anti-NINJ1, pAb (IN114)

CHF 250.00
In stock
AG-25B-6002-C05050 µgCHF 250.00
More Information
Product Details
Synonyms Ninjurin-1; Nerve Injury-induced Protein 1
Product Type Polyclonal Antibody
Source/Host Rabbit
Immunogen/Antigen Synthetic peptide corresponding to aa at the N-terminal human NINJ1.

Western Blot: (1:500-2000)

ELISA: (1:5000 - 1:10000)

Optimal conditions must be determined individually for each application.

Crossreactivity Human

Recognizes full-length human NINJ1. It is predicted to cross-react with mouse and rat NINJ1, based on the homology of the immunogen, but has not been tested.

Purity ≥95% (SDS-PAGE)
Purity Detail Epitope-affinity purified.
Concentration 1mg/ml
Formulation Liquid. In PBS containing 50% glycerol and 0.02% sodium azide.
Isotype Negative Control

Rabbit IgG

Other Product Data

UniProt link Q92982: NINJ1 (human)

Accession Number Q92982
Shipping and Handling
Shipping BLUE ICE
Short Term Storage +4°C
Long Term Storage -20°C
Handling Advice After opening, prepare aliquots and store at -20°C.
Avoid freeze/thaw cycles.
Use/Stability Stable for at least 1 year after receipt when stored at -20°C.
MSDS Download PDF
Product Specification Sheet
Datasheet Download PDF

Ninjurin-1 (NINJ1), a 16-kDa cell-surface protein, is an adhesion molecule that is associated with inflammation and tumour suppression. NINJ1 has been identified to be highly induced by nerve injury in Schwann cells and dorsal root ganglion. NINJ1 is also expressed in myeloid cells (macrophages). NINJ1 plays a role in nerve regeneration, in progression of multiple sclerosis (an autoimmune inflammatory CNS disease characterized by demyelination and axonal damage), in angiogenesis by modulating neovessel formation. NINJ1 is capable of suppressing cancer cell invasion.

Recently, NINJ1 has been shown to play an essential role in the induction of plasma membrane rupture (PMR) during pyroptosis. It is crucial for PMR, but dispensable for Gasdermin D pore formation and IL-1β release. NINJ1 is also involved in necrosis and apoptotic PMR. Mechanistically, NINJ1 uses an evolutionarily conserved extracellular domain for oligomerization and subsequent PMR. NINJ1 mediates PMR and the release of DAMP (Danger Associated Molecular Pattern), key events in the propagation of inflammation.

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