Ask about this productRelated genes to: LYPLA1 antibody
- Gene:
- LYPLA1 NIH gene
- Name:
- lysophospholipase 1
- Previous symbol:
- -
- Synonyms:
- LPL1, APT-1
- Chromosome:
- 8q11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-29
- Date modifiied:
- 2018-10-25
Related products to: LYPLA1 antibody
Related articles to: LYPLA1 antibody
- Colorectal cancer (CRC) persists as a significant public health burden due to its high morbidity and mortality rates worldwide, yet the molecular events that govern its initiation and progression remain incompletely understood. We recently conducted microRNA (miRNA) profiling and identified multiple dysregulated miRNAs in CRC compared to adjacent normal tissue. Among those, miR-138-5p emerged as a potential tumor suppressor due to its marked downregulation in CRC tissue; however, the stage-specific expression of this miRNA during CRC progression and underlying molecular mechanisms remains to be unraveled. In this study, we performed differential expression profiling of healthy colon, adenomatous polyp (AP), and CRC tissues based on public datasets, revealing significant downregulation of miR-138-5p in CRC compared to controls, but not during the AP stage, suggesting a role in later stages of malignant progression. Forced expression of miR-138-5p in HCT116 and HT-29 CRC models suppressed clonogenic survival, proliferation, and migration while inducing cell death. Additionally, miR-138-5p significantly inhibited tumor formation under three-dimensional culture settings, reinforcing its tumor-suppressive function in a physiologically relevant context. Transcriptomic profiling of miR-138-5p-overexpressing CRC models revealed widespread changes in the pathways related to zinc ion binding, cilium morphogenesis, smoothened signaling, and nuclear transport. Integrated computational and experimental analyses identified 41 potential gene targets, among which , and were validated as potential miR-138-5p-regulated genes. Collectively, these findings establish miR-138-5p as a stage-specific tumor suppressor in CRC, acting through coordinated regulation of oncogenic networks across multiple pathways. Downregulation of miR-138-5p appears to be a late oncogenic event, conferring proliferative, survival, and invasive advantages to tumor cells. Restoration of miR-138-5p or therapeutic targeting of its downstream effectors may represent promising avenues for CRC therapeutic intervention. - Source: PubMed
Publication date: 2026/04/09
Shaath HibahVishnubalaji RadhakrishnanAlajez Nehad M - Protein S-acylation is a lipid-based, often reversible post-translational modification that can regulate many aspects of protein behavior, including subcellular localization, proteininteractions, and activity. Emerging evidence has identified roles for individual protein acyltransferases encoded by the ZDHHC in cancers, yet the roles of de-S-acylation enzymes are less clear. Recent evidence suggests that acyl-protein thioesterase (APT1)/LYPLA1 can impact epithelial-mesenchymal transition and metastasis. This study integrates patient datasets, CRISPR dependency data, and in vitro assays to find APT1 as a context-dependent vulnerability in triple-negative breast cancer (TNBC). Despite the highest protein abundance in luminal A MCF7 cells, basal-like MDA-MB-468 cells exhibited the most prominent specific APT1 activity, reflecting subtype-specific regulation. Inhibition of APT1 with ML348 increased S-acylation of nuclear and mitochondrial proteins without altering global acylation. Functionally, APT1 inhibition reduced cell proliferation while inducing minimal apoptosis, consistent with cytostatic growth arrest. Cell-cycle analysis revealed G1 accumulation and reduced S/G2 transition, linking proteomic changes to impaired replication. These findings establish APT1 as a regulator of TNBC proliferation through dynamic de-S-acylation of cell-cycle and mitochondrial proteins, highlighting it as a potential therapeutic vulnerability in aggressive breast cancers. - Source: PubMed
Publication date: 2026/04/16
Salsaa MichaelTavasoli MahtabZein Haggag SPani ShubhashreeKathayat RahulDickinson BryanFairn Gregory D - Repair and remodeling following myocardial infarction (MI) are complex processes with a wide array of cellular and molecular mechanisms; however, the cell source mediating repair is still poorly understood in terms of heterogeneity and temporal dynamics. - Source: PubMed
Publication date: 2026/03/06
Zhao JianfengGong JunhuiZhu Cunzhi - Evidence from genome-wide association studies (GWAS) links genetic variants near the locus to variations in sheep muscle development. To further investigate whether expression plays a role in fetal sheep myoblast development, we performed gain-of-function/loss-of-function analyses targeting using siRNA and recombinant vectors. CCK-8 assays, EdU staining, and flow cytometry were used to investigate the effects of both knockdown and overexpression on the proliferation of fetal sheep myoblasts. Furthermore, this study investigated the effect of on myogenic differentiation by means of indirect immunofluorescence staining with MyHC and quantitative analysis of myogenic regulatory factor (MRF) expression. The results showed that downregulation of significantly reduced cell viability and proliferation rate, arrested myoblasts in the G2 phase, and inhibited proliferation. These effects were reversed when was overexpressed. Furthermore, knockdown significantly impaired myotube formation during terminal differentiation (days 5-7). This defect was correlated with a marked reduction in the expression of myogenic regulatory factors (MRFs). This effect was reversed when was highly expressed. In summary, this study demonstrates that promotes the proliferation and differentiation of fetal sheep myoblasts, establishing its potential as a target for the molecular breeding of sheep. - Source: PubMed
Publication date: 2025/12/02
Zhang ZhanpengYin YiYang HuiguoShalike KanatiNie YanglinCao XiukaiYuan ZehuSun Wei - The causal bridge from environmental exposure to endometriosis (Ems) biology remains incompletely defined. Di(2-ethylhexyl) phthalate (DEHP) is repeatedly implicated in elevated Ems risk, yet actionable molecular anchors linking exposure to phenotype are scarce. - Source: PubMed
Publication date: 2025/11/27
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