| 1993 |
Antisense oligonucleotide-mediated knockdown of Rab3B in rat anterior pituitary cells specifically inhibits calcium-dependent exocytosis without affecting endocytosis, placing Rab3B as a key regulator of exocytosis downstream of calcium-dependent processes. |
Antisense oligonucleotide knockdown introduced via whole-cell patch clamp; Ca2+-dependent exocytosis monitored electrophysiologically |
Nature |
High |
8393147
|
| 1993 |
In human platelets, Rab3B protein is predominantly cytosolic, and thrombin-induced platelet activation leads to phosphorylation of Rab3B; phosphorylation was absent when cAMP-dependent protein kinase was stimulated (PGE1 treatment), suggesting phosphorylation is linked to secretion. |
Subcellular fractionation; phosphorylation assay with thrombin stimulation and PGE1 inhibition |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
8356066
|
| 1996 |
In PC12 neuroendocrine cells, Rab3B and Rab3A both target to large dense core vesicles (LDCVs) and both bind recombinant rabphilin-3A in a GTP-dependent manner; however, Rab3B (and a GTP-binding mutant Rab3B N135I) markedly stimulates Ca2+-evoked norepinephrine secretion and increases NE accumulation into LDCVs, whereas Rab3A modestly inhibits secretion, demonstrating functionally distinct roles despite shared targeting and effector binding. |
Stable expression in PC12 cells; immunofluorescence and membrane fractionation for targeting; GTP-dependent pull-down with recombinant rabphilin-3A; [3H]NE release assay |
The Journal of biological chemistry |
High |
8636125
|
| 1997 |
In bovine chromaffin cells, Rab3B has a much lower GTP[S] binding affinity (Kd ~2700 nM) compared to Rab3A (Kd ~15 nM) and Rab3C; Rab3B localizes distinctly to the plasma membrane rather than vesicle-like structures as seen for Rab3A and Rab3C; C-terminal truncation decreases GTP[S] binding affinity for all three isoforms. |
GTP[S] binding assays; C-terminal truncation/swap mutagenesis; immunofluorescence subcellular localization |
The Biochemical journal |
Medium |
9164844
|
| 1998 |
Antisense knockdown of Rab3B in pituitary cells inhibits both basal and GnRH-induced gonadotrophin release without affecting intracellular gonadotrophin content or Ca2+ transients, placing Rab3B function downstream of cytosolic Ca2+ elevation in GnRH-regulated exocytosis from gonadotrophs. |
Antisense oligonucleotide knockdown; radioimmunoassay for hormone release; Ca2+ imaging; comparison of Rab3B-positive vs Rab3B-negative cells |
The Journal of endocrinology |
Medium |
9659290
|
| 1999 |
Immunoelectron microscopy demonstrates co-localization of Rab3B with oxytocin within the same secretory granules of large luteal cells in the sheep corpus luteum, implicating Rab3B in luteal hormone exocytosis. |
Electron microscopic immunocytochemistry (dual immunogold labeling) |
The Anatomical record |
Low |
9972806
|
| 2000 |
Stable expression of Rab3B (but not Rab3A or the GTP-binding mutant Rab3B N135I) in PC12 cells reorganizes F-actin into filopodia and redistributes the junction-associated protein ZO-1; this effect on ZO-1 is abolished by PI3-kinase inhibitors, whereas Rab3B-dependent norepinephrine secretion is PI3-kinase-independent, indicating Rab3B regulates junctional protein targeting and secretion by distinct mechanisms involving PI3-kinase signaling. |
Stable expression of rab3B, rab3A, and GTP-binding mutant in PC12 cells; immunofluorescence for ZO-1 and F-actin; PI3-kinase inhibitor experiments; [3H]NE secretion assay |
Experimental cell research |
Medium |
10854049
|
| 2001 |
In human platelets, the majority of Rab3B is localized to the particulate (membrane) fraction; RabGDI-alpha pulls Rab3B from the particulate fraction; GST-Rab3B pull-down and reverse Sepharose-CaM bead experiments demonstrate a Ca2+-dependent but guanine-nucleotide-status-independent interaction between Rab3B and calmodulin. |
Subcellular fractionation; GST-RabGDI-alpha pull-down; GST-Rab3B pull-down of calmodulin from platelet cytosol; Sepharose-CaM bead pull-down; EGTA controls |
Biochemical and biophysical research communications |
Medium |
11741295
|
| 2002 |
GTP-bound Rab3B directly interacts with the cytoplasmic domain of the polymeric immunoglobulin receptor (pIgR) in MDCK epithelial cells; binding of dIgA to pIgR dissociates this interaction (requiring dIgA-mediated signaling, Arg657 in pIgR cytoplasmic domain, and possibly GTP hydrolysis by rab3b); overexpression of GTP-locked rab3b inhibits dIgA-stimulated transcytosis, demonstrating that rab3b-pIgR binding controls ligand-stimulated transcytosis. |
Co-immunoprecipitation; direct binding assay with cytoplasmic domain of pIgR; site-directed mutagenesis (Arg657); transcytosis assay with GTP-locked rab3b overexpression; subcellular localization by immunofluorescence |
Developmental cell |
High |
11832247
|
| 2003 |
Overexpression of dominant-negative or constitutively active Rab3B mutants in non-polarized fibroblasts specifically inhibits cell-surface transport of basolateral LDLR but not apical p75NTR or tight junctional Claudin-1, identifying Rab3B as a regulator of basolateral vesicle transport. |
Overexpression of Rab3B mutants in fibroblasts; cell-surface transport assay for p75NTR, LDLR, and Claudin-1 |
Biochemical and biophysical research communications |
Medium |
12901864
|
| 2004 |
Noc2 was identified as a Rab3B effector in epithelial cells: Noc2 binds Rab3B in a GTP-dependent manner (pull-down assay); when co-expressed with GTP-bound Rab3B, Noc2 is recruited from cytosol to perinuclear membranes; Noc2 overexpression inhibits cell-surface transport of basolateral VSV-G protein. |
Degenerate RT-PCR; GST pull-down assay; co-expression localization by immunofluorescence; cell-surface transport assay |
Biochemical and biophysical research communications |
Medium |
15003533
|
| 2006 |
In rat melanotrophs expressing both Rab3A and Rab3B, antisense knockdown of Rab3A (but not Rab3B) blocks Ca2+-dependent secretion; injection of GTP-bound Rab3A with intact C-terminus stimulates secretion while Rab3A T36N (GTP-binding impaired) inhibits it; injection of purified Rab3B protein is ineffective, demonstrating that Rab3A and Rab3B have non-redundant functions in regulated exocytosis in melanotrophs. |
Antisense oligonucleotide knockdown; patch-clamp capacitance measurements; cytosolic dialysis with recombinant proteins; in situ hybridization; immunocytochemistry |
American journal of physiology. Cell physiology |
High |
16822953
|
| 2008 |
Gas8, a microtubule-binding protein involved in dynein motor regulation, was identified as a novel GTP-bound form-specific Rab3B-binding protein using yeast two-hybrid; Gas8 and Rab3B co-localize at the Golgi in NIH 3T3 cells; expression of the Rab3B-binding domain of Gas8 relocates Rab3B, suggesting Gas8 links Rab3B to microtubules. |
Yeast two-hybrid; co-localization by immunofluorescence; overexpression of Gas8 Rab3B-binding domain |
Archives of biochemistry and biophysics |
Low |
18396146
|
| 2009 |
siRNA knockdown of Rab3b/3c in dendritic cells impairs antigen cross-presentation; Rab3b/3c-positive compartments co-localize with MHC class I molecules at perinuclear tubular structures, with internalized transferrin receptor (recycling endosomes), and with a fraction of Rab27a adjacent to phagosomes; depletion of Rab3b/3c reduces fast-phase transferrin receptor recycling, indicating Rab3b/3c-positive recycling vesicles constitute a recycling compartment involved in cross-presentation. |
siRNA knockdown of 57 Rab GTPases (screen); fluorescence protein-tagged β2-microglobulin tracing; co-localization immunofluorescence; transferrin recycling assay |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
19717423
|
| 2009 |
AAV-mediated Rab3B overexpression in rat substantia nigra dopaminergic neurons increases striatal dopamine content, number and size of synaptic vesicles, and levels of presynaptic proteins; extracellular DOPAC measurement after L-DOPA injection indicates enhanced dopamine storage capacity; Rab3B overexpression protects A9 DA neurons against 6-OHDA and improves behavioral outcomes in a retrograde lesion PD model. |
AAV-mediated overexpression in rat SN; electron microscopy (vesicle count/size); HPLC for dopamine/DOPAC; behavioral assays; in vitro toxicity assays (6-OHDA, MG-132) in BE(2)-M17 cells |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
20007772
|
| 2011 |
Rab3B knockout mice show impaired endocannabinoid-dependent long-term depression at inhibitory synapses (i-LTD) in CA1 hippocampus, without altering excitatory/inhibitory synaptic strength, short-term plasticity, or NMDA receptor-dependent LTP; Rab3B is highly enriched in inhibitory synapses; Rab3B KO mice display enhanced reversal learning. Rab3B interacts with RIM1α and RIM2α in a GTP-dependent manner (established by prior studies cited). This places Rab3B in a presynaptic Rab3/RIM-dependent pathway specifically at inhibitory synapses. |
Genetic KO; electrophysiological recordings in acute hippocampal slices; Morris water-maze and fear-conditioning behavioral assays; immunolocalization |
Proceedings of the National Academy of Sciences of the United States of America |
High |
21844341
|
| 2023 |
The lncRNA ENST00000436340 promotes RAB3B mRNA degradation by facilitating binding of PTBP1 to RAB3B mRNA; RAB3B knockdown in podocytes causes cytoskeleton rearrangement and inhibition of GLUT4 translocation to the plasma membrane, leading to podocyte injury. |
RNA immunoprecipitation (RIP); gain/loss-of-function knockdown; Western blot; cytoskeleton/GLUT4 localization assays |
Cell death & disease |
Medium |
36792603
|
| 2024 |
In lung adenocarcinoma cells, Rab3B interacts with DDX6 and enhances its protein stability; DDX6 knockdown phenocopies Rab3B depletion (reduced proliferation, colony formation, migration), and DDX6 overexpression partially rescues Rab3B-depletion phenotypes, placing DDX6 downstream of Rab3B in promoting lung adenocarcinoma aggressiveness. |
Co-immunoprecipitation; gain/loss-of-function overexpression and knockdown; rescue experiments; xenograft mouse model |
Molecular medicine (Cambridge, Mass.) |
Medium |
38834947
|
| 2025 |
In chordoma, RAB3B physically interacts with the phosphatase DUSP12 and blocks DUSP12-mediated dephosphorylation of phospho-S6 at S235/236, thereby enhancing S6 phosphorylation and mTORC1/S6 signaling; RAB3B ablation reduces chordoma stemness and tumorigenicity in vivo and in vitro; mTORC1 inhibition phenocopies RAB3B overexpression effects on stemness. |
Co-immunoprecipitation; phosphorylation assays; in vitro and in vivo loss-of-function (RAB3B ablation); pharmacological mTORC1 inhibition; transcriptome and proteome analyses |
Advanced science (Weinheim, Baden-Wurttemberg, Germany) |
Medium |
40135815
|
| 2026 |
In human amniotic epithelial cells, RAB3B overexpression promotes cell migration, suppresses EMT, reduces epithelial permeability, and upregulates tight junction proteins; RAB3B enhances extracellular vesicle internalization, which in turn potentiates tight junction integrity; RAB3B knockdown produces opposite effects. |
RAB3B overexpression and siRNA knockdown in hAECs; permeability assays; immunofluorescence for tight junction proteins; extracellular vesicle isolation and internalization assay; PROM mouse model |
Biology of reproduction |
Medium |
41792905
|