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AB11887

Anti-C3 antibody

4

(2 Reviews)

|

(38 Publications)

Anti-C3 antibody (ab11887) is a rabbit polyclonal antibody detecting C3/C3b in IHC-P, IHC-Fr. Suitable for Mouse.

- Over 30 publications
- Trusted since 2004

View Alternative Names

Complement C3, HSE-MSF, C3

3 Images
Immunohistochemistry (Frozen sections) - Anti-C3 antibody (AB11887)
  • IHC-Fr

Supplier Data

Immunohistochemistry (Frozen sections) - Anti-C3 antibody (AB11887)

Positive staining of frozen mouse spleen tissue with ab11887 at 20x dilution.

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-C3 antibody (AB11887)
  • IHC-P

Supplier Data

Immunohistochemistry (Formalin/PFA-fixed paraffin-embedded sections) - Anti-C3 antibody (AB11887)

Positive staining of paraffin embedded mouse kidney tissue with ab11887 at 100x dilution.

Immunohistochemistry (Frozen sections) - Anti-C3 antibody (AB11887)
  • IHC-Fr

PubMed

Immunohistochemistry (Frozen sections) - Anti-C3 antibody (AB11887)

Immunohistochemical analysis of rat retina tissue after bright continuous white light exposure, staining C3 with ab11887.

Image from Rutar M et al., Journal of Neuroinflammation 2012, 9:257, 26 November 2012. Fig 5.; doi: 10.1186/1742-2094-9-257.

Key facts

Host species

Rabbit

Clonality

Polyclonal

Isotype

IgG

Carrier free

No

Reacts with

Mouse

Applications

IHC-Fr, IHC-P

applications

Immunogen

The exact immunogen used to generate this antibody is proprietary information.

Specificity

This polyclonal antibody detects a band approximately 120 kDa in Western blot under reducing conditions, corresponding to the C3 alpha chain.

Reactivity data

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Product details

What is this antibody validated in?
Anti-C3 antibody (ab11887) is a rabbit polyclonal antibody and is validated for use in Immunohistochemistry (IHC-P), Immunohistochemistry (IHC-Fr) in Mouse samples.

Trusted by the scientific community
Anti-C3 (ab11887) was first used in a scientific publication in 2004 and has been cited over 30 times in peer-reviewed journals.

Properties and storage information

Form
Liquid
Purification technique
Affinity purification Protein G
Storage buffer
Preservative: 0.02% Sodium azide Constituents: PBS, 0.1% BSA
Shipped at conditions
Blue Ice
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.

Complement component 3 (C3) commonly known as C3 complement is a central protein in the complement system which plays a significant role in immune response. C3b a fragment of C3 is produced when C3 undergoes cleavage. C3 is a large protein with a mass of approximately 185 kDa. The liver primarily secretes C3 into the bloodstream. It circulates in the plasma and is found in high concentration making it one of the most abundant components of the complement system.
Biological function summary

Complement component C3 forms part of the innate immune system by promoting opsonization which enhances phagocytosis of pathogens. C3b binds to pathogens' surfaces facilitating their recognition by phagocytes. C3 as part of a complex with C3 convertase also has a role in amplifying the activation of the complement cascade. The proteolytic cleavage of C3 into C3b and C3a leads to the activation of other components forming the membrane attack complex and orchestrating inflammation.

Pathways

The complement component C3 functions within both the classical and alternative complement pathways. It acts as a convergence point where the complement activation pathways meet. C3 is activated into C3b and C3a which are key to amplifying the cascade. Furthermore C3 interacts with proteins such as factor B and factor D in the alternative pathway and C4 and C2 in the classical pathway facilitating the formation of C3 convertase necessary for pathway progression.

Complement C3 shows associations with immune-related and inflammatory diseases. Deficiencies or malfunctions of complement C3 can lead to increased susceptibility to infections due to impaired opsonization and clearance of pathogens. Additionally overactivation of the complement system involving C3 can contribute to autoimmune disorders such as systemic lupus erythematosus. Other proteins linked to these diseases include C4 in lupus and factor H in age-related macular degeneration which controls complement pathway activation.

Product protocols

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

Target data

C3 plays a central role in the activation of the complement system. Its processing by C3 convertase is the central reaction in both classical and alternative complement pathways. After activation C3b can bind covalently, via its reactive thioester, to cell surface carbohydrates or immune aggregates.. Derived from proteolytic degradation of complement C3, C3a anaphylatoxin is a mediator of local inflammatory process. In chronic inflammation, acts as a chemoattractant for neutrophils (By similarity). It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes. The short isoform has B-cell stimulatory activity.. C3-beta-c. Acts as a chemoattractant for neutrophils in chronic inflammation.. Acylation stimulating protein. Adipogenic hormone that stimulates triglyceride (TG) synthesis and glucose transport in adipocytes, regulating fat storage and playing a role in postprandial TG clearance. Appears to stimulate TG synthesis via activation of the PLC, MAPK and AKT signaling pathways. Ligand for C5AR2. Promotes the phosphorylation, ARRB2-mediated internalization and recycling of C5AR2.
See full target information C3

Publications (38)

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

Molecular therapy. Methods & clinical development 33:101450 PubMed40231247

2025

Enhanced retinal pigment epithelial cells as a delivery vehicle for retinal disease.

Applications

Unspecified application

Species

Unspecified reactive species

Avril Reddy,Chris Greene,Yosuke Hashimoto,Anna-Sophia Kiang,Natalie Hudson,Peter Adamson,Tiago Santos-Ferreira,Matthew Campbell

British journal of pharmacology 181:4028-4049 PubMed38936407

2024

Histone deacetylase inhibition mitigates cognitive deficits and astrocyte dysfunction induced by amyloid-β (Aβ) oligomers.

Applications

Unspecified application

Species

Unspecified reactive species

Luan Pereira Diniz,Juliana Morgado,Ana Paula Bergamo Araujo,Leticia Maria da Silva Antônio,Hannah Paola Mota-Araujo,Pedro de Sena Murteira Pinheiro,Fernanda Savacini Sagrillo,Gabriele Vargas Cesar,Sérgio T Ferreira,Cláudia Pinto Figueiredo,Carlos Alberto Manssour Fraga,Flávia Carvalho Alcantara Gomes

Science translational medicine 16:eadf4601 PubMed38446899

2024

Gamma entrainment using audiovisual stimuli alleviates chemobrain pathology and cognitive impairment induced by chemotherapy in mice.

Applications

Unspecified application

Species

Unspecified reactive species

TaeHyun Kim,Benjamin T James,Martin C Kahn,Cristina Blanco-Duque,Fatema Abdurrob,Md Rezaul Islam,Nicolas S Lavoie,Manolis Kellis,Li-Huei Tsai

Cell reports 43:113801 PubMed38363678

2024

DLK signaling in axotomized neurons triggers complement activation and loss of upstream synapses.

Applications

Unspecified application

Species

Unspecified reactive species

Elham Asghari Adib,Jennifer L Shadrach,Lauren Reilly-Jankowiak,Manish K Dwivedi,Abigail E Rogers,Shameena Shahzad,Ryan Passino,Roman J Giger,Brian A Pierchala,Catherine A Collins

Neural regeneration research 19:2057-2067 PubMed38227536

2024

Unilateral rNurr1-V5 transgene expression in nigral dopaminergic neurons mitigates bilateral neuropathology and behavioral deficits in parkinsonian rats with α-synucleinopathy.

Applications

Unspecified application

Species

Unspecified reactive species

Bismark Gatica-Garcia,Michael J Bannon,Irma Alicia Martínez-Dávila,Luis O Soto-Rojas,David Reyes-Corona,Lourdes Escobedo,Minerva Maldonado-Berny,M E Gutierrez-Castillo,Armando J Espadas-Alvarez,Manuel A Fernandez-Parrilla,Juan U Mascotte-Cruz,C P Rodríguez-Oviedo,Irais E Valenzuela-Arzeta,Claudia Luna-Herrera,Francisco E Lopez-Salas,Jaime Santoyo-Salazar,Daniel Martinez-Fong

Journal of neuroinflammation 20:261 PubMed37953259

2023

NeuroD1 administration ameliorated neuroinflammation and boosted neurogenesis in a mouse model of subarachnoid hemorrhage.

Applications

Unspecified application

Species

Unspecified reactive species

Ping Chen,Xue-Yan Liu,Mou-Hui Lin,Yu-Xi Li,De-Zhi Kang,Zu-Cheng Ye,Qing-Song Lin

Folia neuropathologica 61:273-290 PubMed37818688

2023

Astragaloside IV inhibits experimental autoimmune encephalomyelitis by modulating the polarization of both microglia/macrophages and astrocytes.

Applications

Unspecified application

Species

Unspecified reactive species

Jingwen Yu,Bingtao Mu,Minfang Guo,Chunyun Liu,Tao Meng,Yuqing Yan,Lijuan Song,Jiezhong Yu,Gajendra Kumar,Cungen Ma

Cells 12: PubMed37759539

2023

Differential Effects of Regulatory T Cells in the Meninges and Spinal Cord of Male and Female Mice with Neuropathic Pain.

Applications

Unspecified application

Species

Unspecified reactive species

Nathan T Fiore,Brooke A Keating,Yuting Chen,Sarah I Williams,Gila Moalem-Taylor

Journal of neuroinflammation 20:113 PubMed37170230

2023

β-arrestin1 regulates astrocytic reactivity via Drp1-dependent mitochondrial fission: implications in postoperative delirium.

Applications

Unspecified application

Species

Unspecified reactive species

Fuzhou Hua,Hong Zhu,Wen Yu,Qingcui Zheng,Lieliang Zhang,Weidong Liang,Yue Lin,Fan Xiao,Pengcheng Yi,Yanhong Xiong,Yao Dong,Hua Li,Lanran Fang,Hailin Liu,Jun Ying,Xifeng Wang

Frontiers in immunology 13:1021370 PubMed36591222

2022

The extrafollicular response is sufficient to drive initiation of autoimmunity and early disease hallmarks of lupus.

Applications

Unspecified application

Species

Unspecified reactive species

Lasse F Voss,Amanda J Howarth,Thomas R Wittenborn,Sandra Hummelgaard,Kristian Juul-Madsen,Kristian S Kastberg,Mathias K Pedersen,Lisbeth Jensen,Anastasios D Papanastasiou,Thomas Vorup-Jensen,Kathrin Weyer,Søren E Degn
View all publications

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