GEFT Blocking Peptide
- Known as:
- GEFT Blocking Peptide
- Catalog number:
- 33r-8023
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- GEFT Blocking Peptide
Related genes to: GEFT Blocking Peptide
- Gene:
- ARHGEF25 NIH gene
- Name:
- Rho guanine nucleotide exchange factor 25
- Previous symbol:
- -
- Synonyms:
- GEFT, p63RhoGEF
- Chromosome:
- 12q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2010-09-02
- Date modifiied:
- 2015-11-09
Related products to: GEFT Blocking Peptide
Related articles to: GEFT Blocking Peptide
- Directed migration and rapid process extension-retraction allow microglia to continuously survey the brain and efficiently identify and phagocytose apoptotic neurons. Defining how cytoskeletal regulators coordinate these behaviors could guide strategies for targeted modulation of microglial activity. To this aim, using in vivo imaging in zebrafish, we identified a mechanistic framework in which myosin II-dependent contractility governs transitions between surveillance, migratory, and phagocytic states. Building on this, we engineered an optogenetic RhoA actuator (opto-ArhGEF25) that enables reversible, spatiotemporally precise manipulation of microglial behavior in vivo. We show that patterned RhoA activation can modulate process dynamics and induce front-rear polarity that drives rapid repulsive migration away from the applied light source, overriding injury-evoked cues and preventing migration toward lesions. Together, these results establish optogenetic control of the cytoskeleton as a powerful approach to probe and ultimately modulate microglial function in the living brain. - Source: PubMed
Publication date: 2026/03/27
Biermeier Corinna MariaAlbert MarvinPal Ayush AdityaGallo ElisaWittmann JanaHartmann JonasBill Robert TheofanisJulmi JérômeGilmour DarrenPeri Francesca - Natural killer/T-cell lymphoma (NKTCL) presents highly aggressive clinical behaviour, and the outcomes for relapsed and refractory patients are still poor. Our previous study identified somatic mutations in GNAQ in 8.7% of cases through whole-exome sequencing, revealing the T96S mutation in the Gαq protein. - Source: PubMed
Publication date: 2025/12/09
Gao YuyangZhang ZiheSong YueSong WentingLi HongwenZhang LeiLi ZhaomingZhang Mingzhi - The effect of the conventional treatment methods of glioblastoma (GBM) is poor and the prognosis of patients is poor. The expression of MCL-1 in GBM is significantly increased, which shows a high application value in targeted therapy. In this study, we predicted the prognosis of glioblastoma patients, and therefore constructed MCL-1 related prognostic signature (MPS) and the development of MCL-1 small molecule inhibitors. In this study, RNA-seq and clinical data of 168 GBM samples were obtained from the TCGA website, and immunological analysis, differential gene expression analysis and functional enrichment analysis were performed. Subsequently, MCL-1-associated prognostic signature (MPS) was constructed and validated by LASSO Cox analysis, and a nomogram was constructed to predict the prognosis of patients. Finally, the 17931 small molecules downloaded from the ZINC15 database were screened by LibDock, ADME, TOPKAT and CDOCKER modules and molecular dynamics simulation in Discovery Studio2019 software, and two safer and more effective small molecule inhibitors were finally selected. Immunological analysis showed immunosuppression in the MCL1_H group, and treatment with immune checkpoint inhibitors had a positive effect. Differential expression gene analysis identified 449 differentially expressed genes. Build and validate MPS using LASSO Cox analysis. Use the TSHR HIST3H2A, ARGE OSMR, ARHGEF25 build risk score, proved that low risk group of patients prognosis is better. Univariate and multivariate analysis proved that risk could be used as an independent predictor of patient prognosis. Construct a nomogram to predict the survival probability of patients at 1,2,3 years. Using a series of computer-aided techniques, two more reasonable lead compounds ZINC000013374322 and ZINC000001090002 were virtually selected. These compounds have potential inhibitory effects on MCL-1 and provide a basis for the design and further development of MCL-1 specific small molecule inhibitors. This study analyzed the effect of MCL-1 on the prognosis of glioblastoma patients from the perspective of immunology, constructed a new prognostic model to evaluate the survival rate of patients, and further screened 2 MCL-1 small molecule inhibitors, which provides new ideas for the treatment and prognosis of glioblastoma. - Source: PubMed
Publication date: 2023/07/19
Zhang AoGuo ZhenRen Jia-XinChen HongyuYang WenzhuoZhou YangPan LinChen ZhuopengRen FeiChen YouqiZhang MenghanPeng FeiChen WantingWang XinhuiZhang ZhiyunWu Hui - G protein-coupled receptors (GPCRs) are gatekeepers of cellular homeostasis and the targets of a large proportion of drugs. In addition to their signaling activity at the plasma membrane, it has been proposed that their actions may result from translocation and activation of G proteins at endomembranes-namely endosomes. This could have a significant impact on our understanding of how signals from GPCR-targeting drugs are propagated within the cell. However, little is known about the mechanisms that drive G protein movement and activation in subcellular compartments. Using bioluminescence resonance energy transfer (BRET)-based effector membrane translocation assays, we dissected the mechanisms underlying endosomal G trafficking and activity following activation of G-coupled receptors, including the angiotensin II type 1, bradykinin B, oxytocin, thromboxane A alpha isoform, and muscarinic acetylcholine M receptors. Our data reveal that GPCR-promoted activation of G at the plasma membrane induces its translocation to endosomes independently of β-arrestin engagement and receptor endocytosis. In contrast, G activity at endosomes was found to rely on both receptor endocytosis-dependent and -independent mechanisms. In addition to shedding light on the molecular processes controlling subcellular G signaling, our study provides a set of tools that will be generally applicable to the study of G protein translocation and activation at endosomes and other subcellular organelles, as well as the contribution of signal propagation to drug action. - Source: PubMed
Wright Shane CLukasheva ViktoriyaLe Gouill ChristianKobayashi HiroyukiBreton BillyMailhot-Larouche SamuelBlondel-Tepaz ÉlodieAntunes Vieira NichelleCosta-Neto ClaudioHéroux MadeleineLambert Nevin AParreiras-E-Silva Lucas TabajaraBouvier Michel - Diverse extracellular signals induce plasma membrane translocation of sphingosine kinase-1 (SphK1), thereby enabling inside-out signaling of sphingosine-1-phosphate. We have shown before that G-coupled receptors and constitutively active Gα specifically induced a rapid and long-lasting SphK1 translocation, independently of canonical G/phospholipase C (PLC) signaling. Here, we further characterized G regulation of SphK1. SphK1 translocation by the M receptor in HEK-293 cells was delayed by expression of catalytically inactive G-protein-coupled receptor kinase-2, p63Rho guanine nucleotide exchange factor (p63RhoGEF), and catalytically inactive PLCβ, but accelerated by wild-type PLCβ and the PLCδ PH domain. Both wild-type SphK1 and catalytically inactive SphK1-G82D reduced M receptor-stimulated inositol phosphate production, suggesting competition at Gα. Embryonic fibroblasts from Gα double-deficient mice were used to show that amino acids W263 and T257 of Gα, which interact directly with PLCβ and p63RhoGEF, were important for bradykinin B receptor-induced SphK1 translocation. Finally, an AIXXPL motif was identified in vertebrate SphK1 (positions 100-105 in human SphK1a), which resembles the Gα binding motif, ALXXPI, in PLCβ and p63RhoGEF. After M receptor stimulation, SphK1-A100E-I101E and SphK1-P104A-L105A translocated in only 25% and 56% of cells, respectively, and translocation efficiency was significantly reduced. The data suggest that both the AIXXPL motif and currently unknown consequences of PLCβ/PLCδ(PH) expression are important for regulation of SphK1 by G. - Source: PubMed
Publication date: 2020/09/29
Blankenbach Kira VanessaClaas Ralf FrederikAster Natalie JudithSpohner Anna KatharinaTrautmann SandraFerreirós NereaBlack Justin LTesmer John J GOffermanns StefanWieland ThomasMeyer Zu Heringdorf Dagmar