TXLNA Antibody
- Known as:
- TXLNA Antibody
- Catalog number:
- XW-8134
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- TXLNA Antibody
Related genes to: TXLNA Antibody
- Gene:
- TXLNA NIH gene
- Name:
- taxilin alpha
- Previous symbol:
- -
- Synonyms:
- DKFZp451J0118
- Chromosome:
- 1p35.2
- Locus Type:
- gene with protein product
- Date approved:
- 2005-07-29
- Date modifiied:
- 2016-10-05
Related products to: TXLNA Antibody
Related articles to: TXLNA Antibody
- To evaluate the relationship between N6-methyladenosine (m6A) modification-related genes and the immune microenvironment characteristics of hepatocellular carcinoma (HCC), and to evaluate the potential of targeting m6A regulators to sensitize HCC cells to immunotherapy. RNA sequencing data and clinicopathologic data of HCC patients were obtained from TCGA and ICGC database. Based on the expression levels of 23 m6A modification regulators, the HCC samples were divided into three m6A clusters by ConsensusClusterPlus algorithm. Survival analysis and clinical features was explored in different clusters. Next, univariate Cox analysis and LASSO regression analysis were applied to screened out 4 immune-related prognostic genes from the differentially expressed genes (DEGs) in the three clusters, and a risk model was established. Next, Kaplan-Meier plot, time-dependent receiver operating characteristic (ROC), multivariable Cox regression analysis were applied to evaluate the prognostic value of risk model. The relationship between the immune microenvironment and the risk model was estimated using the ESTIMATE method and single sample Gene Set Enrichment Analysis (ssGSEA). Finally, immunohistochemistry was applied to explore the correlation between the expression levels of PD-L1 and the key m6A regulators METTL3 and YTHDF1. Most m6A regulators were highly expressed in HCC tissues, and positively correlated with each other. The patients in cluster 3 showed the worse prognosis. 449 of the 710 DEGs were immune regulators, and from the 449 genes, a risk model consisting of 4 m6A-related genes (DNTTIP2, SEPHS1, TCOF1 and TXLNA) was established, which was associated with immune microenvironment characteristics of HCC tissues. The risk model was identified as an independent prognostic factor for the overall survival of HCC patients. Higher levels of YTHDF1 and METTL3 expression in HCC tissues were associated with higher expression of PD-L1. m6A modification participates in regulating immune microenvironment of HCC, and targeting m6A may block the immune escape of HCC cells. - Source: PubMed
Publication date: 2025/11/27
Wang WenjuanWang ErxiongHong KunqiaoJiang WeiRuan BanlaiLiu JieTian JinpingDing FengGuo QiuyunDing Qianshan - Pancreatic ductal adenocarcinomas (PDACs) with wild-type KRAS constitute a small fraction of PDACs, and these tumors were recently shown to harbor frequent actionable oncogenic mutations and fusions. However, the clinicopathological features of KRAS wild-type PDAC have not been well studied. Additionally, precancerous lesions occurring in patients with KRAS wild-type PDACs have rarely been characterized. Here, we investigated the clinicopathological characteristics and outcomes of 75 patients with KRAS wild-type PDAC. Molecular analyses were performed in 40 patients using targeted DNA and whole-exome sequencing and targeted RNA sequencing. We demonstrated that patients with metastatic PDAC with wild-type KRAS were younger (median 59.5 years) than those with mutated KRAS (median 67 years, p < 0.000055). The wild-type KRAS status was not a significant prognostic factor for metastatic disease. Molecularly, genes in the RAS pathway are frequently mutated or rearranged (46%, 16/35), including mutations in BRAF, NRAS, HRAS, EGFR, MAP2K1, FGFR1, FGFR3 and ERBB4 and fusions of FGFR2 (FGFR2::CCDC147, FGFR2::CAT, FGFR2::TXLNA), ALK (STRN::ALK, EML4::ALK), and BRAF (TRIP11::BRAF). Mismatch repair deficiency was identified in 10% (4/39) of patients. Potentially actionable alterations were identified frequently in KRAS wild-type PDACs (30%, 12/40), in which nontubular-type carcinomas were significantly enriched with actionable alterations compared with tubular adenocarcinomas [67% (6/9) versus 16% (5/31); p = 0.007]. Finally, we investigated the precursors of PDACs in 13 pancreatectomy specimens from patients with KRAS wild-type PDAC. We identified three pancreatic intraepithelial neoplasias (PanINs) and two intraductal papillary mucinous neoplasms (IPMNs) harboring oncogenic fusions of ALK and BRAF and driver mutations in BRAF and AKT1. This study suggests that in the context of unmutated KRAS, PDAC is driven by alternative oncogenic mutations or fusions of RAS pathway genes, which may be introduced during the early phase of tumorigenesis. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland. - Source: PubMed
Publication date: 2025/05/02
Toriyama KazuhiroMasago KatsuhiroShibata NorikoHaneda MasatakaKuwahara TakamichiNatsume SeijiKobayashi ShotaFujita YasukoSasaki EiichiYamao KenjiKawashima HirokiShimizu YasuhiroHara KazuoYatabe YasushiHosoda Waki - Risk stratification using multi-omics data deepens understanding of immunometabolism in successfully treated people with HIV (PWH) is inadequately explained. A personalized medicine approach integrating blood cell transcriptomics, plasma proteomics, and metabolomics is employed to identify the mechanisms of immunometabolic complications in prolonged treated PWH from the COCOMO cohort. Among the PWHs, 44% of PWH are at risk of experiencing immunometabolic complications identified using the network-based patient stratification method. Utilizing advanced machine learning techniques and a Bayesian classifier, five plasma protein biomarkers; Tubulin Folding Cofactor B (TBCB), Gamma-Glutamylcyclotransferase (GGCT), Taxilin Alpha (TXLNA), Pyridoxal Phosphate Binding Protein (PLPBP) and Large Tumor Suppressor Kinase 1 (LATS1) are identified as highly differentially abundant between healthy control (HC)-like and immunometabolically at-risk PWHs (all FDR<10). The personalized metabolic models predict metabolic perturbations, revealing disruptions in central carbon metabolic fluxes and host tryptophan metabolism in at-risk phenotype. Functional assays in primary cells and cortical forebrain organoids (FBOs) further validate this. Metabolic perturbations lead to persistent monocyte activation, thereby impairing their functions ex vivo. Furthermore, the chronic inflammatory plasma microenvironment contributes to synaptic dysregulation in FBOs. The endogenous plasma inflammatory microenvironment is responsible for chronic inflammation in treated immunometabolically complicated at-risk PWH who have a higher risk of cardiovascular and neuropsychiatric disorders. - Source: PubMed
Publication date: 2025/02/27
Mikaeloff FloraGelpi MarcoEscós AlejandraWang TianqiGupta SohamOlofsson AnnaAkusjärvi Sara SvenssonSchuster SabrinaNaval PrajaktaSood VikasNikouyan NeginKnudsen Andreas DVestad BeateHøgh JulieHov Johannes RBenfield ThomasTrøseid MariusPawar VinayRucevic MarijanaBenfeitas RuiVégvári ÁkosO'Mahony LiamSavai RajkumarBjörkström Niklas KLourda Magdade Magalhães João PedroWeiss SiegfriedMardinoglu AdilVarshney Mukesh KumarKarlsson Annika CSyed Yasir AhmedNielsen Susanne DNeogi Ujjwal - Conventional treatments, including surgery, radiotherapy and chemotherapy, have many limitations in the prognosis of glioma patients. Atorvastatin (ATOR) has a significant inhibitory effect on glioma malignancy. Thus, ATOR may play a key role in the search for new drugs for the effective treatment of gliomas. - Source: PubMed
Publication date: 2024/12/26
Gao KangZhou TaoYin YingChunSun XiaoJieJiang HePingLi TangYue - This study seeks to enhance the accuracy and efficiency of clinical diagnosis and therapeutic decision-making in hepatocellular carcinoma (HCC), as well as to optimize the assessment of immunotherapy response. - Source: PubMed
Publication date: 2024/06/12
Liu ZhiqiangYang LinggeLiu ChunWang ZichengXu WendiLu JueliangWang ChunmengXu Xundi