| 2009 |
RAB27B controls MVE (multivesicular endosome) docking at the plasma membrane; Rab27b silencing redistributes MVEs toward the perinuclear region, distinct from Rab27a which controls MVE size. The Rab27b effector Slac2b (EXPH5) phenocopies Rab27b silencing and inhibits exosome secretion. |
RNAi screen in HeLa cells; siRNA silencing; fluorescence microscopy of MVE localization; exosome quantification |
Nature cell biology |
High |
19966785
|
| 2007 |
Rab27b is required for regulated secretion and correct number of platelet dense granules; Rab27b KO mice exhibit hemorrhagic disease, impaired platelet aggregation, reduced dense granule secretion, and ~50% reduction in dense granule number per platelet. Rab27a partially compensates for the secretory defect but not the reduced granule number. |
Rab27b knockout mouse generation; crossed with Rab27a ashen KO to produce double KO; in vitro platelet aggregation assays; dense granule secretion assays; electron microscopy |
Proceedings of the National Academy of Sciences of the United States of America |
High |
17384153
|
| 2004 |
Rab27B localizes to amylase-containing secretory granules in rat parotid acinar cells and forms a complex with the effector Slac2-c/MyRIP on secretory granules in vivo. Disruption of the Rab27B–Slac2-c complex (by recombinant Slp homology domain or blocking antibodies) strongly inhibits isoproterenol-stimulated amylase release. |
Subcellular fractionation; immunoprecipitation; immunohistochemistry; functional blocking with recombinant protein and antibodies in streptolysin O-permeabilized cells |
Journal of cell science |
High |
15039459
|
| 2007 |
Rab27b is expressed in a wide range of exocytic cells and is involved in delivering secretory granules near the plasma membrane (the exocytic site). In pituitary double Rab27a/Rab27b KO mice, polarized distribution of secretory granules close to the plasma membrane is markedly impaired. |
LacZ knock-in reporter mouse for expression analysis; Rab27a/Rab27b double knockout mice generated by crossing; electron microscopy of secretory granule distribution in pituitary cells |
Molecular biology of the cell |
High |
17761531
|
| 2007 |
Rab27b localizes to secretory granules in mast cells and is required for mast cell degranulation (beta-hexosaminidase release) and passive cutaneous anaphylaxis in vivo. Rab27b-deficient BMMC show ~10-fold increase in granules with fast microtubule-based movement, suggesting Rab27b regulates the transition from microtubule to actin-based granule motility. |
Rab27b KO and double KO mice; bone marrow-derived mast cell (BMMC) cultures; beta-hexosaminidase release assays; passive cutaneous anaphylaxis in vivo; live-cell time-lapse imaging; nocodazole treatment |
Traffic (Copenhagen, Denmark) |
High |
17587407
|
| 2002 |
Rab27b associates with secretory granules and the effector granuphilin in pituitary endocrine cells (AtT20). Overexpression of inactive mutant Rab27b N133I significantly inhibits basal and forskolin-induced ACTH secretion. |
Subcellular fractionation; co-immunoprecipitation with granuphilin; dominant-negative overexpression; ACTH secretion assay |
Endocrinology |
High |
11956164
|
| 2004 |
Rab27b localizes to zymogen granule membranes in pancreatic acinar cells. Constitutively active Rab27b Q78L enhances CCK-induced amylase release by ~92%, while dominant-negative Rab27b N133I inhibits release by ~53%, demonstrating a role for Rab27b GTP/GDP cycling in pancreatic acinar exocytosis. |
Proteomics (MALDI-MS/MS) identification; Western blot and immunocytochemistry for localization; adenoviral overexpression of WT, Q78L, and N133I mutants; amylase secretion assay |
Biochemical and biophysical research communications |
High |
15451418
|
| 2003 |
Rab27b localizes to alpha and dense granules in megakaryocytes. Inhibition of endogenous Rab27 function in primary megakaryocytes causes severe quantitative and qualitative defects in proplatelet formation. NF-E2 transcription factor is recruited to the Rab27B promoter and is required for its expression during terminal megakaryocyte differentiation. |
Immunofluorescence localization; dominant-negative Rab27 inhibition in primary megakaryocytes; chromatin immunoprecipitation (ChIP) for NF-E2 at Rab27B promoter; analysis of gunmetal mice |
Blood |
High |
12907454
|
| 2003 |
Rab27b associates with the cytoplasmic face of fusiform vesicles in bladder urothelial umbrella cells and its expression is differentiation-dependent, suggesting a role in targeting uroplakins to the apical plasma membrane. |
Immuno-electron microscopy; Western blot comparing urothelial tissue vs. cultured cells; differentiation-dependent expression analysis |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
14625374
|
| 2009 |
Rab27a and Rab27b both regulate azurophilic granule exocytosis and NADPH oxidase recruitment to the plasma membrane in neutrophils via independent mechanisms. TIRF microscopy shows both isoforms are required for granule docking near the plasma membrane; upregulation of Rab27b in Rab27a-deficient cells does not compensate for the Rab27a secretory defect. |
Rab27a(ash/ash), Rab27b KO, and double KO mouse neutrophils; azurophilic granule exocytosis assays; TIRF microscopy of granule proximity to plasma membrane; NADPH oxidase activity assay |
Traffic (Copenhagen, Denmark) |
High |
20028487
|
| 2010 |
RAB27B promotes invasive growth of ER-positive breast cancer cells through GTP- and geranylgeranyl-dependent delivery of secretory vesicles. Mass spectrometry of RAB27B-positive vesicles identified HSP90α as a key cargo; RAB27B-dependent HSP90α secretion is required for MMP-2 activation and invasion. |
GFP-RAB27B overexpression; point mutants defective in GTP binding or geranylgeranylation; siRNA silencing; Matrigel and collagen invasion assays; mass spectrometry of purified RAB27B vesicles; orthotopic xenograft mouse model |
Journal of the National Cancer Institute |
High |
20484105
|
| 2010 |
Rab27b is an abundant synaptic vesicle Rab GTPase that, unlike Rab3a, persists on synaptic vesicle membranes upon Ca2+-triggered exocytosis and is resistant to GDI-mediated retrieval. Modulation of the Rab27b GTP/GDP switch impairs synaptic vesicle recycling. |
Quantitative mass spectrometry (iTRAQ) of synaptic vesicles; quantitative immunoblotting; fluorescence microscopy; GDI extraction assay; Rab27b GTP/GDP switch manipulation |
The Journal of neuroscience : the official journal of the Society for Neuroscience |
High |
20926670
|
| 2013 |
In mast cells, Rab27a and Rab27b regulate distinct steps of degranulation: Rab27a/Mlph/MyoVa regulates cortical actin stability upstream of granule exocytosis, while Rab27b/Munc13-4 directly mediates granule exocytosis. Munc13-4-deficient mast cells phenocopy the Rab27b KO secretory impairment. |
Bone marrow-derived mast cells from multiple mutant mouse lines (ashen Rab27a, Rab27b KO, double KO, leaden Mlph KO, dilute MyoVa KO, jinx Munc13-4 KO); beta-hexosaminidase release assays; F-actin immunofluorescence; epistasis analysis |
The FEBS journal |
High |
23281710
|
| 2011 |
Rab27b regulates stimulation-dependent RANKL release from secretory lysosomes in osteoblastic cells. Suppression of Rab27b inhibits fusion of RANKL-containing lysosomal vesicles with the plasma membrane. The effectors Slp4-a, Slp5, and Munc13-4 coordinate Rab27a/b activity in this pathway; Munc13-4-deficient (jinx) mice show increased bone volume due to reduced osteoclast activity. |
siRNA knockdown of Rab27a, Rab27b, Slp4-a, Slp5, Munc13-4 in osteoblastic cells; RANKL release assays; immunofluorescence of vesicle localization; jinx mouse bone phenotype analysis |
Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research |
High |
20939018
|
| 2007 |
Crystal structure of mouse Rab27b-GDP reveals an open conformation with protruding switch and interswitch regions, stabilized through domain-swapping dimerization in the crystal. SAXS measurements show an extended monomer in solution, indicating highly flexible switch regions relevant to effector interaction. |
X-ray crystallography in three distinct crystal lattices; small-angle X-ray scattering (SAXS) |
Acta crystallographica. Section D, Biological crystallography |
High |
17582168
|
| 2012 |
The Rab27b effector Slac2-b (EXPH5) colocalizes with Rab27b and β4 integrin at early adhesion initiation sites in spreading keratinocytes. Loss-of-function of Slac2-b (frameshift mutation in humans or shRNA knockdown) causes keratinocyte adhesion disruption, cytoskeletal disruption, and increased perinuclear vesicles, establishing a role for the Rab27B–Slac2-b complex in keratinocyte biology. |
Whole-exome sequencing of human patients; immunofluorescence co-localization; shRNA knockdown in normal keratinocytes; cell adhesion assays |
American journal of human genetics |
High |
23176819
|
| 2011 |
Rab27b is required for exocytosis of secretory vesicles in lacrimal gland acinar cells. Constitutively active Rab27b increases the average size of secretory vesicles while retaining subapical distribution; dominant-negative Rab27b redistributes Rab27b to cytoplasm. Rab27b KO and double KO mice (but not Rab27a ashen mice) show changes in abundance and organization of secretory vesicles. Disruption of actin filaments inhibits vesicle fusion to the apical membrane but not homotypic fusion. |
Confocal fluorescence microscopy; transmission electron microscopy of lacrimal gland from KO mice; constitutively active and dominant-negative Rab27b expression; syncollin-GFP secretory protein release assay; actin disruption experiments |
American journal of physiology. Cell physiology |
High |
21525430
|
| 2013 |
EPI64B (TBC1D10B) functions as a GTPase-activating protein (GAP) specific for Rab27B in pancreatic acinar cells. EPI64B overexpression almost completely abolishes GTP-Rab27b without affecting GTP-Rab3D, and enhances amylase release in a Rab27B-dependent manner. GAP-dead EPI64B mutations block these effects. |
Adenoviral overexpression in isolated pancreatic acini; GTP-bound Rab27B pulldown; amylase release assay; Rab27b KO mouse acini for epistasis; site-directed mutagenesis of catalytic residues |
The Journal of biological chemistry |
High |
23671284
|
| 2002 |
Rab27b dominant-negative mutants (T23N and N133I) fail to associate with melanosomes and cause redistribution of melanosomes from cell periphery to perinuclear region in melanocytes, implicating Rab27b in outward movement of melanosomes. Wild-type Rab27b co-localizes with TRP-1 and myosin Va at the cell periphery. Dominant-negative Rab27b also reduces dendrite number and length. |
GFP-tagged WT and dominant-negative Rab27b overexpression in melan-a melanocytes; confocal co-localization with TRP-1 and myosin Va; dendrite morphology analysis; intrinsic GTPase activity assay |
The Journal of investigative dermatology |
Medium |
12060386
|
| 2004 |
Rab27b protein is present at extraordinary high levels (0.1% of total protein) on fusiform vesicles in bladder urothelium and is markedly reduced in cultured urothelial cells that fail to form fusiform vesicles, linking Rab27b expression to fusiform vesicle formation/maintenance. |
Immuno-electron microscopy; Western blot quantification; comparison of differentiated urothelium vs. de-differentiated cultured cells |
Proceedings of the National Academy of Sciences of the United States of America |
Medium |
14625374
|
| 2008 |
Slp1 (a Rab27 effector protein) interacts with Rab27B in vivo and co-localizes on zymogen granules in pancreatic acinar cells. Slp1 KO mice show increased number of zymogen granules, implicating the Rab27B–Slp1 complex in amylase secretion. |
Co-immunoprecipitation of Slp1 and Rab27B; co-localization by immunofluorescence; Slp1 KO mouse morphological analysis |
Archives of biochemistry and biophysics |
Medium |
18477466
|
| 2016 |
Kinesin-1 (Kif5b) is recruited to a Slp3/Rab27b effector complex on mast cell secretory granules in a PI3K-dependent and stimulus-dependent manner. PI3K-dependent formation of the kinesin-1/Slp3/Rab27b complex is required for microtubule-dependent movement of secretory granules toward the exocytic site during mast cell degranulation. |
Kif5b conditional KO mice; passive systemic anaphylaxis model; BMMC degranulation assays; SG translocation imaging; co-immunoprecipitation of kinesin-1/Slp3/Rab27b; PI3K inhibitor experiments |
The Journal of cell biology |
High |
27810912
|
| 2015 |
Rab27b mediates shear stress-induced vesicular export of miR-143 from endothelial cells downstream of the KLF2 transcription factor. Rab7a and Rab27b are both required for this extracellular vesicle-based miRNA secretion pathway. |
Rab27b and Rab7a siRNA knockdown; shear stress stimulation; miR-143 vesicular export quantification in endothelial cells |
FEBS letters |
Medium |
26348397
|
| 2009 |
After beta-adrenergic stimulation in parotid acinar cells, Rab27B translocates from secretory granules to the subapical region (5 min) and then dissociates into the cytosol (30 min) through binding to GDI (GDP dissociation inhibitor), which extracts GDP-bound Rab27B from membranes. |
Immunofluorescence time-course after isoproterenol treatment; subcellular fractionation; Rab27B-GDI complex detection in cytosol fractions |
European journal of oral sciences |
Medium |
19583748
|
| 2012 |
In lacrimal gland acinar cells, RAB27B enrichment occurs early in secretory vesicle formation at a basally-localized 'nascent vesicle site' adjacent to the trans-Golgi network. Transport from this nascent vesicle site to the subapical region requires intact microtubules. RAB27B-enriched vesicles in the subapical cytoplasm acquire Myosin 5C for actin-based motility. |
YFP-Rab27b live-cell confocal microscopy in rabbit lacrimal gland acinar cells; vesicle pool depletion-repletion protocol; nocodazole treatment; p150Glued co-localization; Myosin 5C co-localization |
PloS one |
Medium |
22363735
|
| 2010 |
Rab27b localizes to tubulovesicle membranes in gastric parietal cells. Upon stimulation, wild-type Rab27b and constitutively active Rab27b Q78L translocate to the apical membrane, while dominant-negative Rab27b N133I does not. Expression of Rab27b N133I almost completely inhibits acid secretion. |
Mass spectrometry identification in tubulovesicular fractions; YFP-tagged WT, Q78L, N133I adenoviral expression; fluorescence microscopy of resting and stimulated cells; aminopyrine accumulation acid secretion assay |
Gastroenterology |
High |
20888820
|
| 2004 |
Rab27b is upregulated in Griscelli syndrome type II melanocytes (lacking Rab27a) and forms a tripartite complex with melanophilin and myosin Va transcripts containing exon F on the melanosome membrane, partially compensating for loss of Rab27a function. |
Real-time quantitative PCR; Western blot; immunofluorescence co-localization; yeast two-hybrid screening |
Pigment cell research |
Medium |
15357836
|
| 2017 |
RAB27B controls stretch-induced exocytosis of discoidal/fusiform vesicles (DFVs) in bladder umbrella cells. RAB27A-specific shRNA does not inhibit exocytosis. RAB27B operates in a pathway parallel to and independent of the RAB11A-RAB8A-MYO5B pathway. |
Whole bladder filling preparation; shRNA-mediated knockdown of RAB27B and RAB27A; hGH-loaded DFV exocytosis assay; dominant-active/dominant-negative RAB11A and RAB8A mutants; Squassh segmentation quantification of RAB27B-positive DFVs |
American journal of physiology. Cell physiology |
High |
29167152
|
| 2016 |
Rab27b is required for lysosomal exocytosis and surface expression of proteolipid protein (PLP) in oligodendrocytes. Rab27b KD reduces lysosomal exocytosis, decreases PLP surface expression, and reduces myelin-like membrane formation in neuron co-culture. |
shRNA knockdown of Rab27b in oligodendrocytes; lysosomal exocytosis assays; PLP surface expression measurement; oligodendrocyte-neuron co-culture myelination assay |
Neuroscience bulletin |
Medium |
27325508
|
| 2020 |
Rab27b regulates alpha-synuclein release, autophagic clearance, and toxicity in neurons. Rab27b KD increases paracrine αsyn toxicity, shifts released αsyn to higher-molecular-weight species, increases insoluble intracellular αsyn, and impairs autophagic flux (reduced LC3 turnover after chloroquine treatment). |
shRNA knockdown; paracrine αsyn neuronal model; size-exclusion chromatography of released αsyn; immunofluorescence of LC3 puncta; chloroquine autophagic flux assay; Western blot of insoluble αsyn fractions |
The Journal of biological chemistry |
Medium |
32350025
|
| 2023 |
RAB27B controls NRAS palmitoylation and trafficking to the plasma membrane by interacting with ZDHHC9, a palmitoyl acyltransferase. RAB27B depletion selectively abrogates mutant NRAS-mediated ERK signaling and progenitor cell growth in mice, and reduces myelomonocytic leukemia development. RAB27B is upregulated in CBL- or JAK2-mutated myeloid malignancies. |
Proteomic studies; co-immunoprecipitation of RAB27B and ZDHHC9; Rab27b KO mice with NRAS mutant hematopoietic cells; NRAS palmitoylation assays; ERK signaling assays; in vivo leukemia model; primary human AML RAB27B depletion |
The Journal of clinical investigation |
High |
37317963
|
| 2021 |
NRF2 promotes Rab27b expression transcriptionally in urothelial cells, and RAB27B mediates NRF2-dependent UPEC expulsion from urothelial cells. Loss of NRF2 reduces RAB27B expression and impairs UPEC expulsion, increasing bacterial burden both in vitro and in vivo. |
NRF2 KO and overexpression in urothelial cells; RAB27B expression measurement; UPEC expulsion assays; mouse UTI model; dimethyl fumarate (NRF2 inducer) treatment |
Cell reports |
Medium |
34686330
|
| 2021 |
FOXO1 transcriptionally regulates RAB27B expression in kidney proximal tubule cells. In high-glucose conditions (mimicking diabetic kidneys), FOXO1 is phosphorylated and inactivated, leading to RAB27B downregulation and decreased exosome secretion. Constitutively active nonphosphorylatable FOXO1 restores RAB27B and exosome secretion. |
Bioinformatics identification of FOXO1 binding sites in Rab27b promoter; high-glucose treatment of BUMPT cells; RAB27B overexpression rescue; constitutively active FOXO1 overexpression; diabetic mouse model exosome analysis |
Diabetes |
Medium |
33597203
|
| 2023 |
CaSR activates RAB27B through a PI3K/PKA/mTOR/MADD (guanine nucleotide exchange factor) pathway, promoting secretion of cytokines (IL-6, IL-1β, IL-8, IP-10, RANTES) from breast cancer cells. Rab11A interacts with and activates MADD, a GEF for Rab27A/B, linking endocytic recycling endosomes to Rab27B-regulated secretory vesicles via endosomal PI3K (Vps34 and PI3KC2α). |
CaSR stimulation assays; PI3K/PKA/mTOR/MADD pharmacological inhibition; Co-immunoprecipitation of Rab11A and MADD; cytokine secretion ELISA; siRNA knockdown of pathway components |
Cellular signalling |
Medium |
37604243
|
| 2020 |
ZIP4 promotes RAB27B expression through CREB-regulated transcription in pancreatic cancer cells. RAB27B is required for the release of HSP70- and HSP90-associated extracellular vesicles that activate p38 MAPK and induce muscle-wasting gene expression (F-box protein 32, UBR2) in myotubes, causing myofibrillar protein loss and cachexia. |
ZIP4 shRNA knockdown; CREB inhibition; RAB27B expression measurement; EV isolation and Western blot; C2C12 myotube treatment with conditioned media/EVs; p38 MAPK activation assays; orthotopic pancreatic tumor mouse model |
Gastroenterology |
Medium |
30342032
|
| 2013 |
V-ATPase (vacuolar H+-ATPase) activity and subunits (V0a1, V0d1) are required for peripheral localization and size of Rab27B-positive secretory vesicles in breast cancer cells. Inhibition of V-ATPase reduces Rab27B-induced invasion, HSP90α secretion, and MMP-2 activation. |
Mass spectrometry of GFP-Rab27B vesicles identifying V-ATPase subunits; Western blot validation; bafilomycin A1 inhibition; siRNA knockdown of V0a1 and V0d1; invasion and secretion assays |
International journal of cancer |
Medium |
23390068
|
| 2019 |
β-catenin/Tcf-4 transcriptional activation of RAB27B expression is required for secretion of exosomes from colorectal cancer stem cells. Exosomal miR-146a-5p cargo promotes stemness by targeting Numb in recipient cells. |
β-catenin/Tcf-4 transcription factor analysis; RAB27B knockdown; exosome secretion quantification; exosomal RNA sequencing; luciferase reporter and rescue assays |
International journal of cancer |
Medium |
30980673
|
| 2012 |
Rab27b negatively regulates c-kit surface expression in megakaryoblastic cells by promoting autocrine secretion of stem cell factor (SCF). Rab27b knockdown reduces SCF secretion, leading to reduced SCF-induced endolysosomal degradation of c-kit and thus increased c-kit surface expression. |
shRNA knockdown of Rab27b in CMK cells; c-kit surface expression measurement; SCF secretion assay; bafilomycin lysosome inhibition; flow cytometry |
Biochemical and biophysical research communications |
Medium |
22349512
|
| 2025 |
Rab27b promotes lysosomal function in neurons by supporting lysosomal enzyme maturation and acidic vesicle trafficking. Rab27b KO in neurons causes lysosomal proteolytic defects, enzymatic dysfunction, and exacerbated alpha-synuclein aggregation upon preformed fibril treatment. Rab27b overexpression enhances lysosomal activity and reduces insoluble αsyn accumulation. |
Rab27b KO mice; primary neuronal cultures; shRNA KD in αsyn-inducible neuronal model; lysosomal enzyme activity assays; lysosomal pH measurement; αsyn preformed fibril treatment; Rab27b overexpression; brain lysate analysis from postmortem human PD/DLB/iLBD tissue |
The Journal of neuroscience : the official journal of the Society for Neuroscience |
High |
39965930
|
| 2024 |
TGF-β suppresses RAB27B transcription via SMAD3, reducing exosome release from breast cancer cells. RAB27B depletion or TGF-β treatment increases quantity and alters protein composition of EVs, producing recomposed EVs that inhibit CD8+ T cell-mediated cancer killing. |
TGF-β treatment; SMAD3 identification as transcriptional repressor of RAB27B; click chemistry proteomics; RAB27B siRNA; exosome quantification; CD8+ T cell cytotoxicity assay |
Journal of extracellular vesicles |
Medium |
39723610
|
| 2020 |
Rab27b KO in hippocampal mossy fiber (MF)-CA3 synapses completely eliminates long-term potentiation (LTP), an effect rescued by lentiviral re-expression of human Rab27b but not GFP. At SC-CA1 synapses, Rab27b KO increases facilitation. Rab27b and Rab3a act synergistically at presynaptic terminals for LTP expression. |
Rab27b KO mice; electrophysiology at SC-CA1 and DG-MF hippocampal synapses; frequency facilitation measurement; LTP induction; lentiviral rescue with human Rab27b |
Physiological reports |
Medium |
32358861
|
| 2016 |
Genetic deletion of Rab27B in pancreatic acinar cells reduces the size of zymogen granules and moderately decreases digestive enzyme secretion, revealing a role in zymogen granule maturation distinct from Rab3D. |
Rab27B KO mouse model; electron microscopy of zymogen granule size; in vitro secretion assays from isolated acini; comparison with Rab3D |
Biochemical and biophysical research communications |
Medium |
26845357
|
| 2023 |
KIAA1429 stabilizes RAB27B mRNA through the m6A/YTHDF1 axis in chronic myeloid leukemia cells, promoting RAB27B expression and leukemia cell proliferation and drug efflux. Inhibiting KIAA1429 reduces RAB27B mRNA stability, thereby sensitizing CML cells to imatinib. |
KIAA1429 knockdown; m6A modification analysis; YTHDF1 interaction; RAB27B mRNA stability assays; proliferation and apoptosis assays; drug resistance assays |
Genes & diseases |
Medium |
37692484
|
| 2025 |
In neurons, Rab27b KO in A53T alpha-synuclein transgenic mice increases proteinase-K resistant αsyn and phospho-S129 αsyn in cortex, striatum, and substantia nigra, and increases astrocyte/microglial activation. In AAV αsyn model, Rab27b KO accelerates dopaminergic cell loss in the substantia nigra. |
Rab27b KO × A53T transgenic double mutant mice; AAV αsyn overexpression mouse model; proteinase-K resistance assay; phospho-αsyn immunohistochemistry; glia activation markers; nigral dopaminergic cell counting |
bioRxiv : the preprint server for biologypreprint |
Medium |
41509326
|
| 2025 |
DDX10 physically interacts with Rab27b through phase separation and promotes Rab27b-mediated exosome secretion of PD-L1 in oral squamous cell carcinoma cells, contributing to T cell exhaustion. |
Co-immunoprecipitation of DDX10 and Rab27b; DDX10 knockdown; exosome PD-L1 quantification; T cell functional assays |
Research (Washington, D.C.) |
Low |
40352946
|
| 2025 |
Rab27b in neurons is required for amyloid beta (Aβ) secretion via lysosomal exocytosis in hiPSC-derived neurons. Silencing Rab27b (or Munc13-4) significantly reduces lysosomal fusion events at the plasma membrane and blocks Aβ release into the extracellular space, as visualized by TIRF microscopy. |
TIRF microscopy of lysosome-plasma membrane fusion events in hiPSC-derived neurons; siRNA knockdown of Rab27b and Munc13-4; nanoscale flow cytometry of released particles |
bioRxivpreprint |
Medium |
bio_10.1101_2025.03.01.640950
|