Ask about this productRelated genes to: FUNDC1 antibody
- Gene:
- FUNDC1 NIH gene
- Name:
- FUN14 domain containing 1
- Previous symbol:
- -
- Synonyms:
- MGC51029
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2019-02-01
Related products to: FUNDC1 antibody
Related articles to: FUNDC1 antibody
- Circadian disruption exacerbates type 2 diabetes mellitus (T2DM). Time-restricted feeding (TRF) and exercise (EX) improve metabolic health, but their combinatory effect remains unclear. This study investigated whether combined TRF and EX additively ameliorates metabolism via circadian reprogramming in db/db mice. - Source: PubMed
Publication date: 2026/04/11
Li QingxinZhang GuodongZhou SugaoXie Yanli - Autophagy is involved in various stages of the viral life cycle and modulates viral replication. Coronaviruses have developed several strategies to exploit autophagy for their benefit. Nevertheless, the exact mechanisms through which the infectious bronchitis virus (IBV) influences autophagy remain inadequately understood. Here, we demonstrate that IBV infection of chicken embryonic kidney (CEK) cells activates the AKT-mTOR signaling pathway to suppress autophagosome formation and mitophagy. Further investigation reveals that the viral spike protein (S) inhibits cellular autophagy by interacting with the mitophagy receptor FUNDC1. However, FUNDC1-mediated mitophagy promotes degradation of the viral nucleocapsid (N) protein and restricts IBV replication. To counteract this host defense mechanism, the S protein competitively binds to the LC3-interacting region (LIR) motif of FUNDC1, thereby disrupting its interaction with LC3 and ultimately suppressing mitophagy. Molecular docking analysis revealed that a conserved asparagine residue at position 240 (N240) in the S1 subunit of the IBV S protein is essential for binding to FUNDC1. Furthermore, reverse genetics demonstrated that an IBV mutant with an N240A substitution exhibited reduced pathogenicity in the kidneys, trachea, and lungs of specific-pathogen-free (SPF) chickens compared to the wild-type virus. Collectively, these findings unveil a novel mechanism by which IBV antagonizes host mitophagy and provide new insights into the host-virus interplay within the context of autophagic regulation.IMPORTANCEIBV has evolved a mechanism to counteract the host's antiviral defense. Specifically, the viral spike (S) protein blocks a form of autophagy called mitophagy by binding to the mitochondrial receptor FUNDC1. Normally, FUNDC1 helps cells eliminate damaged mitochondria and restricts IBV replication by promoting the degradation of the viral nucleocapsid protein. By interfering with this process, the S protein enhances viral survival. We further identified a single conserved amino acid in the S protein that is critical for this function, and mutation of this residue weakened IBV in chickens. These findings reveal how IBV manipulates host defenses and suggest new strategies for controlling coronavirus infections. - Source: PubMed
Publication date: 2026/04/20
Zhao JunTian JiaxinZhang LiweiLi YingfeiTang LihuaSa QilaLi RuotongZhao JingZhao YeZhang Guozhong - Tris (1,3-dichloro-2-propyl) phosphate (TDCIPP) is a widely used organophosphate flame retardant increasingly linked to reproductive toxicity, yet its placental toxic mechanisms remain unclear. This study demonstrates that TDCIPP exposure disrupts placental homeostasis by inducing oxidative stress, which triggers excessive PINK1/Parkin-mediated mitophagy in both human trophoblasts (HTR-8/SVneo) and pregnant mice. Integrated network toxicology analysis predicted mitochondrial dysfunction and oxidative stress as central pathways, validated by upregulation of ATG5 and HMOX1, downregulation of SOD2, elevated ROS and mitochondrial superoxide, loss of mitochondrial membrane potential, and ultrastructural evidence of mitophagic vacuoles. TDCIPP activated the PINK1/Parkin pathway-evidenced by increased PINK1, Parkin, LC3-II/I, p62, reduced TOMM20, and enhanced Parkin-TOMM20 colocalization-while alternative mitophagy receptors FUNDC1 and BNIP3 remained unaffected. Mechanistically, oxidative stress acted upstream, as N-acetylcysteine (NAC) pretreatment suppressed ROS accumulation and PINK1/Parkin activation. Functionally, TDCIPP impaired trophoblast proliferation, induced apoptosis, and caused fetal growth restriction (FGR) in vivo. Notably, both genetic knockdown of Parkin in vitro and pharmacological inhibition of mitophagy with Mdivi-1 in vivo significantly alleviated trophoblast apoptosis and rescued placental and fetal weights. These findings establish that TDCIPP-induced placental injury is driven by an oxidative stress-PINK1/Parkin-mitophagy axis, revealing dysregulated mitophagy as a pivotal mechanism underlying TDCIPP-associated developmental toxicity and offering new insights into the reproductive risks of environmental flame retardant exposure. - Source: PubMed
Publication date: 2026/04/17
Lin ZimingHu MingqiLi RuijieGong XiaoruiZhao ManZhang HaiyanXuan JinQiao WenlanLi Anna - Ischemic stroke (IS) is a major global cause of disability and death, with its complex pathophysiology posing a significant challenge for effective therapy. Although flavonoids from Ziziphora clinopodioides Flavonoids (ZCF) have demonstrated neuroprotective potential, their comprehensive mechanisms of action remain incompletely understood. - Source: PubMed
Publication date: 2026/04/05
Zhuo XingjieDing ShuxianLi JinhuaDeng MingcongZhang XinyueYang WeijunGu LiliLi Qin - Atherosclerosis is a disease centered on chronic inflammation, in which mitochondrial damage plays a key role in its initiation and progression. Traditionally, atherosclerosis is thought to be triggered by cholesterol accumulation, but recent studies have revealed that mitochondrial dysfunction has emerged as an important driving factor by inducing innate immune imbalance. In atherosclerosis, mitochondria undergo changes in membrane permeability, metabolic disorders, and dynamic imbalance due to oxidative stress and other factors, releasing mitochondrial damage-associated molecular patterns (mt-DAMPs). These mt-DAMPs activate innate immune pathways, promote the production of type I interferons and the release of pro-inflammatory factors such as interleukin 1β, and accelerate plaque progression. Mitophagy exerts a protective effect by eliminating damaged mitochondria. Specifically, the PINK1-Parkin pathway labels damaged mitochondria through ubiquitination; mitophagy receptors (such as NIX, FUNDC1, and BNIP3) directly bind to LC3 to initiate ubiquitination-independent mitophagy; and mitochondrial-derived vesicles selectively encapsulate damaged components and target them to lysosomes for degradation. All these processes can reduce mt-DAMP-induced damage and inhibit excessive immune activation. In this review, we summarize that innate immune imbalance caused by mitochondrial damage is a key mechanism for atherosclerosis progression. Mitochondrial quality control clears damaged mitochondria through multiple pathways, alleviates inflammatory responses and plaque burden, and provides potential targets for atherosclerosis treatment. Its precise regulatory mechanisms and drug development are future research directions. - Source: PubMed
Publication date: 2026/03/16
Liu HaoZhao ShuaiyongGao HuiqinWang YueGao JunyanGuo PingYang YitingCui WenruiZhang ShuanglinShi YapingXie GuanxingHan YutongZhou JunyaZhang QingqiZou Yunzeng