AXIN1 Antibody
- Known as:
- AXIN1 Antibody
- Catalog number:
- AF1130a
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- AXIN1 Antibody
Related genes to: AXIN1 Antibody
- Gene:
- AXIN1 NIH gene
- Name:
- axin 1
- Previous symbol:
- -
- Synonyms:
- PPP1R49
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-17
- Date modifiied:
- 2015-08-24
Related products to: AXIN1 Antibody
Related articles to: AXIN1 Antibody
- Hepatocellular carcinoma (HCC) is a genomically diverse disease, and molecular classification is essential for understanding its biology and improving patient care. Here, integrative analyses of 529 HCC samples across genomic, transcriptomic, epigenomic, and proteomic layers identify nine robust molecular subtypes, validated in 807 external cases. Three common subtypes are defined by alterations in CTNNB1/APC (25%), TP53 (21%), and AXIN1/IRF2 (11%), while four rare subtypes involve TP53+CTNNB1 (6%), BAP1 (6%), CCNA2/E1 (6%), and HNF1A (1%). Two additional immune-related subtypes, U (17%) and U (8%), have undetermined drivers. Using transcriptomic scores, we demonstrate that AXIN1 and TP53 mutations increase β-catenin activity and reduce p53 activity, whereas BAP1 loss functionally inactivates TP53. The rare TP53+CTNNB1 subtype is highly aggressive, associated with poorer outcomes, exhibiting features of both CTNNB1 and TP53-mutated HCC, with TP53 mutation occurring prior to CTNNB1 alteration. The refined molecular classification provides a clinically relevant framework for precision medicine in HCC. - Source: PubMed
Publication date: 2026/05/19
Pan LongHirsch Théo ZFang JingSeretny AgnieszkaImbeaud SandrineJin ShuoshuoGege Olatunji OluwoleRebouissou SandraSidali SabrinaAmmiche NaïmaCalderaro JulienAmaddeo GiulianaBlanc Jean-FrédéricLe Bail BrigitteZiol MarianneCelton-Morizur SéverineParadis ValérieLlovet Josep MTschaharganeh Darjus FelixNault Jean-CharlesDesdouets ChantalCaruso StefanoZucman-Rossi Jessica - Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal interstitial lung disease characterized by an abnormal epithelial‒mesenchymal transition (EMT) and fibroblast activation, although the molecular mechanisms driving these processes remain unclear. Here, we report that the expression of CCAAT enhancer binding protein γ (C/EBPγ), a transcription factor, is significantly upregulated in lung tissues from patients with IPF and the lungs of mice with bleomycin-induced fibrosis. In A549 epithelial cells, C/EBPγ overexpression promoted the EMT, as indicated by decreased E-cadherin expression and increased N-cadherin and vimentin expression. In MRC-5 fibroblasts, C/EBPγ overexpression increased cell migration and upregulated the expression of fibrotic markers, including collagen I, fibronectin, and α-SMA. Mechanistically, C/EBPγ activated the β-catenin pathway by stabilizing β-catenin through the transcriptional repression of AXIN1, a key component of the degradation complex. This repression occurred via an interaction with C/EBPα, antagonizing its promotion of AXIN1 expression, as confirmed by ChIP‒qPCR, luciferase assays, coimmunoprecipitation, immunofluorescence staining, and rescue experiments. In vivo, adeno-associated virus-mediated C/EBPγ overexpression aggravated bleomycin-induced pulmonary fibrosis in mice, increasing collagen deposition, inflammation, and β-catenin expression, whereas C/EBPγ knockdown alleviated these changes. Collectively, these findings suggest that the downregulation of C/EBPγ expression attenuates fibrosis progression through the C/EBPα-AXIN1-β-catenin axis, underscoring its involvement in β-catenin pathway regulation and advancing the understanding of IPF pathogenesis. - Source: PubMed
Publication date: 2026/05/16
Pan XiaoyueXia CongGan YulongCao YingZhao ManLiu HuibingZhou YanlinWang YuqiLi ZhongzhengLi BinWang LanYu Guoying - Simian immunodeficiency viruses (SIVs) have crossed from apes to humans at least four times, but only one event gave rise to the AIDS pandemic. The host barriers that pandemic HIV-1 group M () strains overcame to spread efficiently in humans remain poorly understood. To identify such barriers, we performed CRISPR-Cas9 screens driven by the replication efficiency of SIVcpz, the chimpanzee precursor of HIV-1. Guide RNA libraries targeting more than 500 human genes encoding potential antiviral factors were inserted into the replication-competent SIVcpz MB897 molecular clone, which is phylogenetically closely related to HIV-1 group M strains. Propagation in Cas9-expressing human SupT1 T cells significantly enriched for sgRNAs targeting and . These hits only partially overlapped with those identified in analogous HIV-1-based screens, indicating virus-specific restriction profiles. Functional analyses confirmed that IFITM2 (interferon-induced transmembrane protein 2), PCED1B (PC-esterase domain-containing protein 1B), MEFV (Mediterranean fever protein, pyrin/TRIM20), and AXIN1 (Axis inhibition protein 1) restrict replication of the analyzed SIVcpz strains but not HIV-1 group M strains in primary human CD4 T cells. These findings reveal previously unrecognized host factors that limit SIVcpz replication in human cells and highlight barriers that at least some HIV-1 group M strains overcame during adaptation for pandemic spread. - Source: PubMed
Publication date: 2026/05/07
Xie QinyaWang QingxingNoettger SabrinaGosálbez GuillermoBetzler Annika CVolcic MetaKmiec DorotaKrebs StefanGraf AlexanderGülensoy DilaWeidinger GilbertSparrer Konstantin M JKirchhoff Frank - Nasopharyngeal carcinoma (NPC) is a malignancy associated with genetic alterations and tumor progression. Cadherin genes (CDH1, CDH2, and CDH3) play key roles in cell adhesion, migration, and tissue integrity, and their role in NPC remains underexplored. This study investigates the expression, mutation patterns, and prognostic significance of cadherin genes in NPC. - Source: PubMed
Publication date: 2026/04/28
Yao WenfengQin LitaoLi QianSun ZhanweiWang Guangke - The incidence and mortality of colorectal carcinoma (CRC) continue to rise globally, highlighting the need to identify modifiable risk factors for early detection and prevention. Previous studies have demonstrated significant associations between CRC risk and various serum metabolites as well as inflammatory cytokines; however, due to limitations in study design and potential confounding factors, the causal relationships remain unclear. This study aims to investigate the causal relationships between inflammatory cytokines, serum metabolites, and CRC risk, providing a theoretical basis for the development of novel early diagnostic biomarkers and therapeutic targets. - Source: PubMed
Feng SisiXiao XiaominZhou ManliHuang ZixinZhong Baiyun