Ask about this productRelated genes to: SNAP29 antibody
- Gene:
- SNAP29 NIH gene
- Name:
- synaptosome associated protein 29
- Previous symbol:
- -
- Synonyms:
- SNAP-29, CEDNIK
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-17
- Date modifiied:
- 2016-06-01
Related products to: SNAP29 antibody
Related articles to: SNAP29 antibody
- Emerging evidence implicates premature placental senescence as a central driver of pregnancy complications, though its underlying mechanisms remain elusive. Here, we report marked downregulation of IL33 (interleukin 33) in villi from unexplained recurrent pregnancy loss (URPL) patients, concomitant with elevated trophoblast senescence. More importantly, knockout mice exhibited placental senescence and impaired trophoblast invasion. Mechanistically, senescent trophoblasts displayed metabolic dysregulation - including enhanced glycolysis and lactate accumulation - which disrupted macroautophagic/autophagic flux and mitochondrial function. Lactate-induced lysine lactylation at residue K169 of SNAP29 (synaptosome associated protein 29) promoted its degradation, impairing macroautophagy/autophagy and trophoblast function, ultimately driving pregnancy loss. In interventional studies, senotherapies with metformin or dasatinib plus quercetin restored placental development and improved pregnancy outcomes in both IL33-deficient and inflammation-induced miscarriage models. Our findings establish the IL33-senescence-lactate axis as a critical pathway in URPL pathogenesis and support senomodulation as a therapeutic strategy.: 2-DG: 2-deoxy-D-glucose; BafA1: bafilomycin A1; CHX: cycloheximide; CTB: cytotrophoblasts; D-gal: D-galactose; EVT: extravillous trophoblasts; HDAC: histone deacetylase; H2O2: hydrogen peroxide; IL33: Interleukin 33; LPS: lipopolysaccharide; SA-GLB1/β-gal: senescence-associated galactosidase beta 1; SASP: senescence-associated secretory phenotype; SNAP29: synaptosome associated protein 29; STB: syncytiotrophoblasts; UMAP: uniform manifold approximation and projection; URPL: unexplained recurrent pregnancy loss; VP: etoposide. - Source: PubMed
Publication date: 2026/04/22
Lu Jia-JingSheng Yan-RanHu Wen-TingLiu Yu-KaiXie FengLi Ming-QingZhu Xiao-Yong - Many poxviruses are significant zoonotic pathogens threatening public health. Autophagy, a regulated process vital for cellular homeostasis, can participate in defense against virus invasion. However, the relationship between poxviruses and host cell autophagy is not fully understood. This study shows that vaccinia virus (VACV) induces autophagy but blocks autophagosome-lysosome fusion. Modified vaccinia virus Ankara (MVA), an attenuated VACV strain that cannot replicate in most mammalian cells, fails to do so. Both pharmacological inhibition of early autophagy via 3-MA treatment and genetic ablation of ATG3 and ATG7 led to a significant enhancement of MVA replication. The VACV protein A52 inhibits autolysosome formation by disrupting interactions between SNAP29, STX17, and VAMP8, which is crucial for autophagic flux. Importantly, A52 also promotes the degradation of SNAP29, thereby aiding viral replication. Furthermore, SNAP29 is a newly identified host restriction factor for MVA, as its suppression enables MVA replication in human cells. These findings elucidate how poxviruses modulate autophagy for their own replication and further explain MVA's restriction in human cells. - Source: PubMed
Publication date: 2026/04/13
Niu KangFang YongxiangDeng YiningWang ZiyueXie ShijieZhu JundaSong BaifenWu WenxueJing ZhizhongPeng Chen - The chronic accumulation of ΔFosB in striatal medium spiny neurons has been implicated as a pivotal contributor to the pathogenesis of levodopa-induced dyskinesia (LID). While recent studies have implicated autophagy in the degradation of ΔFosB and the amelioration of LID, the precise mechanisms remain elusive. We induced LID in a unilateral 6-hydroxydopamine-lesioned parkinsonism rat model via chronic levodopa treatment. To modulate the autophagy pathway, we overexpressed ATG14 in the striatum of LID rats and administered chloroquine, an autophagy inhibitor, peripherally. We assessed LID severity using abnormal involuntary movements (AIMs) scores. Western blotting, real-time quantitative polymerase chain reaction, immunofluorescence, immunohistochemistry, transmission electron microscopy, and Golgi staining were employed to measure autophagy flux, synaptic alterations, and ΔFosB levels. Chronic levodopa treatment reduced ATG14 and SNARE complex (STX17, SNAP29, and VAMP8) levels, disrupted their interaction, impaired autophagy flux, affected synaptic function, and led to ΔFosB accumulation in the striatum of PD rats. Upregulating ATG14 in the striatum of LID rats improved AIMs scores, facilitated SNARE-mediated autophagosome-lysosome fusion, restored synaptic deficits, and promoted ΔFosB degradation. However, these beneficial effects of ATG14 upregulation were negated by chloroquine administration. Our findings suggest that upregulating ATG14 enhances SNARE formation, promoting autophagy flux and thereby reducing LID occurrence by facilitating ΔFosB degradation. - Source: PubMed
Wu YiLiu KeZhang ZhaoyuanMa ZhuoranTang ZhichengChang AnOuyang HaoxuanZhai HengCao XuebingXu Yan - T-2 toxin is a persistent, bioaccumulative environmental contaminant that poses major health threats to humans and animals. Endoplasmic reticulum (ER) stress and autophagy are two interconnected stress responses critical for maintaining cellular homeostasis. Berbamine (BBM) is an important member of bis-benzy lisoquinoline alkaloid with diverse biological activities. This study aimed to identify the molecular target of BBM against T-2 toxin-induced hepatotoxicity, focusing on autophagy-ER stress crosstalk. We systematically evaluated autophagy and ER stress in human HepaRG cells using immunoblotting, transmission electron microscopy and an autophagy reporter assay. T-2 toxin was found to concurrently activate PINK1/Parkin-mediated mitophagy and suppress Keap1-mediated FAM134B ubiquitination-dependent ER-phagy, thereby triggering ER stress. Integrated evidence from molecular dynamics and western blot demonstrated that BBM upregulated and stabilized BNIP3, blocking the VAMP8-SNAP29 interaction to inhibit T-2 toxin-induced autophagy and subsequent ER stress. Moreover, in vivo mouse experiments demonstrated that 30 mg/kg BBM significantly alleviated T-2 toxin-induced liver injury by suppressing both autophagic flux and ER stress; BBM significantly reduced serum levels of liver enzymes, ALT, and AST. Collectively, our findings elucidate a novel mechanism wherein T-2 toxin-induced mitophagy inhibits ER-phagy to drive ER stress-mediated liver injury and highlight the therapeutic potential of BBM in alleviating T-2 toxin-induced liver injury. - Source: PubMed
Publication date: 2026/03/06
Xu QiangDeng LuyuXu JintaoWu ZhikaiLin RuqinDeng YiqunWen Jikai - Triple-negative breast cancer (TNBC) remains a clinical challenge due to its heterogeneity and lack of targeted therapies. This study aimed to evaluate the antitumor effects and underlying mechanisms of Z-guggulsterone (Z-GS), a natural product, in TNBC. Human TNBC cell lines (MDA-MB-231 and MDA-MB-468) were treated with Z-GS to assess proliferation, cell-cycle progression, apoptosis, and reactive oxygen species (ROS) accumulation. Autophagic flux and the OGT-SNAP29 signaling axis were investigated via Western blotting, immunofluorescence, molecular docking, and molecular dynamics simulation. In vivo, the antitumor efficacy and safety were evaluated using TNBC xenografts in zebrafish and BALB/c nude mice. Z-GS selectively suppressed TNBC cell proliferation, induced cell-cycle arrest and apoptosis, and increased intracellular ROS. Mechanistically, Z-GS upregulated O-GlcNAc transferase (OGT) expression, enhanced SNAP29 O-GlcNAcylation, disrupted SNARE complex assembly, inhibited autophagosome-lysosome fusion, and blocked late-stage autophagic flux. In vivo, Z-GS significantly inhibited TNBC xenograft growth without detectable toxicity. Z-GS functions as a novel late-stage autophagy inhibitor and exhibits selective anti-TNBC activity, bridging natural product pharmacology and cancer treatment. - Source: PubMed
Publication date: 2026/02/13
Qian DaMu YuxiaoLiu HaotianYang ZhuotaoHu JunsiZeng XinLiu KeHe ChaoqiLiu XiaozhenZhu LiquanZhang JianbinMeng Xuli