clathrin-mediated endocytosis in non-neuronal systems, its physiological role at synapses remains unclear. Here, we investigated the function of FCHO1 in SV endocytosis at central synapses using a combination of shRNA-mediated knockdown and pHluorin-based live imaging. Within defined stimulation paradigms (25-300 action potentials at 10 Hz), depletion of FCHO1 markedly slowed endocytic kinetics across all stimulation intensities and was fully rescued by re-expression of an shRNA-resistant construct. Domain-specific functional analyses revealed stimulation-strength-dependent functional requirements. The F-BAR domain was sufficient to support vesicle retrieval under low stimulation conditions, whereas the μ-homology domain (μ-HD) became essential as stimulation strength increased. These findings support a model in which FCHO1 operates as a demand-sensitive scaffold within the endocytic pathway, with distinct structural domains differentially required as neural activity and consequently endocytic load escalates. Our results establish FCHO1 as a critical regulator of SV endocytosis and suggest that multidomain endocytic proteins may scale their functional contributions according to the magnitude of neuronal activation. - Source: PubMed
Publication date: 2026/04/06
Lee Hyun JungLee WongyoungKim Sung Hyun - - Source: PubMed
Publication date: 2026/02/22
Esenboga SalihaDormus TamerYaz İsmailOkur Fatma VisalCagdas DenizKuşkonmaz Barış - The delivery of nucleic acids into host cells has emerged as an innovative and promising therapeutic approach for various diseases. Despite significant advances in nanoparticle delivery systems, persistent cellular barriers limit the clinical application of most existing technologies. In this study, we developed a programmable device that applies precise uniaxial cyclic stretching to cells cultured on custom polydimethylsiloxane chambers to investigate whether mechanical stimulation can enhance the transfection efficiency (TE) of gold-standard non-viral gene delivery vectors. Applying cyclic mechanical stimulation ( = 0.1 Hz, ε = 10% strain, = 30 min) to HeLa cells and human myoblasts (hMyo) significantly increased nuclear translocation of the mechanosensitive transcription factor Yes-Associated Protein (YAP). Gene expression analysis revealed that this mechanical conditioning orchestrated a coordinated modulation of endocytic machinery, upregulating clathrin-mediated endocytosis (FCHO1) and macropinocytosis (STX1B) pathways while downregulating endocytic inhibitors (DLC1, EHD2). These mechanically induced cellular adaptations resulted in significantly enhanced TE of both plasmid DNA (pDNA)- and mRNA (mRNA)-carrying gold-standard branched polyethylenimine (PEI)-based complexes in both HeLa cells and hMyo, compared to static conditions. Our findings demonstrate that mechanical stimulation is an effective complementary strategy for improving non-viral gene delivery by leveraging endogenous cellular mechanotransduction pathways. Rather than modifying vector chemistry, this mechanobiological approach enhances the performance of existing delivery systems by transiently modulating cellular uptake capacity and nuclear accessibility. This work offers mechanistic insights into how mechanotransduction regulates cellular uptake and highlights opportunities for leveraging controlled mechanical environments in applications such as ex vivo cell engineering. - Source: PubMed
Publication date: 2026/01/08
Fruzzetti FlaminiaRuzzante BeatriceGiagnorio EleonoraBonanno SilviaLauria Pinter GiuseppeMarcuzzo StefaniaCandiani GabrieleBono Nina