LSM7 Antibody (C-term) Blocking Peptides
- Known as:
- LSM7 Antibody (C-terminus) Blocking Peptides
- Catalog number:
- BP11679b
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- LSM7 Antibody (C-term) Blocking Peptides
Related genes to: LSM7 Antibody (C-term) Blocking Peptides
- Gene:
- LSM7 NIH gene
- Name:
- LSM7 homolog, U6 small nuclear RNA and mRNA degradation associated
- Previous symbol:
- -
- Synonyms:
- YNL147W
- Chromosome:
- 19p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-17
- Date modifiied:
- 2015-09-03
Related products to: LSM7 Antibody (C-term) Blocking Peptides
Related articles to: LSM7 Antibody (C-term) Blocking Peptides
- Colorectal cancer (CRC) remains a leading cause of cancer mortality, yet no systematic effort has linked druggable CRC driver genes to downstream ion channel effectors. We integrated differential expression analysis, weighted gene co-expression network analysis (WGCNA), and protein-protein interaction (PPI) network pharmacology to identify CRC hub genes and their ion channel connections, validated by dual single-cell perturbation approaches: variational graph autoencoder-based virtual knockout (VGAE-KO) and experimental HCT116 CRISPRi Perturb-seq (6 genes, 8445 cells). WGCNA identified 100 hub genes spanning three functional programs. Ribosomal proteins link to K channels ( → , targetable by EMA-approved ataluren, passed dual validation at 97.8th-98.7th percentile). RNA processing genes connect to Cl channels ( → , strongest signal at 99.8th-99.4th percentile). Immune checkpoint receptors (, ) connect via PPI intermediates to Ca2+ and K channels, targetable by relatlimab (FDA-approved) and varlilumab (Phase 2). This work maps previously unknown links between CRC driver genes and ion channel regulation, with the ataluren-- axis ready for pharmacological testing. - Source: PubMed
Publication date: 2026/04/10
Dong ZhongyuanMeng XuanlinWang Lianghua - This study explores the impact of histone acetylation-related genes (HARGs) on the PD-1-associated immune microenvironment and prognosis of non-small cell lung cancer (NSCLC) using integrated multi-omics analyses and experimental validation. - Source: PubMed
Publication date: 2026/03/15
Zhou JianyingQiu TingtingHu ZhenzhenXiao DanLiu Zhentian - Ischemic stroke (IS) remains a leading cause of death and disability, with limited effective treatments in the acute phase. Mitophagy, the selective degradation of damaged mitochondria, plays a crucial role in cellular homeostasis and survival during IS. However, its exact mechanisms in stroke pathophysiology remain unclear. This study utilized a multi-omics approach, integrating gene expression data from bulk and single-cell RNA sequencing, to investigate the role of mitophagy-related genes (MRGs) in IS. We identified differentially expressed MRGs (DE-MRGs) in IS using bioinformatics techniques, including weighted gene co-expression network analysis (WGCNA) and machine learning models, which led to the identification of five core biomarkers: SRPRB, ATP5J, LSM7, DEGS1, and TGDS. Validation via qPCR and analysis of immune cell infiltration further supported their relevance. Single-cell analysis revealed significant differences in mitophagy activity in microglial subpopulations, with ATP5J showing dynamic expression patterns linked to stroke-induced mitochondrial dysfunction. Additionally, pseudo-time analysis suggested a progressive shift from homeostatic to disease-associated microglial states. Our findings highlight the complexity of mitophagy regulation in IS and suggest that targeting mitophagy-related pathways, such as ATP5J, could provide novel therapeutic strategies for IS management. - Source: PubMed
Publication date: 2026/03/06
Cao ZhanWang YingluanSun MingjianDu RunyiFeng XuWang LinZhao ZiyiSun Wei - ObjectiveHepatocellular carcinoma (HCC) has a poor prognosis, necessitating novel biomarkers. The role of (Like-Sm protein 7), an RNA-binding protein, in HCC remains unclear.MethodsWe employed a multiomics strategy using transcriptomic data from TCGA, GTEx, GEO, and ICGC to evaluate 's expression and prognostic value. A protein-protein interaction (PPI) network was constructed via STRING, followed by Gene Ontology/KEGG/Gene Set Enrichment Analysis (GSEA) functional enrichment analysis. The relationship between and the immune infiltration landscape was assessed using single-sample GSEA (ssGSEA) and the TISCH single-cell database. Drug sensitivity was analyzed using Genomics of Drug Sensitivity in Cancer, and structure-based virtual screening was performed on the ZINC library to identify potential inhibitors. Key findings were validated in clinical samples and MHCC97H cells and Huh-7 cells using Western blot, IHC, and MTT assays.Results was significantly overexpressed in HCC, correlating with adverse clinicopathological features (higher histological grade, elevated AFP levels, vascular invasion) and shorter overall survival, identifying it as an independent risk factor. Functionally, was implicated in processes such as hormone regulation. Immune analysis revealed that high expression was associated with altered immune cell abundance, upregulation of immune checkpoints, and a higher Tumor Immune Dysfunction and Exclusion score, suggesting a role in immune evasion. The high- group showed increased sensitivity to drugs like sorafenib. Virtual screening identified Velpatasvir as a top -targeting candidate, with in vitro validation confirming that it inhibits MHCC97H cells and Huh-7 cells proliferation and downregulates protein in a concentration- and time-dependent manner.ConclusionsBy integrating multiomics strategy and experimental validation, this study suggests that may play a role in HCC progression and influence the tumor immune microenvironment. may serve as a potential biomarker and therapeutic target, and Velpatasvir appears to be a candidate agent worthy of further investigation. - Source: PubMed
Publication date: 2026/01/19
Fan ShanshanHe YifengKe PeifengJiang JianhongZhang ShengmingZeng DeqinDuan JuanWu Ming - Crystallin proteins serve as both essential structural and as well as protective components of the ocular lens and are required for the transparency and light refraction properties of the organ. The mouse lens crystallin proteome is represented by αA-, αB-, βA1-, βA2-, βA3-, βA4-, βB1-, βB2-, βB3-, γA-, γB-, γC-, γD-, γE, γF-, γN-, and γS-crystallin proteins encoded by 16 genes. Their mutations are responsible for lens opacification and early onset cataract formation. While many cataract-causing missense and nonsense mutations are known for these genes, including the human CRYBB3 gene, the mammalian loss-of function model of Crybb3 remains to be established. Herein, we generated the first mouse model via deletion of the Crybb3 promoter that nearly abolished expression of the βB3-crystallin. Histological analysis of lens morphology using newborn βB3-crystallin-deficient lenses revealed disrupted lens morphology with early-onset phenotypic variability. In-depth lens proteomics at four time points (newborn, 3-weeks, 6-weeks, and 3-months) showed both down- and up-regulation of various proteins, with the highest divergence from control mice observed in 3-months lenses. Apart from the βB3-crystallin, Smarcc1/Baf155 was down-regulated in all four stages. In addition, downregulation of Hspe1, Pdlim1, Ast/Got, Lsm7, Ddx23, and Acad11 was found in three time points. Finally, we show that the βB3-crystallin promoter region, which contains multiple binding sites for the transcription factors AP-2α, c-Jun, c-Maf, Etv5, and Pax6 is activated by FGF2 in primary lens cell culture experiments. Together, these studies establish the mouse Crybb3 loss-of-function model and its disrupted crystallin and non-crystallin proteomes. - Source: PubMed
Publication date: 2025/08/19
Rayêe DanielleWilmarth Phillip AVanSlyke Judy KZientek KeithReddy Ashok PMusil Linda SDavid Larry LCvekl Aleš