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During neural tube formation Rab11-positive recycling endosomes distribute to the medial apical cell junctions in the neural plate. Polarization was under the control of planar cell polarity signalling, and was necessary for neural plate folding.
Rab11 and the associated motor protein Myosin V (show MYO5A Proteins) play essential roles in both endogenous and ectopic apical constriction, and might be involved in Vangl2 trafficking to the cell surface.
Rab11 expression is required throughout the early embryo for proper left-right patterning.
A requirement for Rab11 in multiciliated cells(MCC (show MCC Proteins)) development and support a two-step model, in which the initial polarization of MCC (show MCC Proteins) precursors is critical for their integration into the superficial cell layer.
Pard3 (show PARD3 Proteins) and Rab11a are necessary for lumen formation in the neural rod.
The established transgenic lines ubiquitously express EGFP fusions of Rab5c (show Rab5c Proteins) (early endosomes), Rab11a (recycling endosomes), and Rab7 (show RAB7A Proteins) (late endosomes) to study localization and dynamics during development.
The results suggest that Rab11 regulates anterograde transport from the TGN to the plasma membrane and strongly implicate SYP122, rather than SYP121.
The results from this analysis indicated that Rab11a, Rab11c(Rab25 (show RAB25 Proteins)) and Rab14 (show RAB14 Proteins) were expressed in a wide range of cell lines, including the human placental trophoblastic BeWo cell line.
The results suggest that progressive assembly of vRNA segments may be cell type dependent and that vRNA may be transported through the cytoplasm without Rab11A-containing recycling endosomes in the absence of intact microtubules.
Rac1-Rab11-FIP3 regulatory hub coordinates vesicle traffic with actin remodeling and T-cell activation
In colorectal carcinoma, overexpression of Rab11 was found to promote collective cell migration through the increased distribution of E-cadherin (show CDH1 Proteins), which enhanced cell-cell connections.
A novel tribasic Golgi export signal directs cargo protein interaction with activated Rab11 and AP-1 (show FOSB Proteins)-dependent Golgi-plasma membrane trafficking.
Analysis reveals novel aspects of the PI4KIIIb-Rab11 complex, specifically conformational changes induced in the switch regions of activated Rab11.
Substituted V20 of Rab11A was found to interfere with proper localization of the water molecule, which mediated GTP (show AK3 Proteins) hydrolysis, resulting in GTP (show AK3 Proteins) being locked in an active form of Rab11A S20V.
Data (including data from studies in knockout mice) suggest Munc13-4 binds to Rab11 and regulates trafficking of Rab11-containing vesicles; Munc13-4 appears to regulate final steps of Rab11-positive vesicle docking at plasma membrane in exocytosis.
Rab11A and Rab11B (show RAB11B Proteins) differentially regulate intracellular trafficking of PAR1 (show MARK2 Proteins) through distinct endosomal sorting mechanisms
Rab11a/Rab11 family-interacting protein 2 (show RAB11FIP2 Proteins)-mediated VE-cadherin (show CDH5 Proteins) recycling is required for formation of adherens junctions and restoration of vascular endothelial barrier integrity.
Rab11a inactivation in macrophages as a result of apoptotic cell binding initiates phagocytosis of apoptotic neutrophils via the modulation of ADAM17 (show ADAM17 Proteins)-mediated CD36 (show CD36 Proteins) cell surface expression
Rab8a and Rab11a Are Dispensable for Rhodopsin Transport in Mouse Photoreceptors
The up-regulation of Rab11, Rab7 (show RAB7A Proteins), or RILP (show RILP Proteins), but not its truncated form RILP (show RILP Proteins)-C33 (show CD82 Proteins), rescued LAMP2A-defective trafficking in cystinosis, whereas dominant-negative Rab11 or Rab7 (show RAB7A Proteins) impaired LAMP2A trafficking.
Rab11a-knockdown cells displayed mislocalization of STX3 (show STX3 Proteins) and the presentation of microvilli in the basolateral compartment
Results define Glut3 to be a rab11-dependent trafficking cargo and suggest that impaired Glut3 trafficking arising from rab11 dysfunction underlies the glucose hypometabolism observed in Huntington's disease
LMTK1 (show AATK Proteins) negatively controls dendritic formation by regulating Rab11A-positive endosomal trafficking.
Rab11a critically controls mouse blastocyst development and soluble matrix metalloproteinase secretion
Thus, Rab11a endosome controls intestinal host-microbial homeostasis at least partially via sorting Toll (show TLR4 Proteins)-like receptors, including Tlr9 (show TLR9 Proteins).
The unusual morphology and sorting capacity of Rab11a compartments in primary proximal tubule cells may reflect a unique specialization of these cells to accommodate the functional demands of handling a high endocytic load.
Rab11a promotes Porcine reproductive and respiratory syndrome virus (PRRSV) replication and associates with PRRSV replication sites.
The protein encoded by this gene belongs to the Rab family of the small GTPase superfamily. It is associated with both constitutive and regulated secretory pathways, and may be involved in protein transport. Two transcript variants encoding different isoforms have been found for this gene.
RAB11A, member RAS oncogene family
, ras-related protein Rab-11A
, Rab11 GTPase
, rab11A protein
, Rab11a, GTPase
, rab11A, RAB family GTPase
, RAB 11A, member oncogene family
, rab11 GTP-binding protein
, tubulovesicle-associated protein