Ask about this productRelated genes to: GNAI1 Blocking Peptide
- Gene:
- GNAI1 NIH gene
- Name:
- G protein subunit alpha i1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 7q21.11
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2018-03-05
Related products to: GNAI1 Blocking Peptide
Related articles to: GNAI1 Blocking Peptide
- Late-life depression (LLD) with high prevalence accelerates cognitive impairment and becomes a risk factor for dementia, yet the pathogenesis of LLD is still largely unclear. Delineating the neuromolecular mechanism of LLD is of great significance to its etiology, early diagnosis, and precision treatment. - Source: PubMed
Publication date: 2026/04/16
Chen MeilingZhang HongjiangYu XiaohuiZhang JieZhong JingmeiChen KexuanZi RongWu ZheWang ZhiyuanWu KunhuaWang JiaojianShao HengZhao YingZhu Baosheng - Mesothelin (MSLN) is a glycosylphosphatidylinositol-anchored cell surface protein that is overexpressed in several solid tumors and in one-third of pediatric acute myeloid leukemia (AML) cases. It represents a validated immunotherapeutic target owing to its lack of expression in normal bone marrow. The function of MSLN in AML is unknown, but it is implicated to regulate adhesion in solid tumors through interaction with its only known binding partner, MUC16/CA125. This study uses CRISPR/Cas9 mutagenesis to generate knockout (KO) of MSLN in NOMO-1 and a MSLN-expressing patient-derived xenograft model to investigate its biological role in AML. We show that MSLN-KO cells proliferate slower, have reduced mitochondrial metabolism, are arrested in G1 cell cycle phase, adhere less to extracellular matrix in vitro and engraft slower in vivo. MSLN-KO cells also exhibit increased sensitivity to Ara-C and reduced extracellular matrix-mediated chemoprotection. Using an unbiased approach, we identify Src-family kinase member LYN, and guanine nucleotide-binding protein G(i) alpha subunit proteins, GNAI1, GNAI2, and GNAI3 as novel binding partners of MSLN in AML and show that pharmacological or genetic inhibition of LYN signaling restores NOMO-1 cell sensitivity to Ara-C. Together, these findings demonstrate that MSLN functions as an oncogenic driver in AML and reveal a previously unrecognized MSLN-LYN signaling axis, the therapeutic targeting of which may enhance responses to chemotherapy. - Source: PubMed
Publication date: 2026/03/20
Faust Joshua RHamill DarcyKolb E AndersStevens Alexandra MGopalakrishnapillai AnilkumarBarwe Sonali P - The transcription factor Friend leukemia integration-1 (FLI-1) is implicated in various cellular functions, including the regulation of cardiovascular function. This study aimed to elucidate the role and molecular mechanisms of FLI-1 in myocardial hypertrophy. We conducted FLI-1 overexpression interventions in ISO-induced H9C2 cells and mouse models of myocardial hypertrophy, subsequently assessing their effects on Klotho expression, cardiomyocyte hypertrophy, apoptosis, and IGF-1R/GNAI1PLCG1 signaling pathway activity. Our results demonstrated that ISO induction led to a time-dependent decrease in FLI-1 expression in H9C2 cells. Furthermore, FLI-1 overexpression enhanced Klotho expression in ISO-induced H9C2 cells and significantly inhibited ISO-induced cardiomyocyte hypertrophy and apoptosis. Furthermore, the overexpression of FLI-1 was found to attenuate the activity of the insulin-like growth factor type 1 receptor (IGF-1R)/GNAI1/PLCG1 signaling pathway in ISO-induced H9C2 cells. Notably, the silencing of Klotho negated the protective effects conferred by FLI-1 overexpression on cardiomyocyte hypertrophy and apoptosis, as well as its inhibitory impact on the IGF-1R/GNAI1/PLCG1 signaling pathway. In a murine model of myocardial hypertrophy, FLI-1 overexpression similarly exhibited a protective effect by mitigating myocardial hypertrophy and damage. These findings suggest that FLI-1 exerts a protective role in cardiac hypertrophy and apoptosis, potentially through the modulation of the Klotho and IGF-1R/GNAI1/PLCG1 pathways. - Source: PubMed
Publication date: 2026/03/09
Tang GangLi YunlongWang WeiweiZhong LiSi Liangyi - Ovarian cancer is a rare cancer, it has the worst prognosis and the highest mortality rate, especially in high-grade serous ovarian cancer (HGSOC). High-throughput data generation is developed and provides an opportunity to investigate molecular pathways involved in cancer progression. The purpose of this study is to explore the role of main genes linked to the immune system and immune microenvironment in HGSOC using bioinformatics approaches to introduce promising biomarkers. - Source: PubMed
Publication date: 2025/11/28
Fatehi RaziehTabatabaiefar MohammadAminBehnamfar FaribaKhanahmad Hossein - G proteins and arrestins are key transducers for G protein-coupled receptor (GPCR) signaling, mediating distinct downstream pathways. Recent evidence suggests that G proteins and β-arrestins (βarrs) can directly or functionally interact. However, the molecular details and functional consequences of Gα-βarr interactions remain poorly understood. Here, we quantify the binding affinities between βarr1 and Gαs or Gαi1 in various activation states using microscale thermophoresis (MST). βarr1 in the active conformational ensemble state favors binding, whereas Gα activation status is less determinant. Hydrogen/deuterium exchange mass spectrometry reveals distinct conformational changes between Gαs versus Gαi1 upon βarr1 binding, suggesting differential binding mechanism between Gαs-βarr1 and Gαi1-βarr1 complexes. Both the Ras-like domain and the α-helical domain of Gα contribute to complex formation. Functionally, a BODIPY-FL-GTPγS assay shows that βarr1 does not alter GDP/GTP turnover of Gαs or Gαi1, whereas β-strand XX (βXX) release assays demonstrate that Gαs enhances βarr1 C-tail release. Together, these results propose molecular mechanism of the interaction and asymmetric functional coupling within Gα-βarr complexes and uncover a previously underappreciated layer of GPCR signal transduction. - Source: PubMed
Publication date: 2026/01/20
Duan LonghanKim HyunbinSuh YeongjunAhn DonghoonKim SeungmiHyun JaekyungKwon YonghoonSeong JihyeChung Ka Young