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AB213695

Anti-Ninjurin 1 antibody

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(5 Publications)

Rabbit Polyclonal Ninjurin 1 antibody. Suitable for IHC-P and reacts with Human samples. Cited in 5 publications. Immunogen corresponding to Synthetic Peptide within Human NINJ1 aa 1-100 conjugated to Keyhole Limpet Haemocyanin.

View Alternative Names

Ninjurin-1, hNINJ1, Nerve injury-induced protein 1, NINJ1

2 Images
Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Ninjurin 1 antibody (AB213695)
  • IHC-P

Supplier Data

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Ninjurin 1 antibody (AB213695)

Immunohistochemical analysis of formalin-fixed, paraffin-embedded Human meningioma tissue labeling Ninjurin 1 with ab213695 at 1/200 dilution, followed by conjugation to a secondary antibody and DAB staining.

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Ninjurin 1 antibody (AB213695)
  • IHC-P

Supplier Data

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-Ninjurin 1 antibody (AB213695)

Immunohistochemical analysis of formalin-fixed, paraffin-embedded Human lung carcinoma tissue labeling Ninjurin 1 with ab213695 at 1/500 dilution, followed by conjugation to a secondary antibody and DAB staining.

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Human

Applications

IHC-P

applications

Immunogen

Synthetic Peptide within Human NINJ1 aa 1-100 conjugated to Keyhole Limpet Haemocyanin. The exact immunogen used to generate this antibody is proprietary information.

Q92982

Reactivity data

{ "title": "Reactivity Data", "filters": { "stats": ["", "Species", "Dilution Info", "Notes"], "tabs": { "all-applications": {"fullname" : "All Applications", "shortname": "All Applications"}, "IHCP" : {"fullname" : "Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections)", "shortname":"IHC-P"} }, "product-promise": { "all": "all", "testedAndGuaranteed": "tested", "guaranteed": "expected", "predicted": "predicted", "notRecommended": "not-recommended" } }, "values": { "Human": { "IHCP-species-checked": "testedAndGuaranteed", "IHCP-species-dilution-info": "1/100 - 1/500", "IHCP-species-notes": "<p></p>" }, "Mouse": { "IHCP-species-checked": "predicted", "IHCP-species-dilution-info": "", "IHCP-species-notes": "" }, "Rat": { "IHCP-species-checked": "predicted", "IHCP-species-dilution-info": "", "IHCP-species-notes": "" } } }

Properties and storage information

Form
Liquid
Purification technique
Affinity purification Protein A
Storage buffer
pH: 7.4 Preservative: 0.02% Proclin 300 Constituents: 50% Glycerol (glycerin, glycerine), 48.98% TBS, 1X, 1% BSA
Shipped at conditions
Blue Ice
Appropriate short-term storage duration
1-2 weeks
Appropriate short-term storage conditions
+4°C
Appropriate long-term storage conditions
-20°C
Aliquoting information
Upon delivery aliquot
Storage information
Avoid freeze / thaw cycle

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

Ninjurin 1 also known as ‘NINJ1’ 'ninjurin' or 'ninjurin-1' is a vital protein with a molecular mass of about 16 kDa. This protein is expressed in several tissues such as the neural lineage including Schwann cells and dorsal root ganglion neurons. Ninjurin 1 plays a mechanical role in cell adhesion and communication. Detailed studies reveal that Ninjurin 1 directly participates in the formation of cell-cell junctions indicating an important role in tissue integrity and repair.
Biological function summary

Ninjurin 1 is implicated in neural development and immune response. It is not part of a larger protein complex but it interacts with cell membranes promoting cell migration and regeneration. This makes it essential in processes like nerve injury repair and the maintenance of peripheral nerve structure. As a mediator Ninjurin 1 helps in the coordination between cellular responses and environmental signals influencing how cells react to damage and inflammation.

Pathways

Ninjurin 1 is an important component in nerve regeneration and immune response pathways. It supports the axonal outgrowth and Schwann cell migration essential after nerve damage. Additionally it’s related to molecules involved in inflammatory signaling pathways like cytokines and toll-like receptors. These interactions facilitate Ninjurin 1’s involvement in orchestrating cellular events that lead to wound healing and immune cell trafficking.

Ninjurin 1 shows relevance to neurodegenerative diseases and autoimmune conditions. It supports nerve regeneration making it a focus in neuropathic pain management and multiple sclerosis research. Connection with proteins such as nerve growth factor (NGF) and interleukins further elucidates its disease-related interactions. Research continues to explore how modulating Ninjurin 1 expression can provide therapeutic benefits in these contexts.

Product protocols

For this product, it's our understanding that no specific protocols are required. You can visit:

Target data

Ninjurin-1. Effector of various programmed cell death, such as pyroptosis and necroptosis, which mediates plasma membrane rupture (cytolysis) (PubMed : 33472215, PubMed : 36468682, PubMed : 37196676, PubMed : 37198476, PubMed : 38614101). 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 (PubMed : 38614101). Plasma membrane rupture leads to release intracellular molecules named damage-associated molecular patterns (DAMPs) that propagate the inflammatory response (PubMed : 33472215, PubMed : 36468682, PubMed : 37196676, PubMed : 37198476). Mechanistically, mediates plasma membrane rupture by introducing hydrophilic faces of 2 alpha helices into the hydrophobic membrane (PubMed : 37198476, PubMed : 38614101). Induces plasma membrane rupture downstream of Gasdermin (GSDMA, GSDMB, GSDMC, GSDMD, or GSDME) or MLKL during pyroptosis or necroptosis, respectively (PubMed : 33472215, PubMed : 36468682, PubMed : 37196676, PubMed : 37198476). Acts as an effector of PANoptosis downstream of CASP1, CASP4, CASP8 and RIPK3 (By similarity). Also induces plasma membrane rupture in response to cell swelling caused by osmotic stress and ferroptosis downstream of lipid peroxidation (By similarity). 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 : 33028854, PubMed : 8780658, PubMed : 9261151). Promotes cell adhesion by mediating homophilic interactions via its extracellular N-terminal adhesion motif (N-NAM) (PubMed : 33028854, PubMed : 8780658, PubMed : 9261151). 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).. Secreted ninjurin-1. Secreted form generated by cleavage, which has chemotactic activity (By similarity). Acts as an anti-inflammatory mediator by promoting monocyte recruitment, thereby ameliorating atherosclerosis (PubMed : 32883094).
See full target information NINJ1

Publications (5)

Recent publications for all applications. Explore the full list and refine your search

Cells 14: PubMed40136650

2025

Development of Novel Peptides That Target the Ninjurin 1 and 2 Pathways to Inhibit Cell Growth and Survival via p53.

Applications

Unspecified application

Species

Unspecified reactive species

Jin Zhang,Xiangmudong Kong,Xinbin Chen

Advanced science (Weinheim, Baden-Wurttemberg, Germany) 11:e2402299 PubMed39316370

2024

Embryo-Derived Cathepsin B Promotes Implantation and Decidualization by Activating Pyroptosis.

Applications

Unspecified application

Species

Unspecified reactive species

Meng-Yuan Li,Ying Wu,Hao-Lan Tang,Ying Wang,Bo Li,Yu-Ying He,Gui-Jun Yan,Zeng-Ming Yang

Food science & nutrition 11:6686-6697 PubMed37823117

2023

Effect of vitamin D3 on lipid droplet growth in adipocytes of mice with HFD-induced obesity.

Applications

Unspecified application

Species

Unspecified reactive species

Jingjing Zhang,Yuanfan Zhang,Yong Zhou,Wenxin Zhao,Jialu Li,Dan Yang,Lian Xiang,Tingwan Du,Ling Ma

JID innovations : skin science from molecules to population health 2:100141 PubMed36262667

2022

Ninjurin1 Deletion in NG2-Positive Pericytes Prevents Microvessel Maturation and Delays Wound Healing.

Applications

Unspecified application

Species

Unspecified reactive species

Risa Matsuo,Mari Kishibe,Kiwamu Horiuchi,Kohei Kano,Takamitsu Tatsukawa,Taiki Hayasaka,Maki Kabara,Shin Iinuma,Ryoji Eguchi,Satomi Igawa,Naoyuki Hasebe,Akemi Ishida-Yamamoto,Jun-Ichi Kawabe

American journal of physiology. Heart and circulatory physiology 320:H2438-H2447 PubMed33961504

2021

Pericyte-specific deletion of ninjurin-1 induces fragile vasa vasorum formation and enhances intimal hyperplasia of injured vasculature.

Applications

Unspecified application

Species

Unspecified reactive species

Kiwamu Horiuchi,Kohei Kano,Akiho Minoshima,Taiki Hayasaka,Atsushi Yamauchi,Takamitsu Tatsukawa,Risa Matsuo,Yuri Yoshida,Yui Tomita,Maki Kabara,Naoki Nakagawa,Naofumi Takehara,Naoyuki Hasebe,Jun-Ichi Kawabe
View all publications

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