Arf6 Activation Assay
- Known as:
- Arf6 Activation Assay
- Catalog number:
- STA-407-6
- Product Quantity:
- 20 assays
- Category:
- Peptides
- Supplier:
- Cell Biolabs
- Gene target:
- Arf6 Activation Assay
Related genes to: Arf6 Activation Assay
- Gene:
- ARF6 NIH gene
- Name:
- ADP ribosylation factor 6
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 14q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-01
- Date modifiied:
- 2015-11-19
Related products to: Arf6 Activation Assay
Related articles to: Arf6 Activation Assay
- Genetic studies of serious mental illness (SMI, including schizophrenia and bipolar disorder) have implicated two classes of risk variant: common variants , each of small effect but collectively accounting for most population-level risk, and ultra-rare coding variants which confer large risk in a small number of individuals. Most such studies cannot directly assess the impact of specific variants on SMI, transdiagnostically, as the phenotypic information that they collect is focused on a single diagnosis. Here we report results of association analysis of predicted deleterious variants from exome sequencing of 21,958 cases (SMI and severe major depressive disorder) and 19,826 controls from the Mision Origen biobank in the Paisa genetic isolate of Colombia. We identified transdiagnostic associations to seven genes, three at an exome-wide and four at a false discovery rate significance threshold. Five of these genes have not previously been implicated in SMI ( , , , , and - ); for the first four of these the association is driven by variants enriched in the Paisa due to a founder effect, filling the gap between ultra-rare and common variants. The strongest association that we observe is to a frameshift variant (7:904169:T:TC) in that is genome-wide significant for SMI, schizophrenia, and bipolar disorder and increases risk for both diagnoses by more than threefold; it truncates , a brain-enriched Arf6 GTPase-activating/scaffolding protein that has been mechanistically linked to post-mitotic neuronal morphogenesis and regulation of dendritic differentiation . Variant carriers differ significantly from other SMI cases in Mision Origen for psychotic, manic, and cognitive item-level phenotypes assessed through analyses of electronic health records and displayed impaired executive function on neurocognitive testing. Variant carriers differ significantly from other SMI cases in Mision Origen for multiple item-level phenotypes (psychotic, manic, and cognitive) assigned through natural language processing of longitudinal electronic health records. Although the 7:904169:T:TC variant is not significantly associated with major depressive disorder, carriers compared to others with this diagnosis display a significant increase in symptoms typical of bipolar disorder. The variant's high allele frequency in Mision Origen (~0.4%) will enable population-level studies to stratify SMI based on causation and identify additional factors influencing risk and resilience. - Source: PubMed
Publication date: 2026/09/27
Gerdes GretaTozzo VeronicaService Susan KFrydman-Gani ClaraDiaz-Zuluaga Ana MValencia-Echeverry JohannaArias AlejandroBicks Lucy KRamirez-Diaz Ana MSealock Julia MLiao CalwingHowrigan Daniel PLiu ChristianaLopera-Maya Esteban APimplaskar AdityaDe la Hoz Juan FArango-Gómez Mario AArango-Restrepo CamilaArbelaez-Herrera Maria CCamacho-Gualteros KatherineCardona-Arango MateoCastaño-Ramirez MauricioCastañeda-Hoyos Jaime ACerrato FeleciaChapman Sinéad BFranco-Gómez Roby ELondoño-Martinez John DMazo-Morales John SMejía-Piedrahita Juan CMir EmaadMoore Tyler MPerez-Jaramillo Luz EPérez-Vallejo MariaPosada-Ricardo Maria ERiscanevo-Posada VladimirRestrepo-Osorio CamilaRestrepo-Osorio DanielaRuparel KoshaSánchez-Patiño DaniloTeshiba TerriValdez JonathanValencia-Londoño WendyValencia-Zuluaga Oscar AVelez-Arango Jorge MCrossley Nicolas APalacio-Ortiz Juan DavidGeschwind Daniel HMartin Alicia RGur Ruben CSawaya Michael REisenberg David SEscobar Javier ISabatti ChiaraReus Victor IBearden Carrie ENeale Benjamin MLopez-Jaramillo CarlosFreimer Nelson BOlde Loohuis Loes - Heat stress (HS) is a major environmental factor limiting plant survival and crop productivity, prompting the evolution of adaptive responses driven by transcriptional reprogramming coordinated by Class A1 HS TRANSCRIPTION FACTORS (HSFA1s). Here, we demonstrate that the miR167-AUXIN RESPONSE FACTOR 8 (ARF8) module functions as a central regulatory hub, enhancing thermotolerance by integrating both HSFA1-dependent and HSFA1-independent signaling cascades. Under HS, the expression of ARF6 and ARF8 is repressed, while miR167 is induced. Disruption of ARF6/ARF8 or overexpression of miR167 significantly improves heat tolerance, whereas ARF8 overexpression increases HS sensitivity. ARF8 directly binds to the promoters of HSFA1 genes and heat shock protein (HSP) genes, repressing their transcription and thereby impairing the heat-responsive gene network. In addition, ARF8 physically interacts with HSFA1 proteins, further inhibiting their transactivation activity post-translationally. Notably, ARF8 also regulates HSFA2, a major amplifier of the HS response, through both HSFA1-dependent and HSFA1-independent mechanisms. Genetic evidence supports a model in which the HSFA1-HSFA2 axis functions downstream of the miR167-ARF8 module, but contributes only partially to the overall thermotolerance phenotype. Beyond the HSFA1-HSFA2 pathway, ARF8 also suppresses the RVE4/8-ERF53/54 transcriptional cascade, a circadian-regulated, HSFA1-independent module that promotes thermotolerance. This dual regulation allows ARF8 to fine-tune HS adaptation through integration of both canonical and noncanonical signaling routes. Together, these findings establish the miR167-ARF8 module as a central integrator of HS response pathways. This work not only reveals new mechanistic complexity in plant heat response networks but also identifies a conserved regulatory node with promising potential for genetic improvement of heat-resilient crops. - Source: PubMed
Publication date: 2026/09/26
Li JieLi YixinChen ChenMa ChenghaoTang GuiliangZhao ZhongYan Jun - Selenomethionine (SeMet) is an organic selenium form with high bioavailability. Its regulation of intestinal barrier dysfunction and immune-inflammatory dysregulation through the microbial-immune axis remains incompletely understood. Forty-eight 7-day-old male Sprague-Dawley rats were randomized into four groups: Control, LPS, SeMet, and SeMet‑LPS four groups. Pups received daily oral SeMet (0.2 mg/kg) from postnatal day 7-21, and LPS (10 mg/kg) was intraperitoneally injected after weaning. SeMet pretreatment significantly alleviated LPS-induced growth suppression. It reduced serum and intestinal levels of IL‑6 and TNF‑α and restored antioxidant enzyme activities. Moreover, SeMet upregulated the expression of tight junction proteins ZO‑1 and Claudin‑1. 16S rRNA sequencing revealed that SeMet enriched the beneficial genera Akkermansia and Parasutterella while decreasing pathogenic taxa. Transcriptomic analysis showed that SeMet suppressed activation of the NF‑κB, TNF, and IL‑17 pathways. Microbial-gene association analysis further linked key bacterial genera with host immune and barrier genes, including Traf1, S100a8, Arf4, and Arf6. Collectively, SeMet attenuates LPS-induced intestinal injury by modulating inflammation, oxidative stress, and the microbial-immune axis. - Source: PubMed
Publication date: 2026/08/27
Wu YaliZhou MaocuoLiu XinyiLiu ShuoYang WanluNi BinLi YuanWang XuGao Pengfei - The postsynaptic density (PSD) of neuronal synapses is a crowded, viscous, membraneless compartment consisting of densely packed protein mixtures formed and maintained through liquid-liquid phase separation. A key regulator of synaptic function within the PSD is IQSEC2, an intrinsically disordered protein (IDP), which functions as a guanine nucleotide exchange factor, promoting the activation of the small GTPase ARF6 by catalyzing the exchange of ARF6-bound GDP for GTP. Experiments have shown that IQSEC2 is inactive in a folded state in the dendritic cytosol but can transiently adopt a catalytically active extended conformation in the PSD upon activation by neurotransmitter-mediated calcium influx. In this study, we performed accelerated molecular dynamics (aMD) simulations of the IQSEC2 folding process in aqueous solvent and applied the Gibbs ergodic hypothesis formulated in statistical ensembles for post-processing and analysis of the results. We compared the effects of two sets of parameters on folding: a force field and a water model. The optimal point charge water model optimized for proteins with disordered structure in the extended state in bulk aqueous solvent predicted an incorrect, distorted, 3D folded structure of IQSEC2. We propose that, due to fundamental biophysical differences between the dendritic cytosol and the PSD, there are two distinct classes of IDPs functioning in these different environments. These differences should be considered when optimizing force fields and parameters of water models for studying protein folding. - Source: PubMed
Publication date: 2026/09/07
Shokhen MichaelAlbeck AmnonLevy Nina SLevy Andrew P - Loss of major histocompatibility complex class I (MHC-I) molecules from the tumor cell surface is a common mechanism of immune evasion; yet, the receptor intrinsic events that initiate their endocytic removal remain unclear. Here, using HLA-A11:01, a human MHC-I heavy chain allotype as a model, we identify a membrane responsive regulatory module within its cytoplasmic tail. The conserved 360-365 segment engages phospholipid membranes and undergoes Cys363-dependent self-association under membrane mimetic conditions, while cooperating with the transmembrane region to shape the molecular proximity of full-length HLA-A. Disruption of this segment weakens association with the trafficking GTPase ARF6, slows receptor internalization, and prolongs HLA-A retention at the cell surface. Consistently, a cell penetrating peptide containing this sequence limits endogenous HLA-A internalization across several tumor cell lines. These findings identify the HLA-A cytoplasmic tail as an active regulator of endocytic trafficking and suggest a strategy for preserving surface HLA-A availability in tumor cells. - Source: PubMed
Publication date: 2026/09/03
Xu XiWang YuxuanWu YihuangCai ZhenjiaZhu JialiWu HuiWen MaorongXue HongjuanLiu JingxinChen ZhifengChou James JZhao Linlin