Ask about this productRelated genes to: MOSPD3 antibody
- Gene:
- MOSPD3 NIH gene
- Name:
- motile sperm domain containing 3
- Previous symbol:
- -
- Synonyms:
- CDS3, NET30
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-23
- Date modifiied:
- 2016-10-05
Related products to: MOSPD3 antibody
Related articles to: MOSPD3 antibody
- Autophagy degrades various intracellular components by sequestering them within membrane vesicles called autophagosomes and delivering them to lysosomes or vacuoles. Previous studies have revealed that the conserved, bridge-like lipid transfer protein Atg2 tethers autophagosome precursors to the endoplasmic reticulum (ER) and mediates lipid supply from the ER to drive their expansion into autophagosomes. However, how Atg2 docks onto the ER has remained unclear. Here, we show in that Atg2 interacts with the ER-resident VAP family protein Scs2. This interaction is mediated by a phospho-FFAT motif in Atg2 and the major sperm protein domain of Scs2 and enhanced by phosphorylation of the motif by the autophagy-initiating kinase Atg1, which is activated at the autophagosome formation site upon autophagy induction. This interaction cooperates with the N-terminal region of Atg2, which contains a weakly amphipathic helix, to mediate Atg2 association with the ER. Thus, the Atg2-Scs2 interaction functions as a spatiotemporal switch that controls Atg2-ER association. We also show that mammalian ATG2 interacts with the VAP-like proteins MOSPD1 and MOSPD3 to promote autophagosome formation. Collectively, this study reveals a conserved mechanism that initiates lipid transfer during autophagosome formation. - Source: PubMed
Publication date: 2026/07/29
Kotani TetsuyaTanabe HarukiKitta ShinriHigashi MomokoNiwa TatsuyaKaminishi TatsuyaKakuta ChikaShimasaki JunkoKosako HidetakaYoshimori TamotsuKuma AkikoNakatogawa Hitoshi - Heart failure (HF) is a major global health challenge, contributing to over 18 million deaths annually. While the roles of genetic and environmental factors are widely studied, the role of DNA methylation in HF pathogenesis is not fully understood. This study leverages the Hybrid Mouse Diversity Panel (HMDP) to investigate the relationship between DNA methylation, gene expression, and HF phenotypes under isoproterenol-induced cardiac stress. Using reduced representational bisulfite sequencing, we analyzed DNA methylation profiles in the left ventricles of 90 HMDP strains. Epigenome-wide association studies identified 56 CpG loci linked to HF phenotypes, with 18 loci predicting HF progression. Key genes, including Prkag2, Anks1a, and Mospd3, were implicated through integration with gene expression and phenotypic data. In vitro validation confirmed the roles of Anks1aand Mospd3 in attenuating isoproterenol-induced hypertrophy. Additionally, treatment with the DNA methyltransferase inhibitor RG108 mitigated cardiac hypertrophy, preserved ejection fraction, and restored methylation-sensitive gene expression, underscoring the therapeutic potential of targeting DNA methylation in HF. This study highlights the interplay between DNA methylation, gene expression, and HF progression, offering new insights into its molecular underpinnings. The findings emphasize the role of epigenetic regulation in HF and suggest DNA methylation as a promising target for therapeutic intervention. - Source: PubMed
Publication date: 2025/07/07
Lahue CaitlinWong EleanorDalal AryanTan Lek Wen WilsonRen ShuxunFoo RogerWang YibinRau Christoph D - Heart failure (HF) is a leading cause of morbidity and mortality worldwide, with over 18 million deaths annually. Despite extensive research, genetic and environmental factors contributing to HF remain complex and poorly understood. Recent studies suggest that epigenetic modifications, such as DNA methylation, may play a crucial role in regulating HF-associated phenotypes. In this study, we leverage the Hybrid Mouse Diversity Panel (HMDP), a cohort of over 100 inbred mouse strains, to investigate the role of DNA methylation in HF progression. - Source: PubMed
Publication date: 2024/10/26
Lahue CaitlinWong EleanorDalal AryanWen Wilson Tan LekRen ShuxunFoo RogerWang YibinRau Christoph D - Genome-wide association studies (GWASs) explain the genetic susceptibility between diseases and common variants. Nevertheless, with the appearance of large-scale sequencing profiles, we could explore the rare coding variants in disease pathogenesis. - Source: PubMed
Publication date: 2024/03/14
Jiang YunkeLi HongruLi ZaimingDu ShaZhang RuyangZhao YangChristiani David CShen SipengChen Feng - Obesity poses significant health risks and can negatively impact an individual's quality of life. The human obesity phenotype results from the differentiation of pre-adipocytes into adipocytes, which leads to hypertrophy and hyperplasia in adipose tissue. The molecular mechanisms by which long non-coding RNAs (lncRNAs) modulate adipocyte differentiation, a process implicated in obesity development, remain poorly characterized. A lncRNA which suppressed the hepatic gluconeogenesis and lipogenesis (lncSHGL) was newly identified. Our research aims to elucidate the functional role and mechanistic underpinnings of suppressor of lncSHGL in adipocyte differentiation. We observed that lncSHGL expression progressively diminished during 3T3-L1 differentiation and was downregulated in the liver and perirenal adipose tissue of ob/ob mice. lncSHGL acts as a molecular sponge for miR-149, with Mospd3 identified as a target of miR-149.Overexpression of lncSHGL and inhibition of miR-149 led to suppressed 3T3-L1 proliferation, decreased lipid droplet accumulation, and attenuated promoter activity of PPARγ2 and C/EBPα. These changes consequently resulted in reduced expression of Cyclin D1, LPL, PPARγ2, AP2, and C/EBPα, as well as inhibited the PI3K/AKT/mTOR signaling pathway. In contrast, lncSHGL suppression yielded opposing outcomes. Moreover, the effects of lncSHGL overexpression and miR-149 inhibition on reduced expression of Cyclin D1, LPL, PPARγ2, AP2, and C/EBPα were reversible upon miR-149 overexpression and Mospd3 suppression. These findings were further validated . We also discovered a significant increase in methylation levels during 3T3-L1 differentiation, with lncSHGL highly expressed in the presence of a methylation inhibitor. In conclusion. lncSHGL methylation facilitates adipocyte differentiation by modulating the miR-149/Mospd3 axis. Targeting lncSHGL expression may represent a promising therapeutic strategy for obesity-associated adipogenesis, particularly in the context of fatty liver disease. - Source: PubMed
Publication date: 2024/01/18
Huang XianweiLiu XiongLin Jiyan