LANPL antibody
- Known as:
- LANPL (anti-)
- Catalog number:
- orb100409
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- LANPL antibody
Related genes to: LANPL antibody
- Gene:
- ANP32E NIH gene
- Name:
- acidic nuclear phosphoprotein 32 family member E
- Previous symbol:
- -
- Synonyms:
- LANPL, MGC5350, LANP-L
- Chromosome:
- 1q21.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-04-15
- Date modifiied:
- 2016-10-05
Related products to: LANPL antibody
Related articles to: LANPL antibody
- Seasonal influenza in humans is predominantly caused by influenza A virus (IAV) and influenza B virus (IBV), but they differ markedly in host range, evolutionary dynamics, and pandemic potential. Such phenotypic divergence reflects the distinct molecular strategies employed by the two viruses at key stages of their life cycles. Hemagglutinin (HA) of IAV possesses prominent structural plasticity, which endows it with the capacity to recognize both avian-type α2,3-linked and human-type α2,6-linked sialic acid receptors, and the function of IAV polymerase is highly dependent on host acidic nuclear phosphoprotein 32 (ANP32) family proteins. Moreover, IAV utilizes multiple pleiotropic virulence factors, such as the nonstructural protein 1 (NS1), to modulate host immune responses and inflammatory processes, thereby contributing to viral fitness, host adaptation, and pandemic potential. In contrast, the HA of IBV preferentially binds to human-type (α2,6-linked) sialic acid receptors and exhibits a more restricted receptor-binding profile.While IBV polymerase is well adapted to human ANP32A and ANP32B, yet shows poor compatibility with avian ANP32 proteins. Additionally, the immunomodulatory machinery is relatively streamlined, engaging host cell death pathways in a more limited manner that may contribute to generally less extensive inflammatory responses in many experimental and clinical settings. As a result, IBV transmission is largely confined to humans, with a narrow host range and a predominantly seasonal epidemic pattern. In this review, we systematically compare IAV and IBV with respect to four core pathogenic processes, namely viral entry, genome replication efficiency and host factor dependence, immune evasion, and the regulation of host cell death pathways, to explain how these mechanisms collectively shape differences in host range, evolutionary dynamics, and pandemic potential. We particularly emphasize the capacity of IAV to achieve efficient replication in a wide range of host species, a trait that facilitates its multi-host circulation and viral gene reassortment. These insights establish a theoretical framework for enhancing influenza surveillance and guiding the development of next-generation influenza vaccines and antiviral therapeutics. - Source: PubMed
Publication date: 2026/07/09
Zhang XiaoyangTang QinZhang YongleGuo JianchaoYao XuejieLuo ZhongGuo XinyuZhao YueZhu HenghuiLiu ChangHuang CanHou ZiyingYang ChendiChen RuiqiMa Jiaqi - BackgroundThe main aim of this study is to identify prognostic biomarkers through integrating bioinformatics analysis in gastric cancer, which is a significant global health challenge.MethodsGene expression datasets related to blood, tissue, and saliva in gastric cancer were downloaded from the Gene Expression Omnibus (GEO) database and analyzed. The bioinformatics approaches included the identification of differentially expressed genes (DEGs) and enrichment analysis, as well as Kaplan-Meier Plotter survival analysis. The DEGs were also validated through The Cancer Genome Atlas (TCGA) database. Additionally, DEGs-associated lncRNAs and microRNAs were identified. Subsequently, Tumor and Immune System Interaction Database (TISIDB) was utilized to examine the correlation of the genes of interest with immune and molecular subtypes.ResultsTwenty-six common DEGs were identified across blood, tissue, and saliva samples. Among them, 17 genes showed significant expression based on TCGA data. RAB23, LOX, ELL2, ELK3, CENPF, CD44, ANP32E, AKR1C2, and SMAD5 displayed significant association with patient survival. Particularly, ELL2 exhibit decreased expression in all specimens. The results indicated that ELL2 has a significant correlation with the immune system. The ELL2 gene regulates immune cell functions in gastric cancer, potentially influencing cancer immune responses, and tumor progression.ConclusionELL2 downregulated expression and its correlation with survival across blood, tissue, and saliva samples using bioinformatics analysis underscores the necessity of more investigation to fully comprehend its function in cancer immunology. - Source: PubMed
Publication date: 2026/06/23
Zare KiarashSalehi ZahraMorovat Ali RezaAghajani AliMohammadi Pour PardisGhanbariasad AliNaghizadeh Mohammad Mehdi - Epigenetic aging clocks offer precise measures of biological age, yet the causal contributions of immune gene expression within specific cell subtypes to epigenetic aging remain poorly understood. By integrating single-cell eQTL data from the OneK1K cohort with GWAS summary statistics for four epigenetic clocks (HannumAge Acceleration, IEAA, PhenoAge Acceleration, and GrimAge Acceleration), we performed two-sample Mendelian randomization across diverse immune cell subtypes, followed by colocalization analysis and gene-level phenome-wide association studies. We identified 11 eGene-cell type pairs surviving Bonferroni correction, including NUCKS1 in CD4 NC T cells and NCR3 in Classic Monocytes as risk-increasing eGenes for HannumAge Acceleration, and HSPA1B in Classic Monocytes as protective across multiple clocks. ANP32E in Classic Monocytes represented the strongest risk signal for GrimAge Acceleration (OR = 2.683), while BCAS4 in CD8 EM T cells was the strongest protective association (OR = 0.683). Colocalization confirmed NUCKS1 (PP.H4 = 87%) and NCR3 (PP.H4 = 69%) as high-confidence causal eGenes, and PheWAS revealed no genome-wide significant off-target associations for the prioritized targets, supporting their specificity. These findings establish cell subtype-specific causal roles for immune gene expression in epigenetic aging and prioritize NUCKS1, NCR3, and ANP32E as candidate targets for interventions aimed at promoting healthy aging. - Source: PubMed
Publication date: 2026/05/26
Zhang ChunZhang Jingqi - Understanding the genetic changes that allow avian influenza A viruses (IAVs) to switch their natural hosts and establish productive infection in humans is important for pandemic risk assessment. Adaptations in the IAV polymerase are required to overcome species-specific restrictions imposed by host ANP32 proteins. Notably, avian virus polymerase is generally only poorly supported by human ANP32 proteins due to species-specific differences. Consequently, efficient polymerase adaptation to the binding interface of human ANP32 requires distinct amino acid changes, such as PB2 E627K. A separate adaptation, PB2 M631L, has recently been reported in mammalian-adapted IAV; however, its functional role across divergent viral lineages and its relationship to host ANP32-dependent adaptation remain incompletely defined. Here, we examine PB2 M631L in the polymerases of a 1918 pandemic strain, a recombinant contemporary H1N1pdm09, and a recent clade 2.3.4.4b H5N1 virus. Using polymerase activity and protein-interaction assays, we show that PB2 M631L enhances polymerase activity and ANP32 binding in human-but not avian-contexts, and that this effect is conserved across multiple viral backgrounds. In H1N1pdm09, PB2 M631L also increased virus replication in mammalian cells. These findings indicate that PB2 M631L contributes to enhanced polymerase compatibility with human ANP32 proteins and are consistent with a role in adaptation across multiple influenza virus lineages. Our results highlight how analysis of historical pandemic strains can inform risk assessment for future emerging viruses. - Source: PubMed
Publication date: 2026/04/11
Budt MatthiasBarac IrinaKohs JessicaKrischuns TimNaffakh NadiaWolff Thorsten - Skeletal muscle is the largest organ by mass in the human body, and its functional capacity depends on the precise coordination of protein synthesis, mitochondrial bioenergetics, and regenerative potential. Eukaryotic translation initiation factor 3 (eIF3), a 13-subunit complex (~800 kDa) best known for its multifaceted roles in cancer, is now emerging as a key translational regulator in skeletal muscle physiology and disease. Here, we present a perspective that synthesizes recent advances into a unifying "dual-phase guardian" model. In the first phase, eIF3f acts at the level of translation initiation as a scaffold bridging mTORC1 and S6K1, integrating anabolic and catabolic signals, particularly the MAFbx/Atrogin-1 ubiquitin-proteasome axis, to govern net protein synthesis and muscle mass. In the second phase, eIF3e remains bound to 80S ribosomes during early translation elongation (codons 1-60) of approximately 2700 mRNAs encoding mitochondrial and membrane-associated proteins, facilitating co-translational quality control through chaperone recruitment (e.g., CCT/TRiC). Haploinsufficiency of eIF3e in mice produces mitochondrial hyperfusion, diminished respiratory complex I activity, sarcomeric degeneration, and progressive loss of grip strength, a phenotype recapitulating features of mitochondrial myopathy. Complementing these findings, eIF3b supports satellite cell-mediated muscle regeneration by resolving RNA G-quadruplex structures in the 5'-UTR of Anp32e mRNA, while eIF3a modulates fibrotic remodeling through TGF-β/Smad3 signaling. We situate these subunit-level findings within the broader landscape of translational regulators in muscle (eIF2α/ISR, eIF5A, eEF2) and critically evaluate the translational potential and therapeutic challenges, including the absence of human clinical data, tissue-selectivity concerns, and species-specific limitations, that must be addressed before these mechanistic insights can inform treatment of sarcopenia, disuse atrophy, and mitochondrial myopathy. - Source: PubMed
Xia JianingLiao KexinWang JiahuanLu MinghaoMu YonghaoLin Yingying