Browse our CNTN2 Proteins (CNTN2)

Zebrafish Contactin 2 (Axonal) (CNTN2) interaction partners

1. The expression patterns of contactin-2 at different time points after spinal cord injury were studied at the mRNA level.

2. two guidance cues, TAG-1 and laminin-alpha1, influence the behavior of growth cones during axon pathfinding in vivo

3. tag1, lama1 (show LAMA1 Proteins) and vangl2 (show VANGL2 Proteins) participate in a common mechanism that integrates signaling between the FBMN and its environment to regulate migration.

Mouse (Murine) Contactin 2 (Axonal) (CNTN2) interaction partners

1. 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.

2. 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.

3. Tag1 is crucial for the olfactory circuit formation in mice.

4. Interaction proteomics revealed the interactors of Caspr2 (show CNTNAP2 Proteins), including CNTN2, KCNAs, members of the ADAM family (ADAM22 (show ADAM22 Proteins), ADAM23 (show Adam23 Proteins) and ADAM11 (show ADAM11 Proteins)), members of LGI family and MAGUKs (DLGs and MPPs (show MPHOSPH6 Proteins)).

5. Our results clearly demonstrate that mouse and human contactin-2 are physiological substrates for BACE1 (show BACE Proteins)

6. 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

7. This study demonistrated that knockdown of the cell-surface molecule TAG-1 resulted in retraction of neocortical progenitors' basal processes.

8. These results suggest that the Tax-induced decline in p53 (show TP53 Proteins) function, which is independent of NF-kappaB (show NFKB1 Proteins) activation in the early stage, might be the first stage in the onset of ATLL.

9. two novel genes, Cntnap2 (show CNTNAP2 Proteins) and Tag1, are implicated in the regulation of diet-induced obesity.

10. These observations identify a novel role for TAG1 in modulating the intracellular sorting of signaling receptor complexes.

Human Contactin 2 (Axonal) (CNTN2) interaction partners

1. the selective distribution of Caspr2 (show CNTNAP2 Proteins) and TAG-1 may be regulated, allowing them to modulate the strategic function of the Kv1 (show KCNA5 Proteins) complex along axons

2. the ectodomains of CNTNAP2 (show CNTNAP2 Proteins) and contactin 2 (CNTN2) bind directly and specifically, with low nanomolar affinity.

3. RACK1 (show GNB2L1 Proteins) interacts with CNTN2, and the effects of RACK1 (show GNB2L1 Proteins) on glioma cell growth and differentiation are mediated by CNTN2.

4. Our results clearly demonstrate that mouse and human contactin-2 are physiological substrates for BACE1 (show BACE Proteins)

5. 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.

6. allelic variation in TAG-1 does not play a major role in determining multifocal motor neuropathy susceptibility.

7. single nucleotide polymorphisms in TAG-1 are related to the IVIg responsiveness of Chronic inflammatory demyelinating polyneuropathy patients.

8. 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.

9. TAG-1 homophilic interaction is based on dimer formation rather than formation of a molecular zipper as proposed for the chicken ortholog.

10. 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.