Ask about this productRelated genes to: MYO1D antibody
- Gene:
- MYO1D NIH gene
- Name:
- myosin ID
- Previous symbol:
- -
- Synonyms:
- KIAA0727, myr4, PPP1R108
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-04
- Date modifiied:
- 2015-09-04
Related products to: MYO1D antibody
Related articles to: MYO1D antibody
- One of the most characteristic morphogenetic processes in Drosophila is the 360° rotation of the male pupal genital disc. This movement is driven by the myosin Myo1D, whose expression in the genital disc is controlled by the Hox gene Abdominal-B (Abd-B). The rotation takes place in contact and relative to the posterior abdomen, yet the contribution of abdominal tissues has remained unclear. - Source: PubMed
Publication date: 2026/07/07
Prieto NuriaForonda DavidMartín PalomaSimon EléanorBischoff MarcusNoselli StéphaneSánchez-Herrero Ernesto - Caspases are best known for promoting apoptosis, yet their role in tissue regeneration by compensatory proliferation remains unclear. Using Drosophila wing discs and a delayed reporter for the initiator caspase-9 ortholog Dronc activity, we identify two apoptosis-resistant epithelial cell populations that mediate regeneration after ionizing radiation: Dronc-activating (DARE) and non-activating (NARE) cells. Dronc activity in DARE cells, independent of Dark and effector caspases, drives regeneration both cell-autonomously and non-cell-autonomously. The TNFR in DARE cells, Wengen, likely activated by ROS, strongly promotes DARE proliferation, while TNF/Eiger and TNFR Grindelwald moderately suppress it. Downstream, p38 MAPK is the main signaling essential for DARE and NARE cell proliferation. Myo1D ensures DARE survival by preventing lethal effector caspase activation, whereas Myo7A/Crinkled supports moderate caspase activity. Dying cells trigger DARE induction, and both DARE and NARE transmit apoptosis resistance to progeny, with DARE progeny showing enhanced resistance. Maintaining balanced DARE-NARE proliferation is crucial for proper regeneration, growth, and differentiation, insights that may be relevant to radiation-resistant cells in cancer therapy. - Source: PubMed
Publication date: 2025/12/04
Braun TslilAfgin NaamaSapozhnikov LenaSivan EhudBergmann AndreasBaena-Lopez Luis AlbertoYacobi-Sharon KerenArama Eli - BACKGROUND: Prostate cancer (PCa) is a prevalent malignancy in men, with exosomes playing a key role in tumor microenvironment and disease progression, yet their molecular mechanisms remain unclear.This study aims to identify potential biomarkers and therapeutic targets in PCa by integrating exosome-related genes with differentially expressed genes (DEGs). METHODS: Four GEO datasets (GSE32448, GSE46602, GSE69223, GSE6956) were analyzed. Batch effects were corrected using the ComBat method, followed by DEG analysis and feature selection via machine learning (LASSO regression, random forest, SVM). Functional enrichment and molecular docking validated the findings. RESULTS: Post-correction, sample clustering improved significantly. Of 49 overlapping DEGs and exosome-related genes, EEF2, LGALS3, and MYO1D emerged as key biomarkers, with EEF2 showing the highest predictive power (AUC = 0.786). A risk score model achieved an AUC of 0.886. Immune analysis linked these genes to immune cell subsets, and docking studies revealed strong interactions with small molecules like cycloheximide. CONCLUSION: This study elucidates the molecular role of exosome-related genes in PCa, proposing predictive biomarkers and novel therapeutic targets, warranting further clinical validation. - Source: PubMed
Publication date: 2025/11/04
Huang ShengnanHu ChunyanGuo ZhongqiZhang XiaojingWu TiantianZeng YuqingQing ChenCheng Shulin - Muscle growth is a critical determinant of meat yield and quality in livestock. Although follistatin (FST) is recognized as a key regulator of skeletal muscle development and fat metabolism, its specific function in geese remains largely unexplored. In this study, we identified two transcript variants of goose FST () in Zhedong White geese: gFST-X1 (1125 bp), encoding a 343-amino acid protein with a 28-amino acid signal peptide and four conserved domains, and gFST-X2, which contains a 243 bp insertion within the gFST-X1 transcript. RT-qPCR analysis revealed that mRNA expression varied across tissues from female embryos (25 days), adults (70 days), and laying geese (270 days), as well as in skeletal muscle satellite cells (SMSCs) at embryonic day 16 (E16d). Overexpression of gFST in SMSCs resulted in 3596 differentially expressed genes (DEGs), including 2247 upregulated and 1349 downregulated genes ( < 0.01). Key stemness markers (, ) and myogenic regulators (, , ) were significantly downregulated, whereas genes associated with lipid metabolism (, , ) and myosin-related processes (, , ) were markedly upregulated ( < 0.01). Functional enrichment analysis linked these DEGs to the TGF-β, PPAR signaling, fatty acid metabolism, and Notch signaling pathways. These transcriptomic findings were further validated by qRT-PCR. Collectively, our results demonstrate the dual regulatory role of in skeletal muscle development and provide new mechanistic insights into muscle development in geese. - Source: PubMed
Publication date: 2025/10/16
Wang CuiLiu YiLi MingxiaYang YunzhouDai JiuliChen ShufangWang HuiyingHe Daqian - Genetic predisposition plays a key role in autoimmune and complex diseases such as multiple sclerosis (MS). However, identifying the specific variants or genomic regions responsible for disease susceptibility remains a significant challenge. In this study a family-based fine mapping approach was applied to analyze 142 trios, aiming to identify associated genetic variants linked to MS. The targeted genomic region resides within the 17:30,820,506-32,483,270 bp (Ch37/hg19), which includes the protein-coding gene ASIC2, previously implicated in MS and other neurological conditions, with surrounding genes comprising strongly correlated genetic variants to capture the broader signal from the region. Given the high prevalence of MS in Sardinia and the unique genetic characteristics of the Sardinian population, including reduced heterogeneity and extended linkage disequilibrium, we designed our study specifically within this population and focused on family-based data to enhance the power for detecting genetic signals, avoiding false discoveries. Genotype imputation found 2537 variants, which were then analyzed using the knockoff Trio method to identify loci associated with MS susceptibility. We found rs756787 (3'UTR of MYO1D) increased disease risk (OR 1.57, 95% CI [1.07-2.29], p = 0.02), while rs56175840 (intronic ASIC2) showed a protective effect (OR 0.17, 95% CI [0.04-0.74], p = 0.02), demonstrating the power of knockoff-based fine mapping in family datasets. Integrating LD-based expression and trait analyses helped reveal how rs756787 correlates with variants affecting genes involved in neurodegeneration and the immune response to Epstein-Barr virus, a known environmental factor implicated in MS pathogenesis. Our study highlights the effectiveness of knockoff-based fine mapping combined with expression-trait integration to identify genetic variants influencing MS risk in the Sardinian population. - Source: PubMed
Publication date: 2025/08/30
Baldrighi Giulia NicoleNova AndreaEkstrøm Claus ThornPiras Maria LuisaSaddi Maria ValeriaBernardinelli LuisaFazia Teresa