This NINJ1 Sandwich ELISA Kit is an in-vitro enzyme-linked immunosorbent assay for the measurement of samples in human serum, plasma, tissue homogenates or other biological fluids..
Applications
ELISA
Reactivity
Human
Sensitivity
0.111ng/mL
Detection Limit
0.312-20ng/mL
Note
STRICTLY FOR FURTHER SCIENTIFIC RESEARCH USE ONLY (RUO). MUST NOT TO BE USED IN DIAGNOSTIC OR THERAPEUTIC APPLICATIONS.
Product Properties
Storage Instruction
Store the unopened kit in the fridge at 2-8°C for up to 6 months. Once opened store individual kit contents according to components table provided with the kit.
serum, plasma, tissue homogenates or other biological fluids.
Additional Info
Tissue Specificity
Widely expressed in both adult and embryonic tissues, primarily those of epithelial origin.
Post Translational Modifications
Ninjurin-1: Cleaved by MMP9 protease to generate the Secreted ninjurin-1 form. Ninjurin-1: N-linked glycosylation is required for homooligomerization.
Function
Ninjurin-1: Effector of various programmed cell death, such as pyroptosis and necroptosis, which mediates plasma membrane rupture (cytolysis). Oligomerizes in response to death stimuli and forms ring-like structures on the plasma membrane: acts by cutting and shedding membrane disks, like a cookie cutter, leading to membrane damage and loss that cannot be repaired by the cell. Plasma membrane rupture leads to release intracellular molecules named damage-associated molecular patterns (DAMPs) that propagate the inflammatory response. Mechanistically, mediates plasma membrane rupture by introducing hydrophilic faces of 2 alpha helices into the hydrophobic membrane. Induces plasma membrane rupture downstream of Gasdermin (GSDMA, GSDMB, GSDMC, GSDMD, or GSDME) or MLKL during pyroptosis or necroptosis, respectively. Acts as an effector of PANoptosis downstream of CASP1, CASP4, CASP8 and RIPK3. Also induces plasma membrane rupture in response to cell swelling caused by osmotic stress and ferroptosis downstream of lipid peroxidation. Acts as a regulator of Toll-like receptor 4 (TLR4) signaling triggered by lipopolysaccharide (LPS) during systemic inflammation.directly binds LPS. Involved in leukocyte migration during inflammation by promoting transendothelial migration of macrophages via homotypic binding. Promotes the migration of monocytes across the brain endothelium to central nervous system inflammatory lesions. Also acts as a homophilic transmembrane adhesion molecule involved in various processes such as axonal growth, cell chemotaxis and angiogenesis. Promotes cell adhesion by mediating homophilic interactions via its extracellular N-terminal adhesion motif (N-NAM). Involved in the progression of the inflammatory stress by promoting cell-to-cell interactions between immune cells and endothelial cells. Plays a role in nerve regeneration by promoting maturation of Schwann cells. Acts as a regulator of angiogenesis. Promotes the formation of new vessels by mediating the interaction between capillary pericyte cells and endothelial cells. Promotes osteoclasts development by enhancing the survival of prefusion osteoclasts. Also involved in striated muscle growth and differentiation. Secreted ninjurin-1: Secreted form generated by cleavage, which has chemotactic activity. Acts as an anti-inflammatory mediator by promoting monocyte recruitment, thereby ameliorating atherosclerosis.
Protein Name
Ninjurin-1Hninj1Nerve Injury-Induced Protein 1 Cleaved Into - Secreted Ninjurin-1Soluble Ninjurin-1
