Rab3A pAb;mouse, rat
- Known as:
- Rab3A pAb;mouse, rat
- Catalog number:
- ASAKAP-GP003C
- Product Quantity:
- 25 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Rab3A pAb;mouse rat
Related genes to: Rab3A pAb;mouse, rat
- Gene:
- RAB3A NIH gene
- Name:
- RAB3A, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19p13.11
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2016-10-05
Related products to: Rab3A pAb;mouse, rat
Related articles to: Rab3A pAb;mouse, rat
- A high-fat diet (HFD) combined with sleep deprivation (SD) (collectively termed HSD) is a common modern lifestyle stressor that induces metabolic dysfunction and neurobehavioral alterations. Here, we investigated whether daily coffee (5 g of coffee powder per kg body weight) could alleviate the above-mentioned alterations induced by HSD in male C57BL/6 mice subjected to 20 h day SD for 9 weeks, and explored the underlying mechanisms using multi-omics approaches. Our results showed that the coffee intervention ameliorated HSD-induced anxiety-like behavior, hippocampal synaptic damage, and hepatic steatosis. These improvements may be associated with alterations in the gut microbiota composition (enrichment of , , and ; reduction of ), enhanced hepatic bile acid and lipid metabolism (, upregulation of , ), suppression of profibrotic and proinflammatory signaling, and altered brain transcriptome profiles, including the upregulation of synaptic and neurotransmitter release related genes. Integrated multi-omics network analysis showed that the HSD network was dominated by a single microbial hub with brain inflammatory and hepatic lipid metabolism genes as core features, whereas the coffee treatment group exhibited a more distributed network architecture featuring multiple microbial genera, coffee metabolism related genes (/), and the synaptic gene . Collectively, these findings suggest that moderate coffee consumption may alleviate HSD-induced neurobehavioral and metabolic disturbances, an effect accompanied by coordinated multi-organ adaptation. - Source: PubMed
Publication date: 2026/07/12
Li WentingJiang HuibinWei FenfenLin ZihanWu YanWang YingSong Lihua - Bovine Viral Diarrhea Virus (BVDV) poses a significant threat to the global cattle industry, causing substantial economic losses. Long non-coding RNAs (lncRNAs) play crucial regulatory roles in various biological processes, including viral infections. However, the specific lncRNAs influencing BVDV replication remain poorly characterized. This study identified lncSMIM14 as a key host factor upregulated during BVDV infection in MDBK cells. Functional analyses demonstrated that lncSMIM14 overexpression significantly enhanced BVDV replication, evidenced by increased viral mRNA levels, progeny virus titers, cytopathic effects, and dsRNA abundance, while its knockdown exerted the opposite effect. Mechanistically, we revealed that lncSMIM14 specifically targets and positively regulates the expression of the endocytosis-related GTPase Rab3a. Importantly, Rab3a itself was shown to be essential for efficient BVDV replication, as its overexpression promoted viral replication, and its knockdown inhibited it. Furthermore, Rab3a co-localized with key endocytic regulators Rab5a and Rab7a, and both lncSMIM14 overexpression and Rab3a overexpression promoted the formation of endocytic vesicles, particularly post-BVDV infection. Our findings unveil a novel mechanism wherein BVDV exploits the host lncRNA lncSMIM14 to hijack Rab3a-mediated endocytosis, facilitating its own replication. This study identifies the lncSMIM14-Rab3a axis as a critical host pathway subverted by BVDV, providing new potential targets for antiviral intervention. - Source: PubMed
Publication date: 2026/02/27
Shao ZhiranMa SiqiGao FengSiyueLou YangLiu XinyiYang LiMai ZhanhaiWang LixiaHaiyilati AreayiShi HuijunFu Qiang - Ageing (AG) is associated with cognitive decline and an increased risk of developing neurodegenerative diseases (NDs) like Alzheimer's disease (AD) and Parkinson's disease (PD). While individual diseases have been widely studied, cross-condition convergence at the transcriptomic and regulatory levels has not been systematically defined. - Source: PubMed
Publication date: 2026/03/06
Chaurasiya MonaCholleti Sai NikhithPrasad GajendraVindal Vaibhav - This study aimed to determine the potential mechanism by which pancreatic stem cell-derived beta cells (PSCs-β) assist in the body's glucose-lowering capacity in type 1 diabetes (T1D) rats. - Source: PubMed
Publication date: 2026/03/03
Shan JunlingWang HuifengZhu Guangyu - Deletion of IG20 (also known as MADD), which can encode multiple isoforms, causes diabetes in mice by impairing glucose-stimulated insulin secretion. To evaluate the role of IG20 in mediating the therapeutic potential of glinide-class insulin secretagogues, we tested their effects in Ig20/Madd-knockout (KMA1ko) mice. Glucose tolerance tests revealed that repaglinide, mitiglinide, and nateglinide failed to lower blood glucose levels or enhance insulin secretion in KMA1ko mice, suggesting that IG20 deficiency significantly diminishes the therapeutic efficacy of glinides. The functional relevance of at least 6 IG20 isoforms remains to be defined. Interestingly, among the six IG20 splicing isoforms re-expressed in IG20-deficient Min6 cells, only KIAA0358 was capable of restoring glucose-stimulated insulin secretion. Notably, KIAA0358 re-expression also rescued repaglinide-induced insulin secretion in vivo. Further transmission electron microscopy and total internal reflection fluorescence microscopy analyses showed that KIAA0358 significantly promoted insulin granule transport and docking impaired by IG20 knockout. Furthermore, guanine nucleotide exchange assay and GST pull-down demonstrated that KIAA0358 functions as a Rab GEF to convert Rab3A and Rab27A from the GDP-bound to the active GTP-bound state, thereby restoring their interactions with the downstream effector proteins Rim2α and Slac-2a that were impaired by IG20 deficiency. Therefore, by regulating the activation states of Rab3A and Rab27A, KIAA0358 mediated the transport and docking of insulin granules to the plasma membrane. This study also highlights that the genes encoding non-drug target proteins can influence drug efficacy and provides a novel conceptual foundation for precision medicine strategies aimed at reducing drug resistance and enhancing the clinical efficacy of glinides. - Source: PubMed
Publication date: 2026/02/27
Sui YiWeng Zhao-LeiQian Li-XiaHong Wan-JinPrabhakar Bellur SLi Liang-Cheng