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anti-Human VANGL2 Antibodies:
anti-Mouse (Murine) VANGL2 Antibodies:
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Human Polyclonal VANGL2 Primary Antibody for ELISA, WB - ABIN547850
Kibar, Vogan, Groulx, Justice, Underhill, Gros: Ltap, a mammalian homolog of Drosophila Strabismus/Van Gogh, is altered in the mouse neural tube mutant Loop-tail. in Nature genetics 2001
Expression of constitutively active and dominant-negative isoforms of RHOA revealed that it acts downstream of VANGL2.
VANGL2 interacts with Integrin alphaVbeta3 to regulate matrix metalloproteinase activity and cell adhesion to the extracellular matrix.
Our experimental data demonstrate that high expression of Prickle1 and Vangl2 reduce the growth of neuroblastoma cells and indicate different roles of PCP proteins in tumorigenic cells compared to normal cells.
VANGL2 is overexpressed in basal breast cancers. It is involved in the proliferative signal cascade of the VANGL2-SQSTM1-JNK pathway.
Propose that Arfrp1 exposes a binding site on AP-1 that recognizes the Vangl2 sorting motif for capture into a transport vesicle destined for the proximal surface of a polarized epithelial cell.
The aberrant VANGL2 promoter methylation and the decreased gene expression is associated with Tetralogy of Fallot.
Asymmetry of VANGL2 in migrating lymphocytes as a tool to monitor activity of the mammalian WNT/planar cell polarity pathway.
These results strongly suggest that R181 and R274 play critical roles in Vangl protein function and that their mutations cause neural tube defects in humans.
Van-Gogh-like 2 is frequently methylated in MSI-CRCs with BRAF mutation and may act as a tumour suppressor gene, counteracting WNT/beta-catenin signaling.
these findings strongly implicate VANGL2 in the genetic causation of spinal NTDs in a subset of patients and provide additional evidence for a pathogenic role of PCP signaling in these malformations.
Loss of membrane targeting of Vangl1 and Vangl2 proteins causes neural tube defects.
The planar cell polarity genes Celsr1 and Vangl2 are required for normal lung branching morphogenesis.
identified 3 novel missense mutations in fetuses with neural-tube defects
Van Gogh-Like 2 regulates tumor cell migration and matrix metalloproteinase-dependent invasion.
Results suggest that there is no specific mutation responsible for the Tetralogy of Fallot phenotype in the Vangl2 gene [Vangl2].
we observed a striking additive genetic interaction between Grhl2 and Grhl3 gain-of-function alleles. moderate Grhl3 overexpression also interacted with the Vangl2Lp allele to cause SB, demonstrating genetic interaction with the planar cell polarity signalling pathway that is implicated in mouse and human neural tube defects.
Studies indicate that mouse developing tooth required VANGL planar cell polarity 2 protein (Vangl2) at an early step of its morphogenetic program [Review].
a novel chemically induced mutant allele at Vangl2 called Curly Bob that causes a missense mutation p.Ile268Asn (I268N) in the Vangl2 protein, is reported.
disruption of Vangl2-dependent planar-polarised processes in the posterior neuropore neuroepithelium and surface ectoderm preclude zippering point biomechanical accommodation associated with Closure 5 formation at the completion of posterior neuropore closure.
The Vangl2 phosphorylation, which was previously identified to be induced by Wnt5a signaling, is required for Vangl2 functions in mammalian Planar cell polarity (PCP) in multiple tissues.
type II spiral ganglion neurons make a distinctive 90 degrees turn towards the cochlear base to synapse with 10-15 outer hair cells. this axon turning event requires planar cell polarity signaling and is disrupted in Vangl2 and Celsr1 knockout mice and VANGL2 acts non-autonomously from the cochlea to direct turning.
In Pax2-Cre; V1V2 Conditional knockout mice, the loss of both VANGL proteins significantly disrupts planar polarity throughout the utricular maculae
The Celsr3-mediated signaling pathway responds to the inhibitory function of Wnt5a in glutamatergic synapse formation. We also revealed the opposing roles of Wnt-regulated planar cell polarity components, Celsr3 and Vangl2, in glutamatergic synapse formation.
Exogenously introduced expression of green fluorescent protein (GFP)-tagged core PCP factors by electroporation revealed that Vangl1, Vangl2 and Prickle2 are localized on the ovarian side of the cell periphery in the oviduct.Our data collectively suggest that the mechanism for maintenance of Vangl2 asymmetry in mature mouse oviduct is different from the microtubule dependent polarized transport model
heterozygous Looptail (Lp) mice, in which a single copy of the core PCP gene, Vangl2, is disrupted are viable but display severe airspace enlargement and impaired adult lung function.
interacts with Celsr1 in ureteric tree growth
Vangl2 is expressed in the inner dental epithelium (IDE) and in the secondary enamel knots (SEKs) of bell stage tooth germs.
a new and essential role for Vangl2-dependent planar cell polarity signaling in the intraretinal path-finding of retinal ganglion cell axons
Vangl2-regulated polarisation and subsequent acquisition of an epithelial phenotype is essential to lengthen the tubular outflow vessel, a process that is essential for on-going cardiac morphogenesis.
Vangl2 regulates E-cadherin in epithelial cells.
Vangl2 function in podocytes is important for glomerular development and protects against glomerular injury in adult animals.
Vangl1 and Vangl2 may play a key role in the embryo implantation of mice
The first signal, controlled by cadherin, EGF-like, laminin G-like, seven-pass, G-type receptor (Celsr) 2, Celsr3, Frizzled3 (Fzd3) and Van Gogh like2 (Vangl2) organizes multicilia in individual cells (single-cell polarity)
Vangl does not have a critical role in neural crest migration through planar cell polarity signaling
Celsr2-3 and Fzd3 regulate axonal navigation in the forebrain by using mechanisms different from classical epithelial core planar cell polarity, and require interacting partners other than Vangl1-2 that remain to be identified.
Mutation of the canonical planar-cell-polarity gene vangl2, which decouples the asymmetric phenotypes of sibling hair-cell pairs, results in randomly positioned, randomly oriented sibling cells that nonetheless retain specific wiring.
the fibronectin extracellular matrix is essential for cell-surface Vangl2 expression, membrane-protrusive activity and directed migration.
Results demonstrate that anterior guidance decisions by commissural primary ascending (CoPA) axons are dependent on the function of planar cell polarity genes Fzd3a, Vangl2 and Scribble both prior to and after midline crossing; experiments establish CoPA axons as a model system to investigate the mechanism of planar cell polarity signaling in commissural axon guidance.
dynamic Vangl2 intracellular distribution is coordinated with and necessary for the changes in convergence and extension cell behaviors during gastrulation
we found that the critical period for Vangl2 function coincides with the initial stages of FBM neuron migration out of rhombomere 4.
Vangl2 regulates FBM neuron migration by acting in floor plate cells, independently of cilia function
VANGL2 regulates the endocytosis and cell-surface availability of MMP14 in a manner that is dependent on focal adhesion kinase.
Vangl2(R259L) behaved like the wild-type allele in overexpression and morpholino knockdown/rescue assays in zebrafish embryos.
Rack1 has a dominant-negative effect on Vangl2 localization and gastrulation.
data suggest that bbs8 and vangl2 act synergistically on cell polarization to establish and maintain the appropriate length and number of cilia in the Kupffer's vesicle and thereby facilitate correct LR asymmetry
Vangl2 is required for asymmetric localization and posterior tilting of primary motile cilia at the apical membrane of epithelial cells.
show that anterior hindbrain (r2/r3) motor neuron migration appears to be independent of vangl2 and pk1b functions, and suggest that multiple mechanisms regulate motor neuron migration along the anterior-posterior axis of the zebrafish hindbrain
The vangl2 gene product mediates cellular interactions that confer directionality on distinct movements during vertebrate embryogenesis.
tag1, lama1 and vangl2 participate in a common mechanism that integrates signaling between the FBMN and its environment to regulate migration.
Rab11 and the associated motor protein Myosin V play essential roles in both endogenous and ectopic apical constriction, and might be involved in Vangl2 trafficking to the cell surface.
The interaction and interdependence of Vangl2, VAMP1, aPKC and the stable microtubule cytoskeleton in the oocyte, shows that maternal Vangl2 and aPKC are required for specific oocyte asymmetries and vertebrate embryonic patterning.
The protein encoded by this gene is a membrane protein involved in the regulation of planar cell polarity, especially in the stereociliary bundles of the cochlea. The encoded protein transmits directional signals to individual cells or groups of cells in epithelial sheets. This protein is also involved in the development of the neural plate.
, protein strabismus
, van Gogh-like protein 2
, vang-like 2 (van gogh, Drosophila)
, vang-like protein 2
, loop-tail protein 1 homolog
, loop-tail-associated protein
, strabismus 1
, loop tail associated protein
, loop-tail protein 1
, vang (van gogh)-like 2
, protein trilobite
, protein strabismus-B
, van Gogh-like protein 2-B
, vang-like 2 (van gogh, Drosophila) b
, vang-like 2 b
, vang-like protein 2-B
, vang-like 2