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
- Osteoblast dysfunction and altered Wnt/β-catenin-dependent responses accompany bone-remodeling imbalance in rheumatic and degenerative joint disease. Rosavin and salidroside are constituents of Rhodiola rosea preparations used without prescription, and are always encountered together rather than separately. This exploratory in vitro study asked whether the two compounds and their combination differentially affect total β-catenin concentration and cell-covered area in human osteoblasts (HOBs). HOBs from one commercial preparation (passage 7) were cultured in growth medium (GM) or mineralization medium (MM) and exposed to rosavin 50 µM (R50), salidroside 50 µM (Sal50) or both (R50/Sal50). Total β-catenin was quantified by ELISA in four independently cultured, treated, harvested and lysed wells per condition at days 7, 14 and 21. Cell-covered area was estimated from 79 phase-contrast fields. Welch ANOVA with Games-Howell post-hoc testing was pre-specified. Total β-catenin differed between conditions at day 14 (Welch ANOVA p = 0.003, Holm-adjusted p = 0.009; η² = 0.43): 8.9 ± 3.8 ng/mL in R50 versus 28.5 ± 3.8 in Sal50, 26.5 ± 16.9 in R50/Sal50, 23.5 ± 7.9 in MM and 27.4 ± 8.6 in GM. Sal50 versus R50 was the only contrast surviving correction (difference 19.6 ng/mL, 95% CI 13.1-26.1; p = 0.002). No difference was detected at day 7 (p = 0.87) or day 21 (p = 0.23). Cell-covered area differed at days 7 and 21, with R50/Sal50 lowest and most variable (54.5 ± 23.4% versus 98.1 ± 1.8% in GM at day 7). Cell-covered area explained 12% of the variance in group-mean β-catenin (r = - 0.35). Rosavin alone was associated with a marked reduction in total β-catenin at day 14; its combination with salidroside was not. The two constituents therefore do not act interchangeably on human osteoblasts. These observations derive from a single experimental series and require replication before mechanistic or clinical interpretation. - Source: PubMed
Publication date: 2026/08/17
Wojdasiewicz PiotrWróbel EdytaMaślińska MariaTurczyn PawełStolarczyk Elżbieta UStolarczyk KrzysztofMikulska AgnieszkaSzukiewicz Dariusz - Postpartum depression (PPD) is a prevalent psychological condition among birthing women. While several psycho-socio-economic and neurobiological factors influence its development, its relationship with smoking behavior and nicotine addiction remains largely inconclusive. - Source: PubMed
Publication date: 2026/08/17
Abedin FarheenaraDas MadhuparnaBishayi AratrikaSaha ParnaHusna AsmaulHaque ShafiulRana Sandeep SinghSudesh RaviAhmad Faraz - Craniopharyngiomas are benign sellar and parasellar tumors that present significant clinical challenge because of their close proximity to the optic apparatus, hypothalamus, and pituitary gland. Recent molecular studies have identified distinct driver mutations, namely, CTNNB1 in adamantinomatous craniopharyngiomas and BRAF V600E in papillary craniopharyngiomas, leading to a deeper understanding of tumor biology and treatment strategies. Advances in endoscopic endonasal transsphenoidal surgery have improved surgical safety and expanded the indications for minimally invasive resection, whereas radiotherapy remains an effective option for residual or recurrent disease. Molecular targeted therapy with BRAF and MEK inhibitors has resulted in remarkable tumor shrinkage in papillary craniopharyngiomas harboring the BRAF V600E mutation, and recent clinical studies have established this approach as a promising treatment option. These agents have emerged not only as effective treatment options for recurrent or refractory disease but also as promising options for neoadjuvant treatment and function-preserving management. Future treatment strategies are likely to incorporate molecular subtypes, patient age, and functional outcomes to achieve individualized care. In addition, the development of reliable preoperative molecular diagnostic techniques, including liquid biopsy, may further facilitate the integration of targeted therapies into routine clinical practice. - Source: PubMed
Fujio ShingoHanaya Ryosuke - CTNNB1-related neurodevelopmental disorder with spastic diplegia and visual defect (NEDSDV) is a rare genetic condition characterized by developmental delay, axial hypotonia, peripheral spasticity, and ophthalmologic abnormalities. Due to its phenotypic overlap with bilateral spastic cerebral palsy, NEDSDV may be underdiagnosed, and its anesthetic implications remain undocumented. We report the perioperative management of a two-year-old female with NEDSDV undergoing elective adenoidectomy and myringotomy in a hospital-based ambulatory surgical center. Anesthetic care was individualized, with emphasis on airway planning, cautious titration of anesthetic agents, and multimodal opioid-sparing analgesia. The perioperative course was uneventful, and the patient was safely discharged on the same day. Following a comprehensive literature review, no prior anesthetic reports were identified in patients with NEDSDV. To our knowledge, this case represents one of the first published anesthetic descriptions in a pediatric patient with NEDSDV and highlights key considerations for safe and effective anesthesia in this emerging clinical population. - Source: PubMed
Publication date: 2026/07/15
Rocha Ana RitaCardante Santos ConceiçãoAlves PetraPeixoto Gomes Cristina - Histone deacetylase 1 (HDAC1) is frequently dysregulated in various human malignancies; however, the molecular mechanisms underlying its role in non‑small cell lung cancer (NSCLC) remain unclear. HDAC1 expression was evaluated in 157 paired lung adenocarcinoma (LUAD) and adjacent non‑neoplastic tissues using tissue microarray and immunohistochemical analysis. The functional role of HDAC1 was assessed in A549, H1299 and H1975 NSCLC cells following stable knockdown or overexpression, using Cell Counting Kit‑8, colony formation and Transwell assays. Downstream signaling was examined by western blotting and nuclear‑cytoplasmic fractionation. Rescue experiments were performed by overexpressing β‑catenin in HDAC1‑knockdown cells and the findings were further validated in a subcutaneous xenograft tumor model in nude mice. HDAC1 was markedly upregulated in LUAD tissues and associated with lymph node metastasis and poor differentiation. Functionally, HDAC1 knockdown inhibited proliferation, colony formation, migration and invasion in all three NSCLC cell lines. These effects were accompanied by downregulation of c‑Myc, cyclin D1 and vimentin, upregulation of E‑cadherin and reduced nuclear β‑catenin accumulation. Conversely, HDAC1 overexpression enhanced malignant phenotypes and promoted β‑catenin nuclear accumulation. Notably, the phosphorylation of AKT (Thr308 and Ser473) and ERK1/2 remained unaltered following HDAC1 modulation. β‑catenin overexpression effectively eliminated the tumor‑suppressive effects of HDAC1 knockdown both and . These findings indicated that HDAC1 is a critical promoter of LUAD progression, acting at least in part through β‑catenin nuclear accumulation. This provided a mechanistic rationale for targeting the HDAC1/β‑catenin axis as a potential epigenetic therapeutic strategy in LUAD. - Source: PubMed
Publication date: 2026/08/14
Xu ShijieChang XiaoluWu XiayuWang FabaoXiang JingLin ChaoxiangZhao HeLi JunzheXu Xianhua