G4-1 Antibody
- Known as:
- G4-1 Antibody
- Catalog number:
- XW-7782
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- G4-1 Antibody
Related products to: G4-1 Antibody
Related articles to: G4-1 Antibody
- Sterility control is one of the key tools for regulating pest rodent population density. An in-depth analysis of the molecular mechanism of sterility caused by control agents is of great significance for further exploration of novel sterility controls and the development of alternative drugs. In this study, male plateau zokors (Eospalax baileyi) in the breeding period were tested to explore the molecular mechanism of quinestrol-induced sterility. We used RNA-seq technology to investigate key genes and signaling pathways associated with the inhibition of testicular development and spermatogenesis, and validated these findings through qPCR. The findings indicated that in plateau zokors treated with quinestrol, 420 genes were down-regulated and 127 genes were up-regulated. Notch3, Ppp2r3c, Lipe, Il1b, and Tlr2 are the potential new targets for quinestrol to affect testicular development in plateau zokors. Gene ontology (GO) analysis showed that DEGs were enriched in the inflammatory response, positive regulation of ERK1 and ERK2 cascades, and positive regulation of MAPK cascades. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that DEGs were enriched in pathways such as metabolism of xenobiotics by cytochrome P450. GSEA analysis revealed that treatment with quinestrol induced pathway changes related to the positive regulation of the ERK1 and ERK2 cascades and the positive regulation of PI3K/AKT signaling in plateau zokors. Quinestrol influences the ERK1/2 signaling pathway within the MAPK cascade in spermatogonia of plateau zokor testes via the GPER1 receptor, inducing oxidative stress and resulting in male infertility. - Source: PubMed
Publication date: 2026/01/28
Deng YananKang YukunAn KangYao BaohuiTan YuchenOu KejieLiu MengyaoJi WeihongSu Junhu - Centrosomes have critical roles in microtubule organization, ciliogenesis, and cell signaling. Centrosomal alterations also contribute to diseases, including microcephaly, cancer, and ciliopathies. To date, over 150 centrosomal proteins have been identified, including several kinases and phosphatases that control centrosome biogenesis, function, and maintenance. However, the regulatory mechanisms that govern centrosome function are not fully defined, and thus how defects in centrosomal regulation contribute to disease is incompletely understood. Using a systems genetics approach, we find here that PPP2R3C, a poorly characterized PP2A phosphatase subunit, is a distal centriole protein and functional partner of centriolar proteins CEP350 and FOP. We further show that a key function of PPP2R3C is to counteract the kinase activity of MAP3K1. In support of this model, MAP3K1 knockout suppresses growth defects caused by PPP2R3C inactivation, and MAP3K1 and PPP2R3C have opposing effects on basal and microtubule stress-induced JNK signaling. Illustrating the importance of balanced MAP3K1 and PPP2R3C activities, acute overexpression of MAP3K1 severely inhibits centrosome function and triggers rapid centriole disintegration. Additionally, inactivating PPP2R3C mutations and activating MAP3K1 mutations both cause congenital syndromes characterized by gonadal dysgenesis. As a syndromic PPP2R3C variant is defective in centriolar localization and binding to centriolar protein FOP, we propose that imbalanced activity of this centrosomal kinase-phosphatase pair is the shared cause of these disorders. Thus, our findings reveal a new centrosomal phospho-regulatory module, shed light on disorders of gonadal development, and illustrate the power of systems genetics to identify previously unrecognized gene functions. - Source: PubMed
Publication date: 2024/09/23
Ganga Anil KumarSweeney Lauren KRubio Ramos ArmandoWrinn Caitlin MBishop Cassandra SHamel VirginieGuichard PaulBreslow David K - Cellular signaling pathways rely on posttranslational modifications (PTMs) to finely regulate protein functions, particularly transcription factors. The Hedgehog (Hh) signaling cascade, crucial for embryonic development and tissue homeostasis, is susceptible to aberrations that lead to developmental anomalies and various cancers. At the core of Hh signaling are Gli proteins, whose dynamic balance between activator (GliA) and repressor (GliR) states shapes cellular outcomes. Phosphorylation, orchestrated by multiple kinases, is pivotal in regulating Gli activity. While kinases in this context have been extensively studied, the role of protein phosphatases, particularly Protein Phosphatase 2A (PP2A), remains less explored. This study unveils a novel role for the B″gamma subunit of PP2A, PPP2R3C, in Hh signaling regulation. PPP2R3C interacts with Gli proteins, and its disruption reduces Hedgehog pathway activity as measured by reduced expression of Gli1/2 and Hh target genes upon Hh signaling activation, and reduced growth of a Hh signaling-dependent medulloblastoma cell line. Moreover, we establish an antagonistic connection between PPP2R3C and MEKK1 kinase in Gli protein phosphorylation, underscoring the intricate interplay between kinases and phosphatases in Hh signaling pathway. This study sheds light on the previously understudied role of protein phosphatases in Hh signaling and provides insights into their significance in cellular regulation. - Source: PubMed
Publication date: 2024/08/20
Baran BrygidaDerua RitaJanssens VeerleNiewiadomski Paweł - Alcohol use disorder (AUD) induces complex transcriptional and regulatory changes across multiple brain regions including the caudate nucleus, which remains understudied. Using paired single-nucleus RNA-seq and ATAC-seq on caudate samples from 143 human postmortem brains, including 74 with AUD, we identified 17 distinct cell types. We found that a significant portion of the alcohol-induced changes in gene expression occurred through altered chromatin accessibility. Notably, we identified novel transcriptional and chromatin accessibility differences in medium spiny neurons, impacting pathways such as RNA metabolism and immune response. A small cluster of D1/D2 hybrid neurons showed distinct differences, suggesting a unique role in AUD. Microglia exhibited distinct activation states deviating from classical M1/M2 designations, and astrocytes entered a reactive state partially regulated by , affecting glutamatergic synapse pathways. Oligodendrocyte dysregulation, driven in part by , was linked to demyelination and increased TGF-β1 signaling from microglia and astrocytes. We also observed increased microglia-astrocyte communication via the IL-1β pathway. Leveraging our multiomic data, we performed cell type-specific expression quantitative trait loci analysis, integrating that with public genome-wide association studies to identify AUD risk genes such as and , providing a direct link between genetic variants, chromatin accessibility, and gene expression in AUD. These findings not only provide new insights into the genetic and cellular mechanisms in the caudate related to AUD but also demonstrate the broader utility of large-scale multiomic studies in uncovering complex gene regulation across diverse cell types, which has implications beyond the substance use field. - Source: PubMed
Publication date: 2024/10/31
Green NickGao HongyuChu XiaonaYuan QiuyueMcGuire PatrickLai DongbingJiang GuanglongXuei XiaolingReiter Jill LStevens JuliaSutherland Greg TGoate Alison MPang Zhiping PSlesinger Paul AHart Ronald PTischfield Jay AAgrawal ArpanaWang YueDuren ZhanaEdenberg Howard JLiu Yunlong - Previous studies reveal that psoriatic arthritis (PsA) and ankylosing spondylitis (AS) share susceptibility genes, such as HLA-B27, demonstrating a degree of genetic overlap between these diseases. Recent studies have identified a number of novel AS and PsA genetic susceptibility loci, but data on these loci in Chinese PsA patients are limited. To identify candidate genes that confer susceptibility to PsA in Chinese patients with PsA, psoriasis vulgaris (PsV), and healthy controls. Sixteen susceptibility loci, reported in a genome-wide association study of AS, and nine susceptibility loci, reported in candidate gene studies of PsA, were examined. Single-nucleotide polymorphisms (SNPs) were genotyped in 503 patients with PsA, 496 patients with PsV, and 979 healthy controls using the SNPscanTM multiplex SNP genotyping platform. PLINK software and logistic regression analysis were used to estimate the statistical significance of associations. PPP2R3C (rs8006884) was shown to significantly associate with PsA+PsV (p = 1.92×10-3, OR = 1.28) and was suggested to associate with PsV (p = 0.03, OR = 1.19). A suggestive association was also observed between IL-23R (rs12141575) and PsA as well as with axial PsA based on subtype analysis, KIF3A (rs2897442) and PsV, and ERN1 (rs196941) or IFIH1 (rs984971) and axial PsA. Our results suggest that PPP2R3C confers susceptibility to PsA and PsV, and that this gene may be related to the pathogenesis of psoriatic lesions and arthritis. Moreover, our results indicate a possible association between IL-23R, ERN1, or IFIH1 and subtypes of PsA, and between KIF3A and PsV. - Source: PubMed
Wang NaGuo XiaoWang Zhen ZYu Gong QZhao QingYang QingLiu HongZhang Fu R