Seems to play a role in the formation of functional distinct domains critical for saltatory conduction of nerve impulses in myelinated nerve fibers. Seems to demarcate the paranodal region of the axo-glial junction. In association with contactin may have a role in the signaling between axons and myelinating glial cells.
Predominantly expressed in brain. Weak expression detected in ovary, pancreas, colon, lung, heart, intestine and testis.
Belongs to the neurexin family. Contains 2 EGF-like domains. Contains 1 F5/8 type C domain. Contains 1 fibrinogen C-terminal domain. Contains 4 laminin G-like domains.
Lanes 1 - 4: Merged signal (red and green). Green - ab34151 observed at 180 kDa. Red - loading control, ab18058, observed at 130 kDa.
ab34151 was shown to recognize Caspr in wild-type HAP1 cells as signal was lost at the expected MW in CNTNAP1 (Caspr) knockout cells. Additional cross-reactive bands were observed in the wild-type and knockout cells. Wild-type and CNTNAP1 (Caspr) knockout samples were subjected to SDS-PAGE. ab34151 and ab18058 (Mouse anti-Vinculin loading control) were incubated overnight at 4°C at 1/250 dilution and 1/20000 dilution respectively. Blots were developed with Goat anti-Rabbit IgG H&L (IRDye® 800CW) preabsorbed ab216773 and Goat anti-Mouse IgG H&L (IRDye® 680RD) preabsorbed ab216776 secondary antibodies at 1/20000 dilution for 1 hour at room temperature before imaging.
Western blot - Caspr antibody (ab34151)
Anti-Caspr antibody (ab34151) at 1/250 dilution + Brain (Rat) Whole Cell Lysate - normal tissue at 10 µg
ICC/IF image of ab34151 stained SHSY5Y cells. The cells were 4% PFA fixed (10 min), permabilised in 0.1% PBS-Tween (20 min) and incubated with the antibody (ab34151, 1µg/ml) for 1h at room temperature. 1%BSA / 10% normal goat serum / 0.3M glycine was used to block non-specific protein-protein interactions. The secondary antibody (green) was Alexa Fluor® 488 goat anti-rabbit IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red). DAPI was used to stain the cell nuclei (blue).
Immunohistochemistry (PFA perfusion fixed frozen sections) - Anti-Caspr antibody (ab34151)This image is courtesy of an abreview submitted by Sophie Pezet, ESPCI, France
IHC-FoFR image of ab34151 stained sections of mouse brain (30 um). The tissues were from perfused fixed animals perfused with 4% PFA and postfixed 2h in the same fixative. They were cryoprotected in 30% sucrose and cut using a cryostat.
Caspr was immunoprecipitated using 0.5mg Rat Brain whole tissue lysate, 5µg of Rabbit polyclonal to Caspr and 50µl of protein G magnetic beads (+). No antibody was added to the control (-). The antibody was incubated under agitation with Protein G beads for 10min, Rat Brain whole tissue lysate lysate diluted in RIPA buffer was added to each sample and incubated for a further 10min under agitation. Proteins were eluted by addition of 40µl SDS loading buffer and incubated for 10min at 70oC; 10µl of each sample was separated on a SDS PAGE gel, transferred to a nitrocellulose membrane, blocked with 5% BSA and probed with ab34151. Secondary: Mouse monoclonal [SB62a] Secondary Antibody to Rabbit IgG light chain (HRP) (ab99697). Band: 180kDa: Caspr.
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Caspr antibody (ab34151)Image courtesy of an anonymous Abreview.
ab34151 staining Caspr in murine brain tissue by Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections). Tissue was fixed with paraformaldehyde. Samples were blocked with 20% serum for 1 hour at 20°C followed by incubation with the primary antibody at a 1/300 dilution for 12 hours at 20°C. An HRP-conjugated goat anti-rabbit polyclonal was used as the secondary antibody at a 1/200 dilution.
Zhang M et al. Comparative Analysis of the Cell Fates of Induced Schwann Cells from Subcutaneous Fat Tissue and Naïve Schwann Cells in the Sciatic Nerve Injury Model. Biomed Res Int2017:1252851 (2017).
Read more (PubMed: 28713821) »
O'Hare Doig RL et al. Specific ion channels contribute to key elements of pathology during secondary degeneration following neurotrauma. BMC Neurosci18:62 (2017).
Read more (PubMed: 28806920) »