RAB3B (Human) IP-WB Antibody Pair
- Known as:
- RAB3B (Human) IP-Western Blot Antibody Pair
- Catalog number:
- H00005865-PW1
- Product Quantity:
- 1 Set
- Category:
- -
- Supplier:
- Abno
- Gene target:
- RAB3B (Human) IP- Antibody Pair
Related genes to: RAB3B (Human) IP-WB Antibody Pair
- Gene:
- RAB3B NIH gene
- Name:
- RAB3B, member RAS oncogene family
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p32.3
- Locus Type:
- gene with protein product
- Date approved:
- 1989-06-30
- Date modifiied:
- 2016-10-05
Related products to: RAB3B (Human) IP-WB Antibody Pair
Related articles to: RAB3B (Human) IP-WB Antibody Pair
- Lung adenocarcinoma (LUAD) is characterized by high mortality and recurrence. This study investigated the clinical significance and biological role of as a potential biomarker in LUAD. - Source: PubMed
Publication date: 2026/06/29
Liu Xu-ShengChen XiWang NingCheng Zhi-MingXie Yi-ChiJiang TingPei Zhi-Jun - Prenatal metabolic adversity, including fetal growth restriction (FR), programs long-term alterations in systemic and neural insulin sensitivity, yet its impact on insulin signaling within reward-circuit plasticity across development remains poorly understood. Using a rodent model of gestational FR, we examined how early metabolic stress alters insulin regulation of mesolimbic reward circuits using in vivo chronoamperometry to measure nucleus accumbens (NAc) dopamine (DA) release during palatable food exposure, with and without peripheral insulin. We assessed longitudinal consumption behavior and conducted transcriptomic profiling (RNA-Seq) at birth (P0), weaning (P21), and adulthood (P90) following saline or insulin administration. FR blunted immediate NAc DA release in response to palatable food, a deficit specifically reversed by peripheral insulin, indicating altered insulin sensitivity of mesolimbic reward circuits. FR animals also display accelerated initial palatable food consumption. Transcriptomic analysis revealed that FR reprograms the NAc's molecular response to insulin. Across development and sex, only 2-9% of insulin-responsive genes overlap between FR and controls. FR generated condition-specific and frequently inverted transcriptional signatures, affecting genes linked to synaptic plasticity (Cplx3, Rab3b) and neurodevelopment (Ccn3). These findings demonstrate that prenatal adversity reconfigures the NAc by altering its molecular and neurochemical responsiveness to insulin. This developmental reprogramming reveals how early metabolic stress reshapes insulin sensitivity within reward circuitry, a mechanism that may contribute to both metabolic and psychiatric disease vulnerability. - Source: PubMed
Publication date: 2026/06/19
Alberry BonnieBarth BarbaraBatra AashitaAlves Marcio BonessoMiguel Patricia MaidanaO'Toole NicholasPatel SachinLupinsky DerekZhang Tie YuanWen XianglanArcego Danusa MarLaureano Daniela PereiraPokhvisneva IrinaDalle Molle RobertaSilveira Patricia Pelufo - Circular RNA (hsa_circ_0070354), also known as circPTPN13, was demonstrated in our previous study that it can be used as a biomarker for diagnosing non-small cell lung cancer (NSCLC). However, the mechanism of its role in the occurrence and development of NSCLC has not been investigated. - Source: PubMed
Huang YuejiaoQin ShiyiZhang YuGu XinliangZheng MingLing GuojieYang LeiJu Shaoqing - Premature rupture of membranes (PROM) is a major cause of preterm birth and neonatal mortality. Tight junctions are critical for maintaining fetal membrane barrier integrity. Ras-related protein Rab-3B (RAB3B), a key regulator of vesicle trafficking, may influence barrier homeostasis; however, its role in PROM remains unclear. - Source: PubMed
Su ShuguangYe QiantaoChen FeilongTian QinGan CaixiaLi Yanqiu - Semantic variant of primary progressive aphasia is a clinical subtype of frontotemporal lobar degeneration and is marked by TDP-43 subtype C pathology (FTLD-TDP C). It is a sporadic disease, yet has a strikingly homogeneous clinicopathological presentation, suggesting a common pathophysiology. The aim of this study was to discover dysregulated pathways in FTLD-TDP C through transcriptomics of the temporal cortex, its most affected region. Bulk RNA sequencing was conducted on temporal cortices of a post-mortem cohort of 18 FTLD-TDP C patients and 23 sex- and age-matched controls. Differential expression and functional analyses were run to detect differentially expressed genes with FDR<0.05 (DEG) and functionally annotate them. We assessed enrichment of TARDBP's protein interactors and RNA targets in DEG. Our findings were compared to other published RNA sequencing data of tauopathies (Alzheimer's dementia, progressive supranuclear palsy and FTLD with MAPT), FTLD-TDP (subtypes A&B) and available proteomics of this cohort. Furthermore, we performed weighted gene co-expression network analysis (WGCNA). We adjusted for differences in cell type composition between cases and controls using cell deconvolution, and removed genes dysregulated in temporal cortices of other datasets. In DEG of FTLD-TDP we focused on enrichment of synaptic processes using SynGO. We found upregulation of damage response, cell structure, RNA splicing processes and downregulation of synaptic processes in 6322 DEG and five disease-related WGCNA modules. TARDBP-related genes were enriched in DEG. Additionally, transmembrane transport across the neurovascular unit was dysregulated. After cell deconvolution and removal of common tau-genes, postsynaptic processes remained dysregulated, specifically gene ontology terms 'modulation of chemical synaptic transmission' and 'neurotransmitter receptor localisation to postsynaptic specialisation membrane'. We found eleven synaptic FTLD-TDP C-specific genes affected on both RNA- and protein-level in the temporal cortex, which were involved in synaptic adhesion (CADM1, NCAN), signal transmission (COMT, RGS144, SLC1A2, TUBB2B) and synaptic plasticity (BEGAIN, ITPKA, LRFN1, RAB3B, SYNPO). In conclusion, a wide range of processes were dysregulated on RNA-level in the temporal cortex of FTLD-TDP C, including commonly affected processes in neurodegeneration, such as structural cell alterations. Dysregulation of TARDBP-related genes and RNA splicing has also been observed in other TDP-43 proteinopathies. Importantly, we found that postsynaptic processes were downregulated in FTLD-TDP C, after removing tauopathy-related genes and after cell deconvolution. In particular, assembly of receptors at the postsynaptic membrane and synaptic signal transmission were affected, both on RNA and protein level. Future research on these pathways could elucidate distinct pathophysiological mechanisms and guide targeted clinical approaches. - Source: PubMed
Publication date: 2026/03/06
Rajicic AnaMol Merel OMelhem ShamiramKisic Helenavan Swieten John CSeelaar Harrovan Rooij Jeroen G J