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AB121055

Anti-Factor H antibody [C18/3]

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(3 Publications)

Mouse Monoclonal Factor H antibody. Suitable for WB, sELISA and reacts with Human samples. Cited in 3 publications. Immunogen corresponding to Native Full Length Protein corresponding to Human CFH.

View Alternative Names

HF, HF1, HF2, CFH, Complement factor H, H factor 1

Key facts

Host species

Mouse

Clonality

Monoclonal

Clone number

C18/3

Isotype

IgG1

Light chain type

kappa

Carrier free

No

Reacts with

Human

Applications

WB, sELISA

applications

Immunogen

Native Full Length Protein corresponding to Human CFH.

P08603

Reactivity data

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Properties and storage information

Form
Liquid
Purification technique
Affinity purification Protein G
Storage buffer
pH: 7.4 Preservative: 0.1% Sodium azide Constituents: PBS, 2.9% Sodium chloride
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
Storage information
Avoid freeze / thaw cycle

Supplementary information

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

Factor H also known as complement factor H is an important regulatory protein in the complement system. It has a molecular mass of approximately 155 kDa. This protein is mainly expressed in the liver but it can also be found in low levels in other tissues. Factor H serves as a control element for complement activation particularly affecting the alternative pathway. It binds to C3b a central component of the complement system and accelerates the decay of C3 convertase as well as promotes the proteolytic inactivation of C3b by factor I.
Biological function summary

Factor H limits the activity of the complement system to prevent damage to host tissues. The protein exists in the plasma in a soluble form. It functions by recognizing host cell surfaces via specific markers avoiding inappropriate activation. Factor H belongs to a group of proteins which include other regulators of complement activation. These proteins maintain the balance between effective immune defense and protection of host tissue from excessive immune responses.

Pathways

Factor H is a part of the alternative complement pathway. This pathway is important for innate immune response involving proteins like factor P (properdin) which stabilizes C3 convertase. Factor H modulates these interactions to prevent unwarranted complement activity on host cells. Another related pathway is the classic complement pathway although factor H's involvement here is less direct since it primarily regulates the alternative pathway.

Factor H associations include atypical hemolytic uremic syndrome and age-related macular degeneration. Factor H deficiency or dysfunction can lead to uncontrolled complement activation resulting in kidney damage in atypical hemolytic uremic syndrome where it is also related to factor I. Additionally in age-related macular degeneration variants in the factor H gene are linked to increased susceptibility further highlighting the protein's importance in regulating immune responses.

Product protocols

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

Target data

Glycoprotein that plays an essential role in maintaining a well-balanced immune response by modulating complement activation. Acts as a soluble inhibitor of complement, where its binding to self markers such as glycan structures prevents complement activation and amplification on cell surfaces (PubMed : 21285368, PubMed : 21317894, PubMed : 25402769). Accelerates the decay of the complement alternative pathway (AP) C3 convertase C3bBb, thus preventing local formation of more C3b, the central player of the complement amplification loop (PubMed : 19503104, PubMed : 21317894, PubMed : 26700768). As a cofactor of the serine protease factor I, CFH also regulates proteolytic degradation of already-deposited C3b (PubMed : 18252712, PubMed : 23332154, PubMed : 28671664). In addition, mediates several cellular responses through interaction with specific receptors. For example, interacts with CR3/ITGAM receptor and thereby mediates the adhesion of human neutrophils to different pathogens. In turn, these pathogens are phagocytosed and destroyed (PubMed : 20008295, PubMed : 9558116).. (Microbial infection) In the mosquito midgut, binds to the surface of parasite P.falciparum gametocytes and protects the parasite from alternative complement pathway-mediated elimination.
See full target information CFH

Publications (3)

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

Frontiers in cardiovascular medicine 9:1003282 PubMed36172581

2022

Exosomes derived from pericardial adipose tissues attenuate cardiac remodeling following myocardial infarction by Adipsin-regulated iron homeostasis.

Applications

Unspecified application

Species

Unspecified reactive species

Wanrong Man,Xinglong Song,Zhenyu Xiong,Jing Gu,Jie Lin,Xiaoming Gu,Duan Yu,Congye Li,Mengyuan Jiang,Xuebin Zhang,Zhi Yang,Yang Cao,Yan Zhang,Xiaofei Shu,Dexi Wu,Haichang Wang,Gang Ji,Dongdong Sun

Nature communications 12:4858 PubMed34381048

2021

Dendrimer end-terminal motif-dependent evasion of human complement and complement activation through IgM hitchhiking.

Applications

Unspecified application

Species

Unspecified reactive species

Lin-Ping Wu,Mario Ficker,Jørn B Christensen,Dmitri Simberg,Panagiotis N Trohopoulos,Seyed M Moghimi

Cancer immunology research 9:909-925 PubMed34039652

2021

Intracellular Factor H Drives Tumor Progression Independently of the Complement Cascade.

Applications

Unspecified application

Species

Unspecified reactive species

Marie V Daugan,Margot Revel,Romane Thouenon,Marie-Agnès Dragon-Durey,Tania Robe-Rybkine,Carine Torset,Nicolas S Merle,Rémi Noé,Virginie Verkarre,Stephane Marie Oudard,Arnaud Mejean,Pierre Validire,Xavier Cathelineau,Rafael Sanchez-Salas,Mathew C Pickering,Isabelle Cremer,Audrey Mansuet-Lupo,Marco Alifano,Catherine Sautès-Fridman,Diane Damotte,Wolf H Fridman,Lubka T Roumenina
View all publications

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