C3a Anaphylatoxin Chemotactic Receptor (C3AR1) Antibody

Este producto es parte de C3a-C5a - Complement component Receptor
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312€ (0.1 mg)

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935106861
info@markelab.com
name
C3a Anaphylatoxin Chemotactic Receptor (C3AR1) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx347188
tested applications
IHC, FCM

Description

C3a Anaphylatoxin Chemotactic Receptor (C3AR1) Antibody is a mouse monoclonal antibody against C3a Anaphylatoxin Chemotactic Receptor (C3AR1).

Documents del producto

Instrucciones
Data sheet
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Product specifications

Category
Primary Antibodies
Immunogen Target
C3a Anaphylatoxin Chemotactic Receptor (C3AR1)
Host
Mouse
Reactivity
Human
Recommended Dilution
FCM: 1-4 µg/ml. Optimal dilutions/concentrations should be determined by the end user.
Clonality
Monoclonal
Conjugation
Unconjugated
Isotype
IgG2b
Clone ID
T480
Purification
Purified by Protein A affinity chromatography.
Size 1
0.1 mg
Tested Applications
IHC, FCM
Buffer
PBS solution with 15 mM sodium azide.
Availability
Shipped within 5-12 working days.
Storage
Store at 2-8°C. Do not freeze.
Dry Ice
No
UniProt ID
Q16581
Gene ID
719
Alias
C3AR1,C3AR,C3a anaphylatoxin chemotactic receptor,C3a-R,anaphylatoxin C3a receptor,complement component 3a receptor,C3a receptor,AZ3B,HNFAG09
Background
Antibody anti-C3AR1
Status
RUO
Note
Concentration: 1 mg/ml - 

Descripción

C3AR1 is a G protein-coupled receptor that binds C3a, a complement system-derived anaphylatoxin, playing a pivotal role in inflammation and immune responses. C3AR1 is widely expressed on immune cells, including neutrophils, macrophages, eosinophils, and mast cells, where it mediates chemotaxis, degranulation, and cytokine production in response to C3a binding. It is a key regulator of the complement system, promoting immune cell recruitment and activation during infections, injury, and inflammatory responses. C3AR1 signaling activates pathways such as PI3K/Akt and ERK, driving cellular responses that contribute to host defense. Dysregulated C3AR1 activity is implicated in inflammatory and autoimmune diseases, including rheumatoid arthritis, asthma, and sepsis, where excessive complement activation exacerbates tissue damage and inflammation. In cancer, C3AR1 expression on tumor-associated macrophages and other immune cells modulates the tumor microenvironment, promoting immunosuppression and angiogenesis. C3AR1 is also involved in neuroinflammation, contributing to neurodegenerative diseases like Alzheimer’s and multiple sclerosis by mediating microglial activation and cytokine release. Therapeutically, targeting C3AR1 with inhibitors or antagonists is being explored to modulate complement-driven inflammation and reduce tissue damage in autoimmune diseases and cancer.

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