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Membrane localization and dynamics of geranylgeranylated Rab5 hypervariable region has been reported.
study elucidated a novel Malat1-miR-101-STMN1/RAB5A/ATG4D regulatory network that Malat1 activates autophagy and promotes cell proliferation by sponging miR-101 and upregulating STMN1, RAB5A and ATG4D expression in glioma cells
In conclusion, mutant KRAS promotes endosomal degradation in PDAC cell lines, which is impaired by KRAS silencing. Moreover, KRAS silencing activates RAB5A upregulation and drives PDAC subtype-dependent modulation of endosome trafficking.
siRNA knockdown of Rab5a or overexpression of miR (显示 MLXIP ELISA试剂盒)-494 in human macrophages significantly inhibits the survival of the parasites
our results show that Rab5a is overexpressed in pancreatic cancer and promotes aggressive biological behavior through regulation of the Wnt (显示 WNT2 ELISA试剂盒)/beta-catenin (显示 CTNNB1 ELISA试剂盒) signaling pathway.
CMTM3 (显示 CMTM3 ELISA试剂盒) decreases EGFR (显示 EGFR ELISA试剂盒) expression, facilitates EGFR (显示 EGFR ELISA试剂盒) degradation, and inhibits the EGF (显示 EGF ELISA试剂盒)-mediated tumorigenicity of gastric cancer cells by enhancing Rab5 activity.
High RAS-associated protein (显示 RGL2 ELISA试剂盒) RAB5 expression correlated with the presence of lymphatic invasion and venous invasion and low E-cadherin (显示 CDH1 ELISA试剂盒) expression.
downregulated Rab5a led to slowed cell growth, decreased numbers of migrated cells, decreased numbers of cells at the G0G1 phase and a higher apoptosis rate. However, PDGF (显示 PDGFA ELISA试剂盒) significantly rescued these phenomena caused by siRNA against Rab5a
results suggest a new mechanism in which Rab5 induces a change in flexibility of EEA1 (显示 EEA1 ELISA试剂盒), generating an entropic collapse force that pulls the captured vesicle towards the target membrane to initiate docking and membrane fusion
structural differences may provide an opportunity to selectively target one Rab5 state and lead to new approaches in the development of Rab5-specific therapies
SH3GLB1 (显示 SH3GLB1 ELISA试剂盒) controls nicotinic acetylcholine receptors endocytic trafficking in a phosphorylation- and RAB5-dependent manner at steps upstream of autophagosome formation.
E. chaffeensis secretes Etf-1 (显示 ETF1 ELISA试剂盒) to induce autophagy to repurpose the host cytoplasm and capture nutrients for its growth through RAB5 and class III PtdIns3K, while avoiding autolysosomal killing.
These data highlight a requirement of Rab5 and the endosomal system for the regulation of gluconeogenic gene expression that has important implications for metabolic diseases.
Inpp5e (显示 INPP5E ELISA试剂盒), through functional interactions with Rab20 on the phagosome, activates Rab5, which, in turn, increases PtdIns3P and delays phagosome acidification.
FGF21 (显示 FGF21 ELISA试剂盒) has a role in promoting endothelial cell angiogenesis through a dynamin-2 (显示 DNM2 ELISA试剂盒) and Rab5 dependent pathway
In silico screening for palmitoyl substrates reveals a role for DHHC1/3/10 (zDHHC1/3/11)-mediated neurochondrin (显示 NCDN ELISA试剂盒) palmitoylation in its targeting to Rab5-positive endosomes.
In mammalian cells, p110beta acts as a molecular sensor for growth factor availability and induces autophagy by activating a Rab5-mediated signaling cascade.
Data show that Rinl is closely associated with the cytoskeleton and thus contributes to the spatial control of Rab5a and Rab22 signaling at actin-positive compartments.
Data reveal the affinity of Rabex-5 (显示 RABGEF1 ELISA试剂盒)/Rabaptin-5 (显示 RABEP1 ELISA试剂盒)/Rab5-GTP (显示 AK3 ELISA试剂盒) interaction in the cell, which is quantitatively related to the Rabex-5 (显示 RABGEF1 ELISA试剂盒) concentration for the onset of the indirect
Rab5 regulates and coordinates different endocytic mechanisms through its effector Rabankyrin-5 (显示 ANKFY1 ELISA试剂盒)
Expression of dominant negative Rab5 and Rab7 (显示 RAB7A ELISA试剂盒) mutants, but not the dominant negative Rab11 (显示 RAB11A ELISA试剂盒) mutant, significantly inhibited classical swine fever virus replication. These results were confirmed by silencing of Rab5 and Rab7 (显示 RAB7A ELISA试剂盒).
Dominant-negative mutant rab5 inhibits FMDV infection of IBRS-2 cells.
Required for the fusion of plasma membranes and early endosomes (By similarity).
, Rab5a, GTPase
, hypothetical protein
, Ras-related protein Rab-5A
, ras-related protein rab-5a
, RAB5A, member RAS oncogene family
, ras-related protein Rab-5A
, RAS-associated protein RAB5A
, small GTP-binding protein rab5
, GTP-binding protein (rab5)