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anti-Human RAB5 Anticorps:
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Human Polyclonal RAB5 Primary Antibody pour ICC, IF - ABIN266020
Sönnichsen, De Renzis, Nielsen, Rietdorf, Zerial: Distinct membrane domains on endosomes in the recycling pathway visualized by multicolor imaging of Rab4, Rab5, and Rab11. dans The Journal of cell biology 2000
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Human Monoclonal RAB5 Primary Antibody pour ELISA, WB - ABIN532969
Yao-Borengasser, Varma, Bodles, Rasouli, Phanavanh, Lee, Starks, Kern, Spencer, Rashidi, McGehee, Fried, Kern: Retinol binding protein 4 expression in humans: relationship to insulin resistance, inflammation, and response to pioglitazone. dans The Journal of clinical endocrinology and metabolism 2007
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Human Monoclonal RAB5 Primary Antibody pour ELISA, WB - ABIN519585
Chamberlain, Oberg, Furber, Poland, Hawrysh, Knafelc, McBride, Anderson: Deregulation of Rab5 and Rab4 proteins in p85R274A-expressing cells alters PDGFR trafficking. dans Cellular signalling 2010
Human Polyclonal RAB5 Primary Antibody pour IHC (p), WB - ABIN3044162
Han, Jiang, Ding, Liu, Xiao, Shi: Change of Rin1 and Stathmin in the Animal Model of Traumatic Stresses. dans Frontiers in behavioral neuroscience 2017
Cow (Bovine) Polyclonal RAB5 Primary Antibody pour ICC, IF - ABIN361846
Ali, Wasmeier, Lamoreux, Strom, Seabra: Multiple regions contribute to membrane targeting of Rab GTPases. dans Journal of cell science 2004
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Cow (Bovine) Polyclonal RAB5 Primary Antibody pour IHC, WB - ABIN2786773
Coyne, Shen, Turner, Bergelson: Coxsackievirus entry across epithelial tight junctions requires occludin and the small GTPases Rab34 and Rab5. dans Cell host & microbe 2007
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Human Polyclonal RAB5 Primary Antibody pour IP, WB - ABIN1742215
Perlini, Botti, Fornasiero, Giannandrea, Bonanomi, Amendola, Naldini, Benfenati, Valtorta: Effects of phosphorylation and neuronal activity on the control of synapse formation by synapsin I. dans Journal of cell science 2011
Horse (Equine) Polyclonal RAB5 Primary Antibody pour ICC, IF - ABIN4891966
Pera, Larrea, Guardia-Laguarta, Montesinos, Velasco, Agrawal, Xu, Chan, Di Paolo, Mehler, Perumal, Macaluso, Freyberg, Acin-Perez, Enriquez, Schon, Area-Gomez: Increased localization of APP-C99 in mitochondria-associated ER membranes causes mitochondrial dysfunction in Alzheimer disease. dans The EMBO journal 2017
This study showed that the RAB5A predictors of regional brain atrophy in Parkinson disease.
Low RAB5A expression is associated with polycystic ovary syndrome.
The authors demonstrate that RABGEF1, the upstream factor of the endosomal Rab GTPase cascade, is recruited to damaged mitochondria via ubiquitin binding downstream of Parkin. RABGEF1 directs the downstream Rab proteins, RAB5 and RAB7A, to damaged mitochondria, whose associations are further regulated by mitochondrial Rab-GAPs.
Low RAB5 expression is associated with glioma progression.
The expression level of EMC-6 is significantly elevated in cervical cancer, without significant correlation with Beclin1 and Rab5a.
Here the authors show that Rab5 is monoubiquitinated on K116, K140, and K165. Structural analysis combined with biochemical data revealed that interactions with downstream effectors were impeded in Rab5 monoubiquitinated at K140, whereas GDP release and GTP loading activities were altered in Rab5 monoubiquitinated at K165.
Rab5a is overexpressed in oral cancer tissue samples and promotes the malignant phenotype through EMT and the ERK/MMP2 signaling pathway.
Rab5 was found abundantly localized in macrophage rich areas of human atherosclerotic lesions.Rab5 plays an important role in modulating the intracellular cholesterol of macrophages and consequently mediating the formation of foam cells.
The results were indicative that rabies virus N proficiently colocalized with Rab5/EEA1 and Rab7/LAMP1 in both cell lines at 24 and 48 h post-infection, while N titers significantly decreased in early infection of rabies virus.
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-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/beta-catenin signaling pathway.
CMTM3 decreases EGFR expression, facilitates EGFR degradation, and inhibits the EGF-mediated tumorigenicity of gastric cancer cells by enhancing Rab5 activity.
High RAS-associated protein RAB5 expression correlated with the presence of lymphatic invasion and venous invasion and low E-cadherin 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 significantly rescued these phenomena caused by siRNA against Rab5a
results suggest a new mechanism in which Rab5 induces a change in flexibility of EEA1, 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
Data show that rab5 GTP-Binding Protein (Rab5a) is overexpressed in human hepatocellular carcinoma (HCC) and contributes to cancer cell proliferation and invasion through regulation of FAK and AKT signaling.
The authors described a long-distance signaling mechanism of Porcine hemagglutinating encephalomyelitis virus-driven deficits in neurons and suggested that such Ulk1 repression may result in limited NGF/TrkA retrograde signaling within activated Rab5 endosomes, explaining the progressive failure of neurite outgrowth and survival.
SH3GLB1 controls nicotinic acetylcholine receptors endocytic trafficking in a phosphorylation- and RAB5-dependent manner at steps upstream of autophagosome formation.
E. chaffeensis secretes Etf-1 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, through functional interactions with Rab20 on the phagosome, activates Rab5, which, in turn, increases PtdIns3P and delays phagosome acidification.
FGF21 has a role in promoting endothelial cell angiogenesis through a dynamin-2 and Rab5 dependent pathway
In silico screening for palmitoyl substrates reveals a role for DHHC1/3/10 (zDHHC1/3/11)-mediated neurochondrin 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/Rabaptin-5/Rab5-GTP interaction in the cell, which is quantitatively related to the Rabex-5 concentration for the onset of the indirect
Rab5 regulates and coordinates different endocytic mechanisms through its effector Rabankyrin-5
Using retroviral expression and siRNA Rab5a silencing, data demonstrate that Rab5a is essential for the large endosome phenotype and for localization of mannose receptor.
the recruitment of Gapex-5 to phagosomes through the microtubule network induces transient Rab5 activation
the TC10/GAPEX-5/Rab5 axis mediates insulin-stimulated production of PI(3)P, which regulates trafficking of Glut4 vesicles
activation of Rab5, fusion of early endosomes and phagocytosis induced by T. cruzi infection involved Toll-like receptor (TLR)2 but were independent of TLR4 receptors
parasite surface ligands and host cell receptors modulate pathogen residence times in Rab5(+) phagosomes
Expression of dominant negative Rab5 and Rab7 mutants, but not the dominant negative Rab11 mutant, significantly inhibited classical swine fever virus replication. These results were confirmed by silencing of Rab5 and Rab7.
Dominant-negative mutant rab5 inhibits FMDV infection of IBRS-2 cells.
Rab5-mediated endocytosis of E-cadherin is enhanced at the boundary between normal and RasV12 cells.
Required for the fusion of plasma membranes and early endosomes (By similarity).
RAS-associated protein RAB5A
, ras-related protein Rab-5A
, rab5A protein
, Rab5a, GTPase
, hypothetical protein
, Ras-related protein Rab-5A
, ras-related protein rab-5a
, small GTP-binding protein rab5
, GTP-binding protein (rab5)
, RAB5A, member RAS oncogene family
, RAB5A, member RAS oncogene family, a