ARFIP2 Antibody
- Known as:
- ARFIP2 Antibody
- Catalog number:
- XW-8043
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- ARFIP2 Antibody
Related genes to: ARFIP2 Antibody
- Gene:
- ARFIP2 NIH gene
- Name:
- ADP ribosylation factor interacting protein 2
- Previous symbol:
- -
- Synonyms:
- POR1
- Chromosome:
- 11p15.4
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-21
- Date modifiied:
- 2016-10-05
Related products to: ARFIP2 Antibody
Related articles to: ARFIP2 Antibody
- Overuse of insecticides has led to severe environmental problems and rapid evolution of resistance. Incomplete metamorphosis insects, such as cockroaches, are ideal models for studying insecticide resistance mechanisms due to their short generation cycle and rapid development of resistance. Blattella germanica (L.), which endangers human health by causing allergic diseases and asthma, is ranks seventh among the top 20 most insecticide-resistant pest species globally, however, its miRNA-related resistance mechanisms are not well understood. Here, by miRNA-mRNA integration analysis, we identified two novel miRNAs, namely ame-miR-125-5p and ame-miR-3770-5p, that mediate the resistance of B. germanica to beta-cypermethrin (β-cypermethrin). Mechanistically, ame-miR-125-5p, which was significantly upregulated in the resistant (R) strain of cockroach compared with the susceptible (S) strain, promoted insecticide resistance by negatively targeting ARFIP2 (ADP ribosylation factor interacting protein 2). While, ame-miR-3770-5p, which was significantly downregulated in the R strain, impaired insecticide resistance by negatively targeting Rrs1_0 (ribosome biogenesis regulator 1 homolog). This study used cockroach as a model insect to broaden our understanding of the complex mechanisms of insecticide resistance, thereby providing opportunities to develop novel insecticides with enhanced killing effect based on the key molecular targets of the ame-miR-125-5p-ARFIP2 axis and the ame-miR-3770-5p-Rrs1_0 axis, with the aim of delaying or overcoming the resistance development at the genetic level. - Source: PubMed
Publication date: 2025/09/15
Cai TongZhang YutingZhang XiancuiZang YananMa WenxiaoChen XingyuHan YingnanLiu YanLiu WenjieWang XuejunZhang Fan - Lysosome damage activates multiple pathways to prevent lysosome-dependent cell death, including a repair mechanism involving endoplasmic reticulum (ER)-lysosome membrane contact sites, phosphatidylinositol 4-kinase-2a (PI4K2A), phosphatidylinositol-4 phosphate (PI4P), and oxysterol-binding protein-like proteins (OSBPLs) lipid transfer proteins. PI4K2A localizes to the trans-Golgi network and endosomes, yet how it is delivered to damaged lysosomes remains unknown. During acute sterile damage and damage caused by intracellular bacteria, we show that ATG9A-containing vesicles perform a critical role in delivering PI4K2A to damaged lysosomes. ADP ribosylation factor interacting protein 2 (ARFIP2), a component of ATG9A vesicles, binds and sequesters PI4P on lysosomes, balancing OSBPL-dependent lipid transfer and promoting the retrieval of ATG9A vesicles through the recruitment of the adaptor protein complex-3 (AP-3). Our results identify a role for mobilized ATG9A vesicles and ARFIP2 in lysosome homeostasis after damage and bacterial infection. - Source: PubMed
Publication date: 2025/06/02
De Tito StefanoAlmacellas EugeniaDai Yu DanielMillard EmilyZhang Wenxinde Heus CeciliaQueval ChristopheHervás Javier HPellegrino EnricaPanagi IoannaFogde DitteThurston Teresa L MKlumperman JudithGutierrez MaximilianoTooze Sharon A - Drug targets supported by genetic evidence with a several-fold higher probability of success in clinical trials. We performed a comprehensive proteome-wide Mendelian randomization (MR) analysis to identify causal proteins and potential therapeutic targets for four site-specific cancers. A total of 13,248 protein quantitative trait loci for 4853 plasma proteins were utilized for proteome-wide MR analysis. Identification of cancer causal proteins in the discovery cohort and further validation in the replication cohort. Colocalization, summary-data-based MR (SMR) analysis, and transcriptome‑wide association studies (TWAS) were performed to check the accuracy of the candidate proteins. Two-step MR analysis was used to explore the effects of plasma protein-mediated 248 modifiable factors on cancer. Phenome-wide MR (Phe-MR) analysis, druggability evaluation, and single-cell type expression analysis further assessed the potential of causal proteins. Combining the results of the meta-analysis of MR estimates from the two cohorts, 21, 2, 24 and 1 causal proteins were identified in breast, lung, prostate and stomach cancers, respectively. Evidence from colocalization, SMR analysis, and TWAS highlighted CD36, DNPH1, and PLXND1 as the most promising drug targets for breast cancer, and ZNF175 for prostate cancer. 1 new potential biomarker (PLXND1) for breast cancer, 2 new promising targets (RELL1, DEFB119) for lung cancer, and 8 new circulating biomarkers (ARFIP2, CCN6, CTRB2, HTR7, MRPL33, TNFRSF6B, VAMP5, ZNF175) for prostate cancer were firstly reported. Some plasma proteins may mediate the association of these cancers with other systemic diseases. Additionally, genetically predicted higher BMI and overweight may reduce breast cancer risk by altering CASP8, ADM, PLXND1, TNFRSF9, ULK3 and VSIG4 protein levels. Causal proteins of breast and prostate cancer were expressed predominantly on macrophages in cancerous tissues. This study genetically identified several cancer causal proteins which provided new perspectives for the understanding of the etiology and development of novel targeted drugs for cancer. - Source: PubMed
Publication date: 2025/02/06
Yun ZhangjunLiu ZhuSun ZiyiYan XiangYang QianruTian ShaodanLi XiaoHou Li - HER2-positive breast cancer (BC) accounts for 20-30% of all BC subtypes and is linked to poor prognosis. Trastuzumab (Tz), a humanized anti-HER2 monoclonal antibody, is a first-line treatment for HER2-positive breast cancer which faces resistance challenges. This study aimed to identify the biomarkers driving trastuzumab resistance. - Source: PubMed
Publication date: 2024/05/15
Shi XiaoSheng YuanFei HaoranWei BangbangZhang ZhenyuXia XinyuMao ChangfeiSi Xinxin - Hepatocellular carcinoma is one of the most common malignancies, and its prognosis and treatment outcome cannot be accurately predicted. ADP-ribosylation (ADPR) is a post-translationa modification of proteins involved in protein trafficking and immune response. Therefore, it is necessary to explore the ADPR-related genes associated with the prognosis and therapeutic efficacy of hepatocellular carcinoma treatments. - Source: PubMed
Publication date: 2024/01/30
Jiang FenfenXu YanJiang ZhuangHu BinLv QingWang Zhiyong