Ask about this productRelated genes to: PLCG1 antibody
- Gene:
- PLCG1 NIH gene
- Name:
- phospholipase C gamma 1
- Previous symbol:
- PLC1
- Synonyms:
- PLC148, PLC-II, PLCgamma1, NCKAP3
- Chromosome:
- 20q12
- Locus Type:
- gene with protein product
- Date approved:
- 1989-05-31
- Date modifiied:
- 2016-10-05
Related products to: PLCG1 antibody
Related articles to: PLCG1 antibody
- Adult T cell leukemia/lymphoma (ATL) is an aggressive T cell malignancy with poor prognosis. Recurrent genetic alterations in T cell receptor (TCR) signaling components, including , , and , highlight the biological relevance of this pathway in ATL. We focused on mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1), a key regulator of TCR signaling that functions through complex formation with CARD11 and BCL10, and developed a potent and selective MALT1 protease inhibitor, CRD-1441551. CRD-1441551 exhibited variable antitumor effects across ATL models both and . Among three ATL cell lines and five patient-derived xenograft models, two demonstrated marked sensitivity, three showed modest responses, and three were unresponsive. Notably, therapeutic responses were more frequently observed in models with constitutive MALT1 activation accompanied by enhanced MALT1-NF-κB signaling. These findings suggest that CRD-1441551 preferentially targets a subset of ATL, in which tumor growth is dependent on the MALT1-driven NF-κB pathway. - Source: PubMed
Publication date: 2026/07/23
Kamiunten AyakoMorishita DaisukeKameda TakuroSugiyama MidoriEbara ShunsukeKogure YasunoriMizutani AkioHirayama TakaharuKawamoto TomohiroOchi YotaroShide KotaroTokuhara HidekazuTanaka ToshioBanno HiroshiArikawa YasuyoshiMaru TakamitsuOki HideyukiYoda AkinoriTahira YukiIkeda RyomaMatsumoto KengoKarasawa MasayoshiAkizuki KeiichiSekine MasaakiShimoda HarukoHidaka TomonoriKubuki YokoYamaguchi HidekiHasegawa HirooImaizumi YoshitakaYasunaga Jun-IchirouMatsuoka MasaoYoshimitsu MakotoIshitsuka KenjiKataoka KeisukeOgawa SeishiShimoda Kazuya - Primary hepatic angiosarcoma (PHA) is the most common primary malignant mesenchymal tumour of the liver in adults, accounting for only 0.1-2% of all primary hepatic malignancies. It carries a median overall survival of 6-9 months, driven by aggressive biology, non-specific presentation, and almost universal late-stage diagnosis. No disease-specific tumour markers, pathognomonic imaging features, or PHA-exclusive prospective trials exist. - Source: PubMed
Publication date: 2026/07/31
Murshid MohsinNawawi Abrar - Acquired resistance to epidermal growth factor receptor (EGFR)-targeted therapies remain a major challenge in non-small cell lung cancer (NSCLC), particularly in patients with malignant pleural effusion (MPE). The MPE microenvironment, characterized by acidic, cytokine- and metabolite-rich conditions, promotes the emergence of osimertinib-tolerant persister cells (OTPCs), contributing to disease relapse. In this study, we investigated the role of MPE in driving OTPC formation and identified key molecular regulators underlying this adaptive phenotype. MPE samples from advanced EGFR-mutant NSCLC were used to generate OTPCs through coculture with PC9 and H1975 cell lines. In contrast, non-malignant pleural effusions induced only limited tolerance. Transcriptomic profiling revealed extensive reprogramming in OTPCs, with PLCG1 and RAC1 among the most significantly upregulated genes, enriched in pathways related to glycolysis, hypoxia, and epithelial-mesenchymal transition. Functional analyses demonstrated that OTPCs exhibit enhanced macropinocytosis, metabolic flexibility, and invasive capacity. Mechanistically, PLCG1 and RAC1 formed a co-dependent signaling network, as supported by reciprocal knockdown and protein interaction studies. Inhibition of PLCG1 significantly impaired both mitochondrial respiration and glycolytic activity, reduced mesenchymal marker expression, and decreased OTPC viability by >60%, thereby restoring sensitivity to osimertinib. In vivo, combined inhibition of EGFR and PLCG1 resulted in sustained tumor suppression and improved survival without detectable toxicity. Collectively, these findings identify a co-dependent PLCG1-RAC1 signaling network that integrates metabolic adaptation and phenotypic plasticity to sustain drug tolerance in MPE-associated NSCLC. Targeting this pathway represents a promising strategy to overcome resistance to EGFR-directed therapies. - Source: PubMed
Publication date: 2026/07/16
Tiong Tung-YuWang Chieh-YungChen YingLin Yi-HsuanChangchien Chih-YingChian Chih-FengTsai Chen-Liang - The gut-joint axis has been increasingly implicated in osteoarthritis (OA), yet the causal contribution of specific gut microbes and their downstream molecular mechanisms remain unclear. We employed a multi-stage, two-sample Mendelian randomization (MR) framework. This approach utilized summary-level data from large-scale genome-wide association studies (GWAS) for gut microbiota, plasma proteins, and OA. The analysis involved three steps: (1) identifying gut microbial taxa with potential causal associations with OA risk; (2) screening of pyroptosis-related proteins using pQTL data; and (3) performing mediation analysis to evaluate potential intermediate mechanisms. We also performed transcriptomic analysis of human cartilage and in vitro experiments in chondrocytes to support the biological relevance of our findings. Our MR analysis identified Gordonibacter pamelaeae as a suggestive microbial taxon inversely associated with OA risk. Among 11 candidate pyroptosis-related proteins, only Phospholipase C Gamma 1 (PLCG1) showed a significant inverse association with OA. MR analysis further suggested that G. pamelaeae was positively associated with genetically predicted PLCG1 levels. Mediation analysis indicated that PLCG1 partially mediated the association between G. pamelaeae and OA. Consistent with these findings, PLCG1 mRNA levels were reduced in human OA cartilage. Furthermore, our in vitro experiments demonstrated that PLCG1 knockdown enhanced IL-1β-induced inflammatory and pyroptotic responses in chondrocytes. This study suggests a potential link involving gut microbiota and OA through PLCG1-related signaling. PLCG1 may act as a context-dependent regulator that limits excessive inflammatory responses under stress conditions. These findings refine the current understanding of the gut-joint axis and may help identify potential targets for OA intervention. - Source: PubMed
Publication date: 2026/07/03
Li ShengkunZhong ShaoziZeng Chun - 1. Calcium (Ca) is essential for avian embryonic bone mineralisation, yet its metabolic dynamics during duck embryogenesis remain unclear. This study investigated Ca mobilisation in Muscovy duck embryos.2. Eggshell (ES) and yolk samples were collected from embryonic day (ED) 16 to ED31 for analysis of ES physical properties (thickness, strength, mass ratio) and Ca levels. Serum, yolk sac membrane (YSM) and liver tissues were collected from ED16 to the day of hatch (DOH) to assess serum biochemical parameters and relative mRNA expression of genes associated with Ca transport (, , ) and absorption (, , ).3. Results showed ES quality and Ca levels decreased ( < 0.01) linearly with increasing incubation days. Yolk Ca levels decreased ( < 0.01) linearly and quadratically, reaching a minimum on ED25. Serum Ca levels and alkaline phosphatase (ALP) activity increased ( < 0.01) linearly and quadratically during ED16-DOH and achieved a plateau during ED28-DOH. Expression of Ca-related genes in YSM and liver increased quadratically ( < 0.01), peaking during ED25-28.4. In conclusion, ES quality declined with reduced Ca levels during embryogenesis. Concurrently, yolk Ca levels, along with serum Ca and ALP levels, increased significantly during ED25-28, indicating peak embryonic Ca mobilisation during this period. Additionally, relative mRNA expression of Ca mobilisation-related genes in the YSM and liver exhibited a similar increasing trend. This suggested enhanced Ca mobilisation during this phase to support bone mineralisation and growth in duck embryos. - Source: PubMed
Publication date: 2026/06/24
Wang XRen YHu QWu QSun GChen HLin JLiu SWang WQin JZhu Y