Publication for Cntn1 and Negr1
| Species | Symbol | Function* | Entrez Gene ID* | Other ID | Gene coexpression |
CoexViewer |
|---|---|---|---|---|---|---|
| mmu | Cntn1 | contactin 1 | 12805 | [link] | ||
| mmu | Negr1 | neuronal growth regulator 1 | 320840 |
| Pubmed ID | Priority | Text |
|---|---|---|
| 25061880 | 0.98 | Cntn1, Ncam1, Negr1, Nrxn1 and Sh2b3 mRNAs and their respective long non-coding RNAs in an in vitro model of ischemic-reperfusion injury showed an inverse expression profile to the maturation process, thus suggesting their role(s) in maintaining neuronal structure and function. |
| 0.98 | Cntn1, Ncam1, Negr1 and Nrxn1 had differentially expressed mRNAs and lncRNAs associated with them and were also predicted to be targeted by the altered miRNAs (Figure 3A). | |
| 0.98 | Cntn1, Ncam1, Negr1 and Nrxn1 which are responsible for neurite outgrowth and synaptogenesis (Figure 5, genes in bold). | |
| 0.98 | Cntn1, Ncam1, Negr1, Nrxn1, Ntrk2 and Sh2b3 associated mRNAs and lncRNAs during ischemic injury could characterize the exact relationship between 7 mRNA-lncRNA targets (Table 3). | |
| 0.98 | Cntn1, Ncam1, Negr1, Nrxn1, Sh2b3) was observed upon ischemic insult (Table 3). | |
| 0.97 | Cntn1, Ncam1, Negr1, Nrxn1, Ntrk2 and Sh2b3) by both lncRNAs and miRNAs could be implicated in neuronal maturation. | |
| 0.97 | Cntn1, Ncam1, Negr1 and Nrxn1 as well as Sh2b3 in the neurotrophin signalling pathway displayed a mainly inverse relationship between mRNA and antisense lncRNA gene pairs. | |
| 0.97 | Cntn1, Ncam1, Negr1, Nrxn1, Ntrk2 and Sh2b3) that is altered during neuronal maturation (Figure 3), in an ischemic injury model (neuronal). | |
| 0.97 | Cntn1, Ncam1, Negr1, Nrxn1) were targeted by all these miRNAs with miR-377 specifically targeting only the 4 cell adhesion molecules (Figure 5). | |
| 0.94 | Negr1 and Nrxn1 was upregulated and expression of Cntn1 was downregulated upon maturation (Days 6 and 8). | |
| 0.87 | Cntn1, Ncam1, Negr1, Nrxn1, Sh2b3 (Table 3). | |
| 29249937 | 0.95 | NEGR1, OBCAM, and contactin-1 gradually increase during development and reach the highest level at 4 weeks after birth in the cerebral cortex, diencephalon, hippocampus, and cerebellum. |
| 0.94 | NEGR1, OBCAM, Ntm, Thy-1, LAMP, and contactin-1 as components of synaptic vesicles. |
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