Recombinant Human Rab22
- Known as:
- Recombinant Human Rab22
- Catalog number:
- STA-719
- Product Quantity:
- 5
- Category:
- -
- Supplier:
- Cellbio
- Gene target:
- Recombinant Human Rab22
Related genes to: Recombinant Human Rab22
- Gene:
- RAB31 NIH gene
- Name:
- RAB31, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- Rab22B
- Chromosome:
- 18p11.22
- Locus Type:
- gene with protein product
- Date approved:
- 1999-08-20
- Date modifiied:
- 2015-09-02
Related products to: Recombinant Human Rab22
Related articles to: Recombinant Human Rab22
- Glioblastoma (GBM) is an aggressive brain tumor that exhibits resistance to current treatment, making the identification of novel therapeutic targets essential. In this context, cellular prion protein (PrP) stands out as a potential candidate for new therapies. Encoded by the PRNP gene, PrP can present increased expression levels in GBM, impacting cell proliferation, growth, migration, invasion and stemness. Nevertheless, the exact molecular mechanisms through which PRNP/PrP modulates key aspects of GBM biology remain elusive. - Source: PubMed
Publication date: 2024/02/13
Boccacino Jacqueline MarciaDos Santos Peixoto RafaelFernandes Camila Felix de LimaCangiano GiovanniSola Paula RodriguesCoelho Bárbara ParanhosPrado Mariana BrandãoMelo-Escobar Maria Isabelde Sousa Breno PereiraAyyadhury ShaminiBader Gary DShinjo Sueli Mieko ObaMarie Suely Kazue Nagahashida Rocha Edroaldo LummertzLopes Marilene Hohmuth - Vascular smooth muscle cells (SMCs) and their derivatives are key contributors to the development of atherosclerosis. However, studying changes in SMC gene expression in heterogeneous vascular tissues is challenging due to the technical limitations and high cost associated with current approaches. In this paper, we apply Translating Ribosome Affinity Purification sequencing (TRAP-Seq) to profile SMC-specific gene expression directly from tissue. - Source: PubMed
Publication date: 2024/01/30
Ravindran AarthiHolappa LariNiskanen HenriSkovorodkin IlyaKaisto SusannaBeter MustafaKiema MiikaSelvarajan IlakyaNurminen ValtteriAavik EinariAherrahrou RédouanePasonen-Seppänen SannaFortino VittorioLaakkonen Johanna PYlä-Herttuala SeppoVainio SeppoÖrd TiitKaikkonen Minna U - Translation dysregulation plays a crucial role in tumourigenesis and cancer progression. Oncogenic translation relies on the stability and availability of tRNAs for protein synthesis, making them potential targets for cancer therapy. - Source: PubMed
Li PengWang WenlongZhou RuixinDing YingLi Xinying - Extracellular vesicles (EV), important messengers in intercellular communication, can load and transport various bioactive components and participate in different biological processes. We previously isolated glioma human endothelial cells (GhECs) and found that GhECs, rather than normal human brain endothelial cells (NhECs), exhibit specific enrichment of MYO1C into EVs and promote the migration of glioma cells. In this study, we explored the mechanism by which MYO1C is secreted into EVs. We report that such secretion is dependent on RAB31, RAB27B, and FAS. When expression of RAB31 increases, MYO1C is enriched in secretory EVs. Finally, we identified an EV export mechanism for MYO1C that promotes glioma cell invasion and is dependent on RAB31 in GhECs. In summary, our data indicate that the knockdown of RAB31 can reduce enrichment of MYO1C in extracellular vesicles, thereby attenuating the promotion of glioma cell invasion by GhEC-EVs. - Source: PubMed
Publication date: 2023/11/20
Suo JinghaoWang YuxinWang LinQiu BojunWang ZhixingYan AnQiang BoqinHan WeiPeng Xiaozhong - Inhalation anthrax, the deadliest form of the disease, requires inhaled B. anthracis spores to escape from the alveolar space and travel to the mediastinal lymph nodes, from where the vegetative form of the pathogen disseminates, resulting in a rapidly fatal outcome. The role of epithelia in alveolar escape is unclear, but previous work suggests these epithelial cells are involved in this process. Using confocal microscopy, we found that B. anthracis spores are internalized more rapidly by A549 type II alveolar epithelial cells compared to hAELVi type I alveolar epithelial cells. Internalization of spores by alveolar epithelial cells requires cytoskeletal rearrangement evidenced by significant inhibition by cytochalasin D, an actin inhibitor. Chemical inhibitors of macropinocytosis significantly downregulated B. anthracis spore internalization in human alveolar cells, while inhibitors of other endocytosis pathways had minimal effects. Additional studies using a macropinosome marker and electron microscopy confirmed the role of macropinocytosis in spore uptake. By colocalization of B. anthracis spores with four endocytic Rab proteins, we demonstrated that Rab31 played a role in B. anthracis spore macropinocytosis. Finally, we confirmed that Rab31 is involved in B. anthracis spore internalization by enhanced spore uptake in Rab31-overexpressing A549 cells. This is the first report that shows B. anthracis spore internalization by macropinocytosis in human epithelial cells. Several Rab GTPases are involved in the process. - Source: PubMed
Publication date: 2023/08/14
Wu WenxinBooth J LelandLiang ZhiminLi GuangpuMetcalf Jordan P