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
- - Source: PubMed
Publication date: 2026/04/23
Heslin GraceLeiter Sarah MShahipasand ShahabLong Anna-MayGattens MichaelSebire NeilSolman LeaTrotman JamieHook C ElizabethBehjati Sam - Gastric cancer (GC) remains one of the most prevalent and lethal malignancies worldwide. Natural flavonoids are increasingly recognized for their therapeutic potential due to their multi-target actions and favourable safety profiles. Morin, a dietary flavonol found in several plants of the Rosaceae, Moraceae, and Fagaceae families, has not been well explored in GC. In this study, network pharmacology analysis identified ten major morin-associated hub genes (PIK3R3, PIK3CA, PIK3CB, PIK3CD, PIK3R2, PLCG1, JAK2, IGF1R, ZAP70, and ERBB4), several of which are key regulators of the PI3K-Akt signalling axis. Molecular docking showed strong binding affinities of morin toward PIK3CD (-11.01 kcal/mol), ZAP70 (-10.72 kcal/mol), JAK2 (-10.53 kcal/mol), IGF1R (-9.99 kcal/mol), PIK3CA (-9.79 kcal/mol), and ERBB4 (-8.83 kcal/mol). Molecular dynamics simulations of 500 ns, along with PCA, DCCM, FEL, and MM-GBSA analyses further confirmed stable interaction of morin with PIK3CA. In vitro, morin demonstrated selective cytotoxicity, with low IC values in AGS (15.16 ± 0.02 μM) and NCI-N87 (15.85 ± 0.8 μM) GC cells, compared to a significantly higher IC in normal MCF10A cells (101.97 ± 2.61 μM). Wound-healing assays showed that morin inhibits AGS cell migration in a dose- and time-dependent manner. Integrating in silico and in vitro evidence, we propose that morin primarily targets PIK3CA leading to modulation of the PI3K-Akt pathway, thereby contributing to reduced proliferation and migration of GC cells. Together, these findings highlight morin as a promising natural molecule with therapeutic potential against gastric cancer. - Source: PubMed
Publication date: 2026/04/10
Naskar NileshKumar SunilMamgai DeepanshuVishwakarma Harish ChandraKumar Guru SantoshMathew BijoMaliyakkal NaseerKumar Uday RShrivastava ShwetaJeengar Manish Kumar - - Source: PubMed
Publication date: 2026/04/04
Cui HuantianWang NingMin FeitianPei HuanWang YumingLi HanzhouWan QianqianMeng YanHe MingweiLv XiaomanXing LiweiLi ZixuanPan TianzeLi RenlinWen WeiboKong XiangyingBian Yuhong - The eastern and northern parts of Xinjiang are the main camel breeding areas in the region. Currently, there is a lack of systematic comparative genetic studies of local populations with significant phenotypic differences at the whole-genome level. Previous research has shown significant differences in milk production traits between Bactrian camels in the eastern and northern regions of Xinjiang. To further elucidate the genetic differences between the Bactrian camel populations in these two areas and the molecular basis of their lactation traits, this study selected 106 Bactrian camels—55 from three camel farms in the northern region and 51 from one farm in the eastern region—for whole-genome resequencing. - Source: PubMed
Publication date: 2026/03/30
Li YongqingCai ShudongTulafu HanikeziLiu ShihaoLin ChangchunWu WeiweiHuang Juncheng - Large cell transformation (LCT) in mycosis fungoides (MF) is thought to represent the clonal evolution of a single clone and is associated with aggressive clinical behavior and poor outcome not overcome by aggressive treatment regimens. The tumor dynamics leading to LCT-MF are poorly understood and previously determined genetic alterations in MF do not explain nor can predict disease progression and/or transformation, although implicating driver mutations have been identified. Our aim is to describe a distinct case of MF and the evolution of a genomic signature after LCT. This brief report highlights the evolution of genetic mutations seen in a 30-year-old Caucasian female with MF, folliculotropic type, who failed multiple treatment regimens and ultimately progressed with histologically confirmed LCT. The genomic analysis of five separate tumor samples, which originally harbored NRAS and PLCG1, showed molecular evolution with new somatic mutations in ATM, CARD11, TET2, TP53, U2AF1, and copy number variation including amplification of CDK6 and EIF4E, loss of CDKN2A, CDKN2B, and IKZF1 oncogenic isoform and high tumor burden, which were not seen in samples prior to LCT. The new somatic alterations seen with the clinical progression of LCT suggest evolution of the molecular tumor environment. Many of the mutations described implicate driver mutations in advanced-stage MF and have been associated with poor survival. While there is no evidence suggesting a singular mutation for the pathogenesis of LCT, the constellation of mutations may be responsible for histologic progression to LCT. - Source: PubMed
Publication date: 2026/03/23
Cheng MelissaCrisan LilianaZain JasmineAfkhami MichelleQuerfeld Christiane