Ask about this productRelated genes to: RAB40B antibody
- Gene:
- RAB40B NIH gene
- Name:
- RAB40B, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- SEC4L, RAR
- Chromosome:
- 17q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-22
- Date modifiied:
- 2015-08-25
Related products to: RAB40B antibody
Related articles to: RAB40B antibody
- Avian reovirus (ARV) is an oncolytic virus that induces autophagy and apoptosis in cancer cells, modulates the immune response, and exposes tumor-associated antigens to the immune system, making it a promising candidate for cancer therapy. Cancer cell migration and invadopodia formation are essential processes in metastasis, and targeting these mechanisms could be beneficial in limiting cancer progression. - Source: PubMed
Publication date: 2025/06/12
Hsu Chao-YuLi Jyun-YiHuang Wei-RuLiao Tsai-LingWen Hsiao-WeiWang Chi-YoungLye Lon-FyeNielsen Brent LLiu Hung-Jen - HNSCC presents a significant health challenge due to its high mortality resulting from treatment resistance and locoregional invasion into critical structures in the head and neck region. Understanding the invasion mechanisms of HNSCC has the potential to guide targeted therapies, improving patient survival. Previously, we demonstrated the involvement of doublecortin like kinase 1 (DCLK1) in regulating HNSCC cell invasion. Here, we investigated the hypothesis that DCLK1 modulates proteins within invadopodia, specialized subcellular protrusions that secrete matrix metalloproteinases to degrade the ECM. - Source: PubMed
Publication date: 2025/02/24
Arnold LeviYap MarrionFarrokhian NathanJackson LauraBarry MichaelLy ThucArjunan PachiappanKaczorowski-Worthley AngelaTews CarterPandey AvishaMorrison AustinWashburn Michael PStanding DavidGomez Juan PYellapu Nanda KumarJohnson DavidLi LinhengUmar ShahidAnant ShrikantThomas Sufi Mary - This study was aimed at exploring a specific open region of chromatin in the peripheral blood mononuclear cells (PBMCs) of patients with breast cancer and evaluating its feasibility as a biomarker for diagnosing and predicting breast cancer prognosis. We obtained PBMCs from breast cancer patients and healthy people for the assay for transposase-accessible chromatin (ATAC) sequencing (n = 3) and obtained the GSE27562 chip sequencing data for secondary analyses. Through bioinformatics analysis, we mined the pattern changes for chromatin accessibility in the PBMCs of breast cancer patients. A total of 1,906 differentially accessible regions (DARs) and 1,632 differentially expressed genes (DEGs) were identified via ATAC sequencing. The upregulated DEGs in the disease group were mainly distributed in the cells, organelles, and cell-intima-related structures and were mainly responsible for biological functions such as cell nitrogen complex metabolism, macromolecular metabolism, and cell communication, in addition to functions such as nucleic acid binding, enzyme binding, hydrolase reaction, and transferase activity. Combined with microarray data analysis, the following set of nine DEGs showed intersection between the ATAC and microarray data: JUN, MSL2, CDC42, TRIB1, SERTAD3, RAB14, RHOB, RAB40B, and PRKDC. HOMER predicted and identified five transcription factors that could potentially bind to these peak sites, namely NFY, Sp 2, GFY, NRF, and ELK 1. Chromatin accessibility analysis of the PBMCs from patients with early-stage breast cancer underscores its potential as a significant avenue for biomarker discovery in breast cancer diagnostics and treatment. By screening the transcription factors and DEGs related to breast cancer, this study provides a comprehensive theoretical foundation that is expected to guide future clinical applications and therapeutic developments. - Source: PubMed
Publication date: 2024/09/23
Xia LongjieLu JiaminQin YixuanHuang RunchunKong FanbiaoDeng Yu - To explore whether the p17 protein of oncolytic avian reovirus (ARV) mediates cell migration and invadopodia formation, we applied several molecular biological approaches for studying the involved cellular factors and signal pathways. We found that ARV p17 activates the p53/phosphatase and tensin homolog (PTEN) pathway to suppress the focal adhesion kinase (FAK)/Src signaling and downstream signal molecules, thus inhibiting cell migration and the formation of invadopodia in murine melanoma cancer cell line (B16-F10). Importantly, p17-induced formation of invadopodia could be reversed in cells transfected with the mutant PTEN. p17 protein was found to significantly reduce the expression levels of tyrosine kinase substrate 5 (TKs5), Rab40b, non-catalytic region of tyrosine kinase adaptor protein 1 (NCK1), and matrix metalloproteinases (MMP9), suggesting that TKs5 and Rab40b were transcriptionally downregulated by p17. Furthermore, we found that p17 suppresses the formation of the TKs5/NCK1 complex. Coexpression of TKs5 and Rab40b in B16-F10 cancer cells reversed p17-modulated suppression of the formation of invadopodia. This work provides new insights into p17-modulated suppression of invadopodia formation by activating the p53/PTEN pathway, suppressing the FAK/Src pathway, and inhibiting the formation of the TKs5/NCK1 complex. - Source: PubMed
Publication date: 2024/07/17
Hsu Chao-YuLi Jyun-YiYang En-YingLiao Tsai-LingWen Hsiao-WeiTsai Pei-ChienJu Tz-ChuenLye Lon-FyeNielsen Brent LLiu Hung-Jen - Rab40 proteins are an atypical subgroup of Rab GTPases containing a unique suppressor of the cytokine signaling (SOCS) domain that is recruited to assemble the CRL5 E3 ligase complex for proteolytic regulation in various biological processes. A nonsense mutation deleting the C-terminal SOCS box in the gene was identified in a family with axonal peripheral neuropathy (Charcot-Marie-Tooth disease type 2), and pathogenicity of the mutation was assessed in model organisms of zebrafish and . Compared to control fish, zebrafish larvae transformed by the human mutant showed a defective swimming pattern of stalling with restricted localization and slower motility. We were consistently able to observe reduced labeling of synaptic markers along neuromuscular junctions of the transformed larvae. In addition to the neurodevelopmental phenotypes, compared to normal expression, we further examined ectopic expression of in to show a progressive decline of locomotion ability. Decreased ability of locomotion by ubiquitous expression of the human mutation was reproduced not with GAL4 drivers for neuron-specific expression but only when a pan-glial GAL4 driver was applied. Using the ectopic expression model of , we identified a genetic interaction in which down regulation exacerbated the defective motor performance, showing a consistent loss of SOCS box of the pathogenic RAB40B. Taken together, we could assess the possible gain-of-function of the human mutation by comparing behavioral phenotypes in animal models; our results suggest that the mutant phenotypes may be associated with CRL5-mediated proteolytic regulation. - Source: PubMed
Son WonseokJeong Hui SuNam Da EunLee Ah JinNam Soo HyunLee Ji EunChoi Byung-OkChung Ki Wha