RGS4 antibody - C-terminal region (ARP30354_P050)
- Known as:
- RGS4 (anti-) - C-terminal region (ARP30354_P050)
- Catalog number:
- arp30354_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- RGS4 antibody - C-terminal region (ARP30354_P050)
Related genes to: RGS4 antibody - C-terminal region (ARP30354_P050)
- Gene:
- RGS4 NIH gene
- Name:
- regulator of G protein signaling 4
- Previous symbol:
- SCZD9
- Synonyms:
- -
- Chromosome:
- 1q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-09
- Date modifiied:
- 2017-04-13
Related products to: RGS4 antibody - C-terminal region (ARP30354_P050)
Related articles to: RGS4 antibody - C-terminal region (ARP30354_P050)
- Despite a growing body of evidence implicating genetic variants and proteins encoded by them with risk and pathogenesis of Alzheimer's disease (AD), this knowledge has not been successfully translated into effective AD treatments. We integrated current genomic, transcriptomic and proteomic profiles of AD into a network pharmacology framework that leverages comprehensive gene-gene and drug-target interactions. This approach allowed us to screen 2,413 drugs for repurposing opportunities in AD. Computational validation and drug prioritization was followed by experimental validation in 33 cell culture-based phenotypic assays combined with Bayesian hypothesis testing. Our network-based screen rediscovered drugs in clinical trials for AD, providing computational validation. Besides many cancer drugs, the screen identified three drugs previously implicated in AD-related endophenotypes: the primary bile acid chenodiol, arundine (3,3'-diindolylmethane), and cysteamine. In analysis of results from culture-based phenotypic assays, large Bayes factors supported the hypothesized benefits of arundine and the chenodiol derivative, tauroursodeoxycholic acid (TUDCA), in amyloid- clearance and release and neuroinflammation. Follow-up network analyses mechanistically implicated Regulator of G protein signaling 4 (RGS4) in the plausible therapeutic actions of arundine and TUDCA. A network pharmacology approach identified TUDCA and arundine as promising repurposing candidates in AD that rescue disease-relevant molecular phenotypes by acting on AD-associated genes through regulation of G protein signaling. - Source: PubMed
Publication date: 2026/03/09
Jones AttilaLoeffler TinaWu EvanVarma Vijay RIm Hae KyungThambisetty Madhav - Heat stress (HS), an escalating environmental threat, induces cognitive impairment, but the underlying mechanisms remain incompletely understood. This study investigated the role of ferroptosis, an iron-dependent cell death pathway, in HS-induced neurotoxicity. Using murine models and HT22 hippocampal neurons subjected to subacute HS (42.5 °C, 1 h/day, 7 days in vivo; 41 °C, 48 h in vitro), we demonstrate that HS triggers hippocampal ferroptosis. HS impaired spatial learning and memory (Morris water maze, shuttle box) and induced neuronal damage in the CA3 region. Untargeted serum metabolomics showed a systemic shift in arachidonic acid (AA) metabolism after heat stress, including decreased free AA and increased oxidized AA metabolites (5-HETE and 15(S)-HPETE). Because serum changes are peripheral correlates, we next assessed the hippocampus and observed oxidative stress (increased MDA, decreased SOD), molecular dysregulation (upregulated ACSL4, TfR1, COX2, CHAC1; downregulated GPX4, SLC7A11, RGS4), and histopathological damage. Critically, the ferroptosis inhibitor Ferrostatin-1 (Fer-1) attenuated cognitive deficits, neuronal damage, and molecular/metabolic dysregulation in vivo and in vitro. Pharmacological inhibition of ACSL4, the key enzyme incorporating peroxidation-susceptible PUFAs into membranes, using rosiglitazone, similarly suppressed ferroptosis markers, lipid peroxidation, ROS, and cell death in HT22 neurons, while restoring GPX4 expression. These findings establish that HS induces cognitive impairment via an ACSL4-driven lipid peroxidation-ferroptosis axis in hippocampal neurons, identifying ACSL4 as a potential therapeutic target for mitigating heat-related neurodegeneration. - Source: PubMed
Publication date: 2026/02/18
Zhou QichengLiu XinyaoPan WenlanQu YicuiShi WenjingMiao GenHuang LuLi XinCai MengyuLi HongxiaShen Hui - Mechanical force is a universal language of cells, yet which transcripts report tension on individual cytoskeletal polymers has remained unknown. Existing stretchers and drugs distort every filament simultaneously, blurring the signal. Here we apply a magnetogenetic approach, using antibody-guided 10 nm FeO nanoparticles to exert ∼0.5 pN force on β-actin, α-tubulin, or vimentin in human mesenchymal stem cells, and record the 20-h transcriptional response by bulk RNA-seq. Tension on microtubules amplifies Wnt, focal-adhesion, and extracellular-matrix modules; vimentin loading activates Hippo signalling, DNA-replication, and cell-cycle engines; actin loading elicits a TGF-β-centred oxidative-stress and ferroptosis programme, revealing a striking division of labour among the three polymers. Only four genes: KLHL24, RGS4, FMN2, and PDE4DIP are shared across the 384-405 differentially expressed transcripts per condition, exposing an orthogonal "filament code" for mechanosensation. The data overturn the view that the cytoskeleton transmits force through common pathways and identify a minimal, four-gene set that reports intracellular tension regardless of where it is applied. Because magnetic fields penetrate tissue centimetres deep and can be shaped in space and time, this platform offers a non-invasive route to steer stem-cell migration (via tubulin), proliferation (via vimentin), or cytoprotection (via actin), informing the design of mechano-responsive biomaterials and remotely controllable cell therapies. STATEMENT OF SIGNIFICANCE: Cells sense mechanical forces, but standard stretch devices and drugs activate the whole cytoskeleton at once, making it hard to isolate each filament's role. We used antibody-guided 10 nm FeO nanoparticles to apply ∼0.5 pN tension specifically to actin, microtubules, or vimentin in mesenchymal stem cells, then read out the 20 h response by RNA sequencing. Each filament triggers a largely distinct gene program, with only four shared genes, revealing a simple filament code for force signaling. This resolves a long-standing assignment problem and provides testable markers of intracellular tension. Because magnetic fields penetrate tissue and are easily shaped, our strategy suggests non-invasive ways to guide migration, proliferation, or cytoprotection, informing mechano-responsive biomaterials and remotely controllable cell therapies. - Source: PubMed
Publication date: 2026/02/11
Pozdina Varvara AKaravashkova Olga YPechnikova Nadezhda AMinin Artem SMaltseva Alexandra EDemin Alexander MAbakumov Maxim AYaremenko Alexey VZubarev Ilya V - Bladder cancer (BC) is characterized by a high incidence and frequent recurrence. Despite efforts to improve survival and reduce mortality among BC patients, significant progress remains elusive. The role of the cell cycle in BC has been increasingly studied, and our analysis revealed that BC exhibits elevated expression of BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B). However, the role of BUB1B in BC remains not fully understood. A Multi-omics analysis was performed by integrating BUB1B expression with clinical data, and the results indicated that the upregulation of BUB1B was associated with poor prognosis. Moreover, our study demonstrated that BUB1B promotes bladder cancer (BC) cell proliferation, migration, invasion, and tumorigenicity both in vitro and in vivo. Finally, subsequent analysis revealed a positive correlation of BUB1B expression with CDC25A and IFI6, and a negative correlation with CXCR6 and RGS4. In addition, our findings implicate the NF-κB signaling pathway in the function of BUB1B. These findings provided insights into the potential role of BUB1B as a therapeutic target for BC. - Source: PubMed
Publication date: 2026/01/12
Zhou HuidongPeng ShaoLing ZhixinCai JiaodiLiu JinghongKong YingZhang HuaOuyang JunZhang Jianglei - Benz/imidazole-2-thione/selone-based triazoles, particularly their thione and selone analogs, are gaining attention for anticancer drug development due to their structural diversity and biological activity. However, their potential as targeted inhibitors of cancer-related proteins remains underexplored. This study reports the design, synthesis, and evaluation of novel benz/imidazole-2-thione/selone-based triazoles, focusing on cyclin-dependent kinase 1 (CDK1), a key regulator of cancer cell proliferation. The compounds were synthesized via a multistep approach involving imidazolium salt intermediates, followed by sulfur or selenium incorporation. Structural confirmation was achieved using FT-IR, NMR, and mass spectrometry. Molecular docking against CDK1, TERT, and VEGFR2 revealed strong binding affinities (-9.7 to -7.3 kcal/mol), with CDK1 selected for further in vitro study using MCF-7 breast cancer cells. Molecular dynamics (MD) simulations confirmed stable CDK1 binding for Compounds 2, 4, and 9, although Compound 9 showed conformational instability after 60 ns. ADMET profiling indicated favorable drug-likeness and permeability but highlighted metabolic liabilities and hERG inhibition risks, particularly for Compounds 4 and 9. The target prediction and pathway enrichment analyses predict that benz/imidazole-2-thione/selone-based triazoles exert their pharmacological effects primarily through the regulation of GPCR signaling pathways, likely via direct interaction with key regulators such as RGS8 and RGS4. In vitro assays demonstrated dose-dependent cytotoxicity, with Compound 4 showing the highest potency (IC = 106.12 ± 1.03 µg/mL), followed by 9 and 2. These findings suggest that benz/imidazole-2-thione/selone-based triazoles are promising CDK1 inhibitors and support their further optimization as targeted breast cancer therapies. - Source: PubMed
Abdulkareem Alameer EzatMageed Ahmed Hassoon