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The ninjurin protein is upregulated after nerve injury both in dorsal root ganglion neurons and in Schwann cells (Araki and Milbrandt, 1996. Additionally we are shipping Ninjurin 1 Antibodies (44) and Ninjurin 1 Proteins (6) and many more products for this protein.
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Data show that Ninj1 assembles into a homomeric protein complex and that N-glycosylation is a prerequisite for Ninj1 homomer assembly.
Ninj1 suppresses migration, invasion and metastasis of lung cancer via inhibition of the IL-6 signaling pathway in vitro and in vivo.
High ninjurin 1 expression is associated with Prostate Cancer.
Ninj1 expression was detected in both HSMCs and HUVECs, and was higher in the former. Ninj1 expression was enhanced by hypoxia in HUVECs.
Ninj1 modulates TLR4 signaling, which itself plays a major role in systemic inflammatory response syndrome and sepsis.
The NINJ1 gene polymorphism plays an important role in nerve degeneration in leprosy patients.
Data show an important cell-specific role for Ninjurin-1 in the transmigration of inflammatory APCs across the BBB.
Ninjurin1 is able to induce the senescence program. Ninjurin1 may be involved in the regulation of cellular senescence in the liver during carcinogenesis.
Our data suggests that Ninjurin 1 asp110ala SNP could be a valuable genetic marker of nerve damage in leprosy.
Ninjurin1 is a key regulator molecule for macrophage migration and Tumor-associated macrophages (TAM) mediated tumorigenesis in vivo.
Ninj1 negatively regulates the formation of neovessels, that is, the EC-tube, by reducing the trophic effects of capillary pericytes.
Ninjurin1-deficient bone marrow-derived macrophages exhibited reduced membrane protrusion formation and dynamics, resulting in the impairment of cell motility.
Inhibition of Ninjurin 1 restores erectile function through dual angiogenic and neurotrophic effects in the diabetic mouse.
The dual neurotrophic and angiogenic effects of Ninj1 blockade may provide a good opportunity for treating erectile dysfunction resulting from radical prostatectomy.
Ninjurin1 deficiency attenuates susceptibility of experimental autoimmune encephalomyelitis in mice
Ninj1 plays a role in p53-mediated tumor suppression in addition to nerve regeneration.
the N-terminal ectodomain of mouse Ninjurin1, which may act as a chemoattractant, is cleaved by MMP9.
Ninj1 protein has an important role in vascular regression mediated by macrophages during early eye development and suggest the biological relevance of Ninj1 on vascular homeostasis.
The ninjurin protein is upregulated after nerve injury both in dorsal root ganglion neurons and in Schwann cells (Araki and Milbrandt, 1996
, nerve injury-induced protein 1
, nerve injury-induced protein-1