Ask about this productRelated genes to: Arf4 Blocking Peptide
- Gene:
- ARF4 NIH gene
- Name:
- ADP ribosylation factor 4
- Previous symbol:
- ARF2
- Synonyms:
- -
- Chromosome:
- 3p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1992-07-09
- Date modifiied:
- 2015-11-19
Related products to: Arf4 Blocking Peptide
Related articles to: Arf4 Blocking Peptide
- Formalin-fixed, paraffin-embedded (FFPE) archives underpin dermatopathology and translational oncology, enabling clinically annotated melanoma cohorts, but cohort-scale proteomics remains limited by labor and variability in upstream processing. We established a plate-scale, acoustic FFPE proteomics workflow and integrated it with AI-assisted digital pathology to support composition-aware molecular profiling from routine sections. The optimized pipeline reduces handling steps, is designed to improve reproducibility, and supports rapid parallel processing in a 96-well format. Deep data-independent acquisition mass spectrometry of 40 primary melanomas spanning acral lentiginous, lentigo maligna, superficial spreading, and nodular subtypes quantified more than 8,200 protein groups and a mean of 5,200 proteins per tumor. Proteome profiles resolved melanoma subtypes and defined an acral lentiginous melanoma program enriched for translation/biogenesis and extracellular matrix/adhesion processes with relative depletion of lipid and fatty-acid metabolism and peroxisomal pathways. Supervised feature selection highlighted TNC, POSTN, EIF4A1, and ARF4 and uncovered selective depletion of ATP5IF1, a regulator of mitochondrial ATP synthase, in acral lentiginous melanoma. ATP5IF1 depletion persisted after adjustment for mitochondrial proxies and QuPath-derived tumor content, and coincided with higher glycolysis relative to Complex V. This pathology-integrated, high-throughput FFPE proteomics framework enables scalable retrospective discovery and suggests subtype-specific metabolic alterations consistent with mitochondrial remodeling in an underrepresented melanoma subtype. - Source: PubMed
Publication date: 2026/07/13
Fernández-Coto Diana LashiduaAyala MarisolAlonso RamiroPalmqvist AliciaGarcía Ma FernandaBalderas-López Scarlett FOskolas HenriettChristersson LukasFulöp LiviaSzigeti BalazsOlivera-Rodríguez Victor HMarko-Varga MatildaHorvatovich PeterMalm JohanSzadai LeticiaHerrera-Goepfert RobertoSzasz Attila MarcellEncarnación-Guevara SergioMarko-Varga GyörgyGil Jeovanis - The central nervous system responds to acute injury with plastic remodeling of its network. However, the temporal and structural dynamics of this response in the denervated dentate gyrus remain poorly understood. Therefore, we examined the transcriptional programs activated after perforant path transection, focusing on the outer molecular layer (OML) and the granule cell layer (GCL). - Source: PubMed
Publication date: 2026/05/19
Schlaudraff JessicaDel Turco DomenicoKey JanaDeller ThomasAuburger Georg - Luminal breast cancer is rising rapidly among East Asian women, particularly younger patients, with variable clinical outcome, yet current risk-stratification models inadequately predict early recurrence of under-studied young-onset cases. We hypothesize that the interplay between endogenous mutagenic processes and overlooked environmental carcinogen exposure drives molecular diversity, revealing novel etiologic and therapeutic insights. - Source: PubMed
Publication date: 2026/06/03
Chang Ya-HsuanChen Yi-JuHong Zhi-JieHsiao Yi-JingLin Kuen-TyngLiao Guo-ShiouSu Sheng-FangLin Ze-ShiangChen Huei-WenHan Chia-LiChen Eric Sheng-WenHsu Yin-ChenChen Yan-MingFang HaoYang Hao-ChinChen Yan-SiLin Chien-YuHsu Hsiang-EnLin Ching-HungJiang Pin-LianWu Pei-ShanChen Ching-WenHung Chen-TingWu EthanChiu Wei-TzuHsing Fan-NiLiu Tsai-PeiWang Chia-YuWang Yu-TaiYeh Chang-WeiLiao Ki-HokRobles Ana IRodriguez HenryYang Show-LingHung Mien-ChieLu Yen-ShenChen Hsuan-YuYu Sung-LiangYu Jyh-CherngChen Yu-Ju - Anaplastic thyroid cancer (ATC) patient develops resistance to radioactive iodine (RAI) due to diminished sodium-iodide symporter (NIS) expression and mislocalization to the cell membrane. MAPK pathway inhibitors have demonstrated efficacy in enhancing RAI avidity in radioiodine-refractory papillary thyroid carcinoma and ATC. Elucidating this mechanism may lead to novel therapeutic approaches for ATC treatment. The cytotoxic effects of three MAPK pathway inhibitors (selumetinib, vemurafenib, dabrafenib) were assessed in ATC cell lines and xenograft models via viability assays and F-FDG PET/CT. We investigated their impact on radioiodine metabolism by analyzing the expression of key genes (NIS, TSHR, and TPO) and trafficking regulators (ARF4, PIGU, and β-catenin) via Western blotting, and assessing NIS localization and function through immunofluorescence and uptake assays. The protein interaction between NIS and ARF4 was examined via co-immunoprecipitation (co-IP) and immunofluorescence. MAPK pathway inhibitors reduced the viability of ATC cell lines. ATC cells exhibited restored iodine metabolism-related gene expression after treatment, and pronounced increases in membrane-localized NIS were detected via the promotion of ARF4 expression. Furthermore, MAPK pathway inhibitors increased radioiodine uptake in ATC cells. The MAPK pathway inhibitors enhance NIS function through two mechanisms: upregulation of NIS expression and increased ARF4-mediated NIS membrane transport. - Source: PubMed
Publication date: 2026/06/04
Wang JunfangZeng ZhenzhenXu ShashaWang XiaoxianWu KeliuChang YongguangWang GuanzhengLiu BaopingWang RuihuaHan Xingmin - Sepsis-associated acute lung injury (S-ALI) represents a significant clinical challenge due to its high incidence and mortality rates. Macrophages play a central and dual role in the pathogenesis of S-ALI, they serve as a critical component of the innate immune defense against pathogen invasion, while simultaneously contributing to the propagation of excessive inflammatory responses and tissue damage. Consequently, modulation of macrophage function has emerged as a promising therapeutic strategy for S-ALI. Accumulating evidence indicates that heme oxygenase-1 (HO-1, encoded by HMOX1) exerts endogenous protective effects in S-ALI. Our prior studies demonstrated that HO-1 ameliorates S-ALI by modulating oxidative stress in macrophages. Furthermore, emerging reports suggest that HO-1 may also mitigate this pathological process through regulation of Golgi stress; however, the underlying molecular mechanisms remain poorly defined. In this study, using both in vivo and in vitro models of S-ALI, we demonstrate that HO-1 in alveolar macrophages directly interacts with the transcriptional activation domain (TAD) of CREB3, leading to the degradation of the CREB3/ARF4 signaling pathway. Moreover, activated CREB3 suppresses HO-1 gene transcription, establishing a negative feedback regulatory loop. This mechanism effectively restricts CREB3 trafficking from the endoplasmic reticulum to the Golgi apparatus and its subsequent nuclear translocation, thereby preventing excessive activation of CREB3-dependent signaling pathways during S-ALI and attenuating Golgi stress. Additionally, clinical analyzes reveal that the expression levels of HO-1, CREB3, and ARF4 in peripheral blood mononuclear cells (PBMCs) from sepsis patients are significantly elevated compared to those in non-septic controls and positively correlate with APACHE II and SOFA scores. These markers demonstrate significant positive associations with established severity indices, suggesting that HO-1, CREB3, and ARF4-either individually or in combination-may serve as potential novel biomarkers for the diagnosis of sepsis, the assessment of disease severity, and the prediction of clinical outcomes. Collectively, these findings indicate that HO-1 alleviates Golgi stress in macrophages by inhibiting the CREB3/ARF4 axis, thus improving cellular functional homeostasis, and highlight their potential as both a diagnostic biomarker and a therapeutic target in sepsis. - Source: PubMed
Publication date: 2026/04/10
Kong ChangZhang YuanLi XiangyunRen GuangzhenGuo ChenxuLi MenghanLiu WeiqiangZhang DongchaoLi ChengyuShi JiaGong LirongYu Jianbo