Ctnnb1
- Known as:
- Ctnnb1
- Catalog number:
- 060587A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Ctnnb1
Related genes to: Ctnnb1
- Gene:
- CTNNB1 NIH gene
- Name:
- catenin beta 1
- Previous symbol:
- CTNNB
- Synonyms:
- beta-catenin, armadillo
- Chromosome:
- 3p22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-13
- Date modifiied:
- 2019-04-23
Related products to: Ctnnb1
ACTN4 & CTNNB1 Protein Protein Interaction Antibody PairACTN4 & CTNNB1 Protein Protein Interaction Antibody Pair pairsAnserine Catenin, Beta Elisa Kit (CTNNb1)Anserine anti - Catenin, Beta Elisa Kit (CTNNb1)anti-CTNNB1 Beta Catenin (4D5)anti-CTNNB1 Beta Catenin (4D5) type: Primary antibodies host: Mouseanti-CTNNB1 Beta Catenin (EM-22)anti-CTNNB1 Beta Catenin (EM-22) type: Primary antibodies host: Mouseanti-CTNNB1 (4D5)Anti-CTNNB1 (4D5), Mouse Monoclonal to CTNNB1, Isotype IgG1, Host MouseAnti-CTNNB1 (EM-22), Mouse Monoclonal to CTNNB1, Isotype IgG1, Host Mouseanti-CTNNB1 / Beta Catenin (4D5)anti-CTNNB1 / Beta Catenin (EM-22)Anti-CTNNB1, Rabbit Polyclonal to CTNNB1, Isotype , Host RabbitAnti-CTNNB1, Rabbit Polyclonal to CTNNB1, Isotype IgG, Host Rabbit Related articles to: Ctnnb1
- Age-related macular degeneration (AMD) is a common degenerative eye disease that eventually leads to irreversible vision loss. CircRNAs have received increasing attention for their regulatory role in AMD. In this study, whole transcriptome sequencing identified differentially expressed circRNA (circMETTL3) in AMD. Previous studies have unlocked the potential mechanism of circMETTL3 in cancer, but its role in AMD has not been studied. - Source: PubMed
Publication date: 2026/08/20
Xin XiangyangZhao XinLing FengQin LiruLiu XinyueLiu Changhe - Chronic exposure to the widely used organophosphate pesticide chlorpyrifos has been associated with reproductive dysfunction; however, the early subclinical events preceding overt reproductive dysfunction remain poorly understood due to cell-specific and non-monotonic responses to the toxicant. The present study investigated the effect of chronic CPF exposure on the spermatogenic niche and sperm epigenome in a mouse model. Despite the absence of detectable oxidative stress or reproductive toxicity, chronic CPF exposure induced significant changes in the testicular microenvironment. Testicular proteomic analysis revealed dysregulated expression of proteins involved in extracellular matrix remodeling in CPF-exposed mice. These changes were associated with increased expression of Ctnnb1 and Axin1 indicating modulation of β-catenin-associated signaling in the testis. Furthermore, CPF exposure was associated with dysregulation of Sertoli cell function characterized by a significant reduction in Kitlg expression, increased c-kit levels, and reduced expression of the gap junction protein Connexin 43. CPF exposure also led to a significant dose-dependent increase in the expression of Tet1 suggesting altered epigenetic regulation in the testis. Interestingly, there was a trend toward increased sperm DNA methylation in CPF-exposed mice. Overall, these findings reveal that chronic CPF exposure induces early remodeling of the spermatogenic niche and alters testicular epigenetic regulation prior to overt reproductive dysfunction, identifying the Sertoli cell-extracellular matrix axis as a potential early target underlying CPF-induced testicular toxicity. - Source: PubMed
Publication date: 2026/08/20
Mansukhani MeenakshiTasneem RuqaiyaSen Sharma Souvik - Exercise-related genes (ERGs) have emerged as potential modulators of tumor biology, yet their systematic characterization in hepatocellular carcinoma (HCC) remains incomplete. Here we integrated 320 ERGs from MSigDB with TCGA-HCC cohort to construct an interaction-perturbation network, identifying two distinct subtypes with divergent prognostic outcomes. Cluster1 (44.4% of patients) exhibited significantly higher network perturbation scores, activated proliferation and epithelial-mesenchymal transition pathways, and elevated immune checkpoint gene expression, collectively contributing to poorer survival. This subtype also demonstrated enhanced immune evasion potential and lower predicted immunotherapy response rates. Conversely, Cluster2 (55.6%) was characterized by metabolic pathway enrichment, increased CTNNB1 mutations, higher tumor mutational burden, and more favorable immunotherapy prediction. Notably, integrated analysis of intratumoral microbiota revealed that Streptomyces abundance was significantly associated with immune exclusion features and negatively correlated with both exercise-related and lactate metabolic pathways. Mediation analysis further suggested that elevated lactate metabolism was statistically associated with adaptive microbial changes, which in turn showed directional associations with exercise-related pathway activity and clinical outcomes. Using Streptomyces-associated host genes, we developed an 8-gene prognostic signature that effectively stratified patient outcomes and predicted immunotherapy response across multiple independent cohorts. Our findings delineate exercise-related molecular subtypes with distinct immune-microbiota-metabolic crosstalk and provide a clinically applicable signature for risk stratification in HCC. - Source: PubMed
Publication date: 2026/08/20
Zhao XiaotingHe YuZhang YibinLiu DapengWang YingweiWang ZuopengHuang Yudiao - Conventional therapies for inflammatory bowel disease (IBD) are associated with significant adverse effects, highlighting the need for safer and effective alternatives. Krill oil (KO), a rich source of long-chain omega-3 polyunsaturated fatty acids (PUFAs) and astaxanthin, has shown therapeutic potential in several disorders but remains understudied in chronic colitis. This study evaluates the potential therapeutic efficacy of KO, alone or in combination with dexamethasone (DEX), in a spontaneous chronic colitis mouse model that closely mimics human IBD. The molecular mechanisms underlying the health benefits of KO were also explored. - Source: PubMed
Publication date: 2026/08/04
Liu YingyingRobinson Ainsley MNurgali KulmiraSu Xiao Qun - BRAF-mutant colorectal cancer (CRC) is a clinically aggressive subtype arising from the serrated pathway and is associated with poor prognosis and therapy resistance. The mechanisms driving malignant transformation in microsatellite-stable (MSS) BRAF-mutant CRC remain incompletely understood. We aimed to define the role of WNT pathway activation in serrated CRC progression and tumor-immune interactions. - Source: PubMed
Publication date: 2026/08/18
Mastel ManuelGuiseris Martinez AitanaPozza UmbertoMeier JasminChiotakakos IoannisJaun SandraArtmann CarolinDiamante GabrieleGeorgakopoulos NikolaosAlbrecht PhilippPetersen YvonneReuter SaskiaSchmitt BarbaraGünther MichaelThiran AlexandraNurfauziah IstiffaGhezzi IanOuyang Kyanna SMilsom Michael DPuschhof JensReitsam Nic GBoonekamp Kim EBetge JohannesOrmanns SteffenBoutros MichaelJackstadt Rene