Ask about this productRelated genes to: PLCG2 antibody
- Gene:
- PLCG2 NIH gene
- Name:
- phospholipase C gamma 2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-16
- Date modifiied:
- 2019-04-23
Related products to: PLCG2 antibody
Related articles to: PLCG2 antibody
- Chronic lymphocytic leukemia (CLL) is a paradigmatic malignancy driven by intraclonal diversity and dynamic evolutionary processes. High-resolution genomic profiling has demonstrated that CLL progression rarely follows a linear trajectory; rather, it is characterized by a complex and evolving (sub)clonal architecture shaped by intrinsic biological features and extrinsic factors, including therapeutic pressure. Recurrent genetic alterations affect key signaling pathways and cellular processes, including B-cell receptor and NF-κB signaling, DNA damage response, RNA processing, and apoptosis. Many of these lesions arise as subclonal events and subsequently expand, thereby influencing disease progression, therapeutic resistance, and transformation. Over the past decade, the treatment paradigm in CLL has shifted from chemoimmunotherapy to targeted agents, resulting in substantial clinical benefit. Nevertheless, the emergence of therapeutic resistance remains a major challenge. In this review, we summarize current knowledge of clonal evolution and resistance mechanisms in CLL. Resistance to chemoimmunotherapy is frequently driven by genetic lesions, such as TP53 aberrations, and by expansion of resistant microclones. In contrast, targeted therapies select for distinct resistance mechanisms, such as BTK and PLCG2 mutations in patients treated with BTK inhibitors, as well as activation of alternative survival pathways. We further discuss emerging technologies, including single-cell sequencing and integrative multi-omics approaches. Finally, we highlight the need for future studies addressing resistance in evolving clinical contexts, such as combination targeted therapies, bispecific antibodies, and CAR T-cell therapy. Taken together, a deeper understanding of clonal evolution is central to the development of personalized therapeutic strategies and to improving long-term outcomes for patients with CLL. - Source: PubMed
Publication date: 2026/04/17
Mansouri LarryChatzikonstantinou ThomasScarfò LydiaRosenquist Richard - - Source: PubMed
Publication date: 2026/04/15
Hong DandanDai JialinZhou Xinyi - Nonalcoholic fatty liver disease (NAFLD) is a major clinical challenge and a growing global public health burden, yet no pharmacological therapy specific to this disease has been approved to date. Notably, Astragalus membranaceus (Huangqi, HQ) is incorporated into approximately 80% of multi-herb formulations employed for treating liver diseases. Fuzhuan brick tea, a distinctive Chinese fermented tea, is widely recognized for its unique fermentation process and hypolipidemic properties. However, whether co-fermentation with HQ enhances its lipid-lowering efficacy against NAFLD remains unexplored and unreported. - Source: PubMed
Publication date: 2026/03/31
Chen TingYang ShusenZhang XinyueChen JuanYang XinkeLi ChengjunYang MingjieLi JingtaoJi XumingYan Shuguang - We developed a high content screening to investigate how Alzheimer disease (AD) genetic risk factors may affect synaptic mechanisms in rat primary neuronal cultures. Out of the target genes identified, we found that downregulation in mouse dentate gyrus neurons consistently disrupted dendritic morphology and synaptic function. In human neuronal cultures (hNCs), downregulation also impaired synaptic function and increased Aβ levels and Tau phosphorylation. Very rare loss-of-function (LoF) variants were associated with a 10-fold increased AD risk. LoF carriers exhibit low mRNA/protein /PLCγ2 levels and the R953* LoF mutation compromised synaptic function and increased AD hallmarks in hNCs. Single nuclei RNAseq analyses confirmed that the downregulation of impacted pathways related to synaptic and neuronal functions, potentially through neurexin in neurons. In conclusion, PLCγ2 downregulation could increase AD risk by impairing synaptic functions and increasing the Aβ levels and Tau phosphorylation in neurons. - Source: PubMed
Publication date: 2026/03/27
Coulon AudreyRabiller FlorianTakalo MariRoy AvishekPelletier AlexandreMartiskainen HennaSiedlecki-Wullich DoloresLannette-Weimann NinaMajerníková Nad'aGrenon ArthurGao VanceErhardt AnaëlPernodet AnneLemaire MorganeLimoge FlorianeWalle PaulineMendes TiagoGuyot KarineLemeu CéliaCarvalho Lukas-Iohande Farias Ana Raquel MeloHulsman MarcNajdek ChloéFreire-Regatillo AlejandraSaha OrthisAmouyel PhilippeCharbonnier CamilleDeleuze Jean-FrançoisDols-Icardo OrioJeskanen HeliWillman Roosa-MariaKuulasmaa TeemuKurki MitjaHardy JohnHeikkinen SamiHolstege HenneMäkinen PetraNicolas GaëlMead SimonWagner MichaelRamirez AlfredoRauramaa TuomasPalotie AarnoSims RebeccaSoininen Hilkkavan Swieten JohnWilliams JulieBellenguez CélineGelle CarlaLambert ErwanCosta Marcos RTcw JuliaGlaab EnricoAyral Anne-MarieDemiautte FlorieGrenier-Boley BenjaminMuntaner ManonEberlé DelphineDeforges SéverineHaas JoelKilinc DevrimMulle ChristopheChapuis JulienHiltunen MikkoDumont JulieLambert Jean-Charles - Bisphenol A (BPA) is a widely used endocrine-disrupting chemical that has been implicated in neurodevelopmental and psychiatric disorders; however, the molecular mechanisms linking BPA exposure to major depressive disorder (MDD) remain poorly understood. In this study, we systematically investigated the potential toxicological effects of BPA on MDD by integrating network toxicology, summary-data-based Mendelian randomization (SMR), single-cell RNA sequencing (scRNA-seq), molecular docking, and experimental validation. BPA-related targets were collected from multiple databases and intersected with MDD-associated genes, followed by functional enrichment analyses and construction of a protein-protein interaction network to identify core targets. Causal relationships between candidate targets and MDD were assessed using SMR analysis based on genome-wide association study (GWAS) and expression quantitative trait loci (eQTL) data. Cell-type-specific expression patterns were examined using scRNA-seq data from MDD patients, while molecular docking was employed to evaluate the binding affinities between BPA and core target proteins. Differential expression of key targets was further validated using public bulk RNA-seq datasets, Enzyme-Linked Immunosorbent Assay (ELISA), and BPA exposure were further confirmed via quantitative real-time PCR (qRT-PCR) in BPA-induced MDD mouse models, together with behavioral assessments. A total of 571 shared targets between BPA and MDD were identified, enriched in pathways related to neurodevelopment, synaptic plasticity, and cognitive function. Six core targets (ESR1, SRC, EGFR, AKT1, PLCG2, and JAK3) were highlighted. MR and SMR analyses supported causal roles for AKT1, SRC, PLCG2, and JAK3 in MDD, whereas EGFR exhibited a protective effect. These findings provide integrative evidence for molecular mechanisms underlying BPA-associated susceptibility to MDD and identify potential targets for future therapeutic intervention. - Source: PubMed
Publication date: 2026/03/30
Lu ZhenbinShi Wenhan