a_catenin (Phospho_Ser641) antibody
- Known as:
- a_catenin (Phospho_Ser641) (anti-)
- Catalog number:
- E011330-2
- Product Quantity:
- 100ug
- Category:
- -
- Supplier:
- EnoGene
- Gene target:
- a_catenin (Phospho_Ser641) antibody
Related products to: a_catenin (Phospho_Ser641) antibody
Related articles to: a_catenin (Phospho_Ser641) antibody
- Melanotic neuroectodermal tumour of infancy is primarily treated by complete surgical excision; however, recurrence rates range from 20% to 25%. Recurrent lesions often exhibit more aggressive behaviour, which complicates surgical management and may preclude radical resection, thereby necessitating the use of adjuvant therapies. The limited molecular characterization of MNTI has impeded the development of targeted therapeutic strategies, particularly for aggressive or recurrent cases. Given the biological similarities between MNTI and melanoma - both of which arise from neural crest-derived cells and demonstrate melanin production - it is plausible that MNTI may harbour oncogenic alterations commonly observed in melanoma, such as the BRAFV600E mutation. Furthermore, mutations in CTNNB1, which have been associated with aggressive behaviour in certain melanoma subtypes, may also contribute to the tumour biology of MNTI. Therefore, the present study aims to evaluate key molecular alterations in MNTI using immunohistochemical analysis. - Source: PubMed
Publication date: 2026/05/20
N SivakumarTrimukhe AkshayJot KiranKaur SharanjeetSurya VarunMishra DeepikaNayyar Vivek - Our previous research has shown that lipopolysaccharide (LPS) derived from Gram-negative bacteria in the intestine promoted rheumatoid arthritis (RA) after entering peripheral blood, but the specific molecular mechanism was unclear. - Source: PubMed
Publication date: 2026/07/03
Wang BingSong YingqiuXu WenboChen JiaqingHuang YurongZhou XinyueCai YikangXia AixinLi YanpingJiang LiweiLiao FaxueHuang JianMiao Chenggui - The β-catenin destruction complex (BDC) regulates WNT-β-catenin signaling and is a prime therapeutic target in colorectal cancer, yet its biochemical complexity has hindered mechanistic understanding. We mapped the sequence-function landscape of the BDC using tiled base editor screens across its components CTNNB1, AXIN1, APC and GSK3B. Amongst ~150 previously unreported mutations that affected WNT signaling, we discovered gain-of-function and separation-of-function alleles that reveal mechanisms of complex assembly, including a β-catenin region regulating TCF/LEF transcription factor binding. Critically, we found that the AXIN1-β-catenin interface controls signaling flux through the oncogenic BDC found in APC-mutant cancers. In cells expressing truncated APC, β-catenin itself scaffolds BDC assembly, establishing a substrate-assisted autoregulatory mechanism. This architecture represents an unexploited therapeutic vulnerability: strengthening the AXIN1-β-catenin interaction restores destruction complex function and impairs the growth of colorectal cancer cells. Our mutational resource provides a foundation for mechanistic understanding and therapeutic targeting of the WNT pathway. - Source: PubMed
Publication date: 2026/07/02
Padmanarayana MurugeshSakalas SairaSarkar ParijatMa MengxiaoGarvin Ethan RLee EthanCorsello Steven MGuettler SebastianPusapati Ganesh VRohatgi Rajat - We generated two mouse models, p21 and p21, expressing either telomerase reverse transcriptase (Tert) or a catalytically inactive variant under the control of the p21 promoter. By 18-20 mo of age, ∼15% of mice from both genotypes developed liver tumors with histopathological features resembling human hepatocellular carcinoma (HCC). Whole-exome sequencing identified activating Ctnnb1 mutations and recurrent PP1 subunit alterations in p21 tumors, whereas p21 tumors harbored activating Hras mutations associated with elevated C > A transversions. Both models exhibited chromosomal aberrations commonly observed in human HCC. Transcriptomic analyses revealed that β-catenin-activated tumors recapitulated gene expression signatures of human HCC, whereas MAPK-mutated tumors showed profiles consistent with MAPK/ERK pathway activation. All HCCs suppressed the gluconeogenic genes and , but diverged into two distinct groups based on their glycolytic and target gene expression profiles. Spatial profiling further revealed reduced HNF4α-positive hepatocytes across tumors, independent of HNF4α transcription, and markedly diminished immune cell infiltration, particularly in β-catenin-activated tumors. Collectively, these findings uncover telomere-independent functions of Tert and identify molecular and metabolic features with potential relevance for predicting immunotherapy response. - Source: PubMed
Publication date: 2026/07/02
Braud LauraVernerey JulienGuille ArnaudCordier PierreGinet ClémenceEgger TomBernabe ManuelChurikov DmitriDa Costa QuentinMeghraoui AïdaDesdouets ChantalGu LiBertucci FrançoisLachaud ChristopheGéli Vincent - Rare or compound EGFR variants in non-small cell lung cancer (NSCLC) can create substantial therapeutic uncertainty, particularly when accompanied by additional co-alterations with potential resistance implications. In such settings, molecular tumor boards (MTBs) may integrate genomic, functional, and clinical data to guide treatment selection. - Source: PubMed
Publication date: 2026/07/02
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