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NINJ1 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, IHC-P, IF, E |
|---|---|
| Primary Accession | Q92982 |
| Other Accession | NP_004139, 148922911 |
| Reactivity | Human, Mouse, Rat |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | IgG |
| Calculated MW | Predicted: 17 kDa Observed: 16 kDa |
| Application Notes | NINJ1 antibody can be used for detection of NINJ1 by Western blot at 1 - 2 µg/ml. Antibody can also be used for immunohistochemistry starting at 5 µg/mL. For immunofluorescence start at 20 µg/mL. |
| Gene ID | 4814 |
|---|---|
| Target/Specificity | NINJ1; NINJ1 antibody is human, mouse and rat reactive. |
| Reconstitution & Storage | NINJ1 antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. |
| Precautions | NINJ1 Antibody is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | NINJ1 {ECO:0000303|PubMed:33472215, ECO:0000312|HGNC:HGNC:7824} |
|---|---|
| Function | [Ninjurin-1]: Effector of necroptotic and pyroptotic programmed cell death that mediates plasma membrane rupture (cytolysis) (PubMed:33472215, PubMed:36468682, PubMed:37196676, PubMed:37198476). Acts downstream of Gasdermin (GSDMA, GSDMB, GSDMC, GSDMD, or GSDME) or MLKL during pyroptosis or necroptosis, respectively: oligomerizes in response to death stimuli and promotes plasma membrane rupture by introducing hydrophilic faces of 2 alpha helices into the hydrophobic membrane, leading to release intracellular molecules named damage- associated molecular patterns (DAMPs) that propagate the inflammatory response (PubMed:33472215, PubMed:36468682, PubMed:37196676, PubMed:37198476). Acts as a regulator of Toll-like receptor 4 (TLR4) signaling triggered by lipopolysaccharide (LPS) during systemic inflammation; directly binds LPS (PubMed:26677008). Involved in leukocyte migration during inflammation by promoting transendothelial migration of macrophages via homotypic binding (By similarity). Promotes the migration of monocytes across the brain endothelium to central nervous system inflammatory lesions (PubMed:22162058). Also acts as a homophilic transmembrane adhesion molecule involved in various processes such as axonal growth, cell chemotaxis and angiogenesis (PubMed:8780658, PubMed:9261151, PubMed:33028854). Promotes cell adhesion by mediating homophilic interactions via its extracellular N-terminal adhesion motif (N-NAM) (PubMed:33028854). Involved in the progression of the inflammatory stress by promoting cell-to-cell interactions between immune cells and endothelial cells (PubMed:22162058, PubMed:26677008, PubMed:32147432). Plays a role in nerve regeneration by promoting maturation of Schwann cells (PubMed:8780658, PubMed:9261151). Acts as a regulator of angiogenesis (PubMed:33028854). Promotes the formation of new vessels by mediating the interaction between capillary pericyte cells and endothelial cells (By similarity). Promotes osteoclasts development by enhancing the survival of prefusion osteoclasts (By similarity). Also involved in striated muscle growth and differentiation (By similarity). |
| Cellular Location | [Ninjurin-1]: Cell membrane; Multi-pass membrane protein. Synaptic cell membrane {ECO:0000250|UniProtKB:O70131}; Multi-pass membrane protein |
| Tissue Location | Widely expressed in both adult and embryonic tissues, primarily those of epithelial origin |
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abcepta to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
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Provided below are standard protocols that you may find useful for product applications.
Background
Ninjurin-1 (NINJ1) is a homophilic adhesion molecule that is strongly induced in dorsal root ganglion (DRG) and Schwann cells following nerve injury and promotes neurite outgrowth of DRG neurons (1,2), suggesting that NINJ1 may play a role in nerve regeneration. NINJ1 is transcriptionally regulated by p53 and is induced by DNA damage in a p53-dependent manner. A deficiency of NINJ1 increases p53 expression, suppresses cell proliferation, but enhances apoptosis and premature senescence in a p53-dependent manner as well as radiation-induced cell mortality (3).
References
Araki T and Milbrandt J. Ninjurin, a novel adhesion molecule, is induced by nerve injury and promotes axonal growth. Neuron 1996; 17:353-61.
Araki T, Zimonjic DB, Popescu NC, et al. Mechanism of homophilic binding mediated by ninjurin, a novel widely expressed adhesion molecule. J. Biol. Chem. 1997; 212:21373-80.
Cho SJ, Rossi A, Jung YS, et al. Ninjurin1, a target of p53, regulates p53 expression and p53-dependent cell survival, sensecence, and radiation-induced mortality. Proc. Natl. Acad. Sci. USA 2013; 110:9362-7.
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