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anti-Mouse (Murine) CNTN2 Antibodies:
anti-Human CNTN2 Antibodies:
anti-Rat (Rattus) CNTN2 Antibodies:
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Human Polyclonal CNTN2 Primary Antibody for IHC, IHC (p) - ABIN4300032
Peng, Tran, Krishnaswamy, Kostadinov, Martersteck, Sanes: Satb1 Regulates Contactin 5 to Pattern Dendrites of a Mammalian Retinal Ganglion Cell. in Neuron 2017
These data demonstrate distinct roles for zebrafish cntn2 in neuronal migration and axon fasciculation, and in the function of sensorimotor circuits.
The expression patterns of contactin-2 at different time points after spinal cord injury were studied at the mRNA level.
two guidance cues, TAG-1 and laminin-alpha1, influence the behavior of growth cones during axon pathfinding in vivo
tag1, lama1 and vangl2 participate in a common mechanism that integrates signaling between the FBMN and its environment to regulate migration.
we identify an additional variant (N407S) with a dominant-negative effect on axon growth although it is well-localized at the membrane and properly binds to Contactin2
During development, CNTN2 absence can transiently affect the expression levels of myelin and myelin-regulating genes, and results in impaired oligodendrocyte branching and hypomyelination of fiber tracts. During de- and remyelination, Cntn2 absence did not affect oligodendrocyte survival or the extent of remyelination.
We further demonstrate that Cre expression initiates after birth with preservation of native Cntn2 protein. Finally, we show that Cntn23'UTR-IRES-Cre-EGFP/+ mice maintain normal cardiac mechanical and electrical function.
Tag1 is crucial for the olfactory circuit formation in mice.
Interaction proteomics revealed the interactors of Caspr2, including CNTN2, KCNAs, members of the ADAM family (ADAM22, ADAM23 and ADAM11), members of LGI family and MAGUKs (DLGs and MPPs).
Our results clearly demonstrate that mouse and human contactin-2 are physiological substrates for BACE1
the TAG-1-mediated cell-to-cell interaction between the unpolarized multipolar cells and the pioneering axons regulates the polarization of multipolar cells partly through Lyn kinase and Rac1
This study demonistrated that knockdown of the cell-surface molecule TAG-1 resulted in retraction of neocortical progenitors' basal processes.
These results suggest that the Tax-induced decline in p53 function, which is independent of NF-kappaB activation in the early stage, might be the first stage in the onset of ATLL.
two novel genes, Cntnap2 and Tag1, are implicated in the regulation of diet-induced obesity.
These observations identify a novel role for TAG1 in modulating the intracellular sorting of signaling receptor complexes.
These findings are consistent with a regulatory role for Tag-1 in axon emergence as well as migratory behavior by developing mouse cerebellar granule neurons.
Data show that TAG1 and F3 act antagonistically to control SHH-induced proliferation: F3 suppresses SHH-induced GNP proliferation and induces differentiation, whereas TAG1 antagonises F3.
Ultrastructural and behavioral analysis of Tag-1 knockout mice shows that the expression of glial TAG-1 is sufficient to restore the axonal and myelin deficits
These findings suggest that an age-related reduction of TAG-1 expression may predispose neurons to cell death, induced by the binding of TGFbeta2 to APP.
Although several aspects of the role of TAG-1 in developing sensory axons are consistent with the defects seen in Brn3a knockout mice, it is unlikely that changes in TAG-1 expression directly mediate these defects.
In the absence of TAG-1, axonal Caspr2 did not accumulate at juxtaparanodes, and shaker-type K+ channels in these regions were severely disrupted, in the central and peripheral nervous systems.
The TAX-1 upstream sequence includes elements not only sufficient to restrict expression to the nervous system, but also to recapitulate to a great extent the endogenous pattern of the TAG-1 expression in the developing CNS.
TAG-1 function is required for survival of the neurons of some precerebellar nuclei, while it is not required for cortical interneuron migration in vivo.
a TAG1-APP signalling pathway negatively modulates neurogenesis through Fe65
The data of this study reveal that the contactin-2 changes observed in tissues are reflected in CSF, suggesting that decreased contactin-2 CSF levels might be a biomarker reflecting synaptic or axonal loss.
the selective distribution of Caspr2 and TAG-1 may be regulated, allowing them to modulate the strategic function of the Kv1 complex along axons
the ectodomains of CNTNAP2 and contactin 2 (CNTN2) bind directly and specifically, with low nanomolar affinity.
RACK1 interacts with CNTN2, and the effects of RACK1 on glioma cell growth and differentiation are mediated by CNTN2.
A single nucleotide deletion in exon 6 of CNTN2 results in a frameshift mutation, segregating in a recessive manner in a consanguineous Egyptian family with epilepsy.
The single-nucleotide polymorphism (SNP) rs2275697 in the TAG-) gene was not associated with treatment responsiveness, treatment dependence, disability, or mortality in chronic inflammatory demyelinating polyneuropathy
allelic variation in TAG-1 does not play a major role in determining multifocal motor neuropathy susceptibility.
single nucleotide polymorphisms in TAG-1 are related to the IVIg responsiveness of Chronic inflammatory demyelinating polyneuropathy patients.
The domains responsible for the neurite outgrowth promoting activity of TAG-1 have been investigated as well as its interactions with other cell adhesion molecules.
TAG-1 homophilic interaction is based on dimer formation rather than formation of a molecular zipper as proposed for the chicken ortholog.
Contactin-2 is expressed by various neuronal populations and sequestered in the juxtaparanodal domain of myelinated axons both at the axonal and myelin sides; is an autoantigen targeted by T cells and autoantibodies in MS.
immune response to CNTN2 and possible involvement in multiple sclerosis and EAE [REVIEW]
The protein encoded by this gene is a member of the immunoglobulin superfamily. It is a glycosylphosphatidylinositol (GPI)-anchored neuronal membrane protein that functions as a cell adhesion molecule. It may play a role in the formation of axon connections in the developing nervous system. It may also be involved in glial tumorigenesis and may provide a potential target for therapeutic intervention.
, transiently expressed axonal glycoprotein
, contactin 2 (axonal)
, axonal glycoprotein TAG-1
, transient axonal glycoprotein 1
, transiently-expressed axonal glycoprotein
, axonin-1 cell adhesion molecule
, contactin 2 (transiently expressed)