ARF6 Antibody (Center) Blocking Peptide
- Known as:
- ARF6 Antibody (Center) Blocking Peptide
- Catalog number:
- BP6814c
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- ARF6 Antibody (Center) Blocking Peptide
Related genes to: ARF6 Antibody (Center) Blocking Peptide
- 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 Antibody (Center) Blocking Peptide
Related articles to: ARF6 Antibody (Center) Blocking Peptide
- Nymphaea prolifera employs a unique asexual reproductive strategy in which its normal flowers transform into branching flowers. These are specialized structures that develop vegetative propagules. These propagules can directly sprout into new plants. As the branching flowers mature, they detach from the parent plant and form new, independent individuals. However, the underlying molecular mechanisms that govern this distinctive reproductive phenomenon remain unclear. - Source: PubMed
Publication date: 2026/05/29
Tang YuweiLi JiahuiWei MiaoqinBin ZhenjunLu ZuzhengZhao JiahuiGao XiaoyuSu Qun - DS-1471a is a humanized antibody that targets CD147, a transmembrane glycoprotein frequently overexpressed in cancer cells, and has undergone a phase 1 clinical study for advanced solid tumors. To further investigate DS-1471a's therapeutic potential and the underlying molecular mechanisms involved, we examined its efficacy in patient-derived xenograft (PDX) models of liver cancer. DS-1471a exhibited potent antitumor effects in multiple PDX models, with positive correlations observed between DS-1471a efficacy and expression of CD147 and related proteins such as SMAD4, ARF6, and FBXO22. Among these proteins, overexpression of FBXO22, a ubiquitin ligase, enhanced DS-1471a efficacy in liver cancer xenograft models. Mechanistic analysis showed that FBXO22 overexpression was associated with reduced expression of p21/CDKN1A, a cyclin-dependent kinase inhibitor previously characterized as a degradation target of FBXO22, suggesting a potential regulatory relationship between these proteins. Moreover, in tumor models lacking p21, DS-1471a efficacy was also enhanced, whereas DS-1471a-resistant tumors expressed higher levels of p21 protein. Although direct causal relationships remain to be fully established, these results suggest possible mechanisms underlying DS-1471a efficacy involving not only CD147 expression but also FBXO22 and p21. Taken together, these preclinical findings indicate a potential clinical benefit of DS-1471a and provide useful mechanistic insights for liver cancer treatment. - Source: PubMed
Publication date: 2026/05/29
Yuita HiroshiWatanabe SadanoriTsukada JunJohmura YoshikazuAratani SaeIshikawa HirokazuNakamura RyuichiYokoyama MikiHashimoto MariYukinaga HideoHung Huynh TheNakanishi MakotoFukuchi Keisuke - Circular RNAs (circRNAs) are noncoding RNAs formed by back-splicing, characterized by covalently closed-loop structures with enhanced stability. Although growing evidence highlights their regulatory roles in plants, the precise biological functions of circRNAs remain largely unclear. In this study, we identified Arabidopsis thaliana circP5CS1, a circRNA derived from the delta-1-pyrroline-5-carboxylate synthase (P5CS1) gene through back-splicing of exons 11 to 13. The junction between exons 11-13 generates a de novo miR167 binding site, validated by sequence alignment and RNA pull-down assays, which indicate that circP5CS1 preferentially binds miR167a/b. circP5CS1 acts as a miR167 sponge to upregulate auxin response factors 6 (ARF6) and ARF8, fine-tuning salicylic acid (SA)- and jasmonic acid (JA)-mediated immunity during Pseudomonas syringae pv. tomato (Pst) DC3000 infection. In addition, circP5CS1 suppresses its host gene P5CS1, a rate-limiting enzyme for proline biosynthesis, through both splicing competition and post-transcriptional mechanisms, thereby linking circRNA biogenesis with gene expression control. Our results suggest that circP5CS1 directly modulates plant immunity via both hormone and proline pathways. circP5CS1 expression was induced by both Pst DC3000 and AvrRpt2 infections. Consistent with this, resistance to these pathogens was compromised in circP5CS1-OE, p5cs1, and miR167-STTM plants, whereas circP5CS1-RNAi, P5CS1-1-OE, and miR167-OE showed enhanced resistance. Proline levels increased in P5CS1-1-OE and circP5CS1-RNAi plants but decreased in circP5CS1-OE and p5cs1 mutants, supporting a link between circP5CS1 activity and proline metabolism. Our findings suggest that circP5CS1 may be an immuno-hub integrating hormone signaling and proline homeostasis through miRNA sponging and host gene suppression, revealing its dual regulatory role in coordinating RNA-mediated regulation with plant immune response. - Source: PubMed
Publication date: 2026/05/20
Wang LinSong XiaoningWei RanShi XuechaoXu LeYu ZeTang ChengLi LeyaoGuo BaohuanLiu HongxiaSun XiaoyongZhao Hongwei - The mortality rate associated with hepatocellular carcinoma (HCC) remains alarmingly high, positioning it as a primary lethal cancer worldwide, primarily driven by its high degree of malignancy, recurrence, and metastasis. The high heterogeneity of HCC necessitates the urgent identification of new therapeutic targets and molecular pathways. Our previous research observed that alpha-fetoprotein (AFP) deficiency led to pro-metastatic roles in HCC with specific genotypes. Here, we further investigated the underlying molecular mechanism. Through proteome microarray screening, we identified that ADP-ribosylation factor 6 (ARF6) was a key AFP-interacting protein and AFP deficiency upregulated ARF6 activity, which subsequently promoted the metastatic capacity of HepG2 cells. Mechanistically, the abnormal activation of ARF6 induced the dissociation of β-catenin from its membrane-bound anchors, specifically E-cadherin. The consequent increase in free cytoplasmic β-catenin facilitates its nuclear translocation, which in turn activates Wnt/β-catenin pathway. Crucially, we discovered that the pro-metastatic function of activated ARF6 and the sensitivity to the ARF6 inhibitor were strictly dependent on the CTNNB1 genotype. In highly invasive MHCC-97H cells, which harbor a CTNNB1 nonsense mutation, ARF6 inhibitor SecinH3 failed to inhibit migration and invasion. However, the overexpression of CTNNB1 mutation in MHCC-97H cells further amplified the increasing transcriptional activity of β-catenin triggered by the ARF6 abnormal activation. Importantly, the reintroducion of CTNNB1 mutation restored the inhibitory effect of SecinH3 in vitro and significantly suppressed the hepatic and pulmonary metastasis in a tail vein injection HCC metastasis mouse model. These findings establish a CTNNB1-dependent mechanism for ARF6-mediated metastasis, indicating that CTNNB1 activating mutations serve as a "permissive signal" for ARF6's pro-metastatic program. Our study underscores the importance of CTNNB1 genotype screening for precisely stratifying patients for ARF6-targeted therapies, offering new medication guidance for highly heterogeneous HCC. - Source: PubMed
Publication date: 2026/05/21
Zhang RuitianDong LongxuanYang JunyiGuo QinglongPan DiXun ChenWei Libin - Disorders of glucose metabolism, particularly type 2 diabetes and obesity, remain major therapeutic challenges because they involve dysfunction across multiple tissues, including pancreatic β-cells, peripheral insulin-sensitive tissues, and immune cells. ADP-ribosylation factor 6 (ARF6) is a regulator of membrane trafficking and cytoskeletal dynamics and may represent a mechanistically relevant link across these compartments. In this review, we summarise evidence suggesting that ARF6 may contribute to sustained second-phase insulin secretion, glucose transporter type 4 trafficking and recycling, and metabolic inflammation through effects on receptor and membrane trafficking. We also discuss pharmacological and nucleic acid-based approaches targeting ARF6 or its regulatory network. Current evidence suggests that direct systemic inhibition may be difficult to translate because of off-target risks, including possible disruption of endothelial barrier integrity. In addition, because cellular uptake of some delivery systems depends on endocytic pathways associated with ARF6, broad inhibition may also interfere with drug entry. Given these limitations, tissue-targeted and microenvironment-responsive nanodelivery systems may provide a more feasible strategy for modulating the ARF6 axis with greater spatial and temporal control. Overall, this review presents ARF6 as a potentially important mechanistic and translational entry point within the broader network that regulates glucose homeostasis, rather than as a single master regulator. - Source: PubMed
Wang YangyangHe YanXiu ZhimingWang Huiyan