C1ra

Host Animal Rat
Specie Reactivity Mouse
Antibody Clone CTJS-412
Isotype IgG2a
Applications WB
Host Animal Sheep
Specie Reactivity Mouse
Isotype IgG
Applications WB; ELISA
Host Animal Rat
Specie Reactivity Mouse
Antibody Clone CTJS-431
Isotype IgG2a
Applications WB
Specie Reactivity Mouse
Sensitivity 0.156-10 ng/mL
Applications ELISA
Specie Reactivity Mouse
Type Recombinant Protein
Expression Host E. Coli, yeast, insect, or mammalian cell
Applications WB; ELISA
Specie Reactivity Mouse
Type Recombinant Enzyme
Expression Host Mouse myeloma cell line, NS0
Applications Enzyme Activity Assays
Specie Reactivity Mouse
Type Recombinant Protein
Expression Host Yeast
Applications WB; ELISA
Specie Reactivity Mouse
Type Recombinant Protein
Expression Host E.coli/Mammalian cell/Baculovirus
Applications WB; ELISA
Clear All
Specie Reactivity Mouse
Type Expression Plasmid
Vector pCMV6-Entry
Tag Myc-DDK
Specie Reactivity Mouse
Type Expression Plasmid
Vector pLenti-C-Myc-DDK-P2A-Puro
Tag Myc-DDK
Specie Reactivity Mouse
Type Expression Plasmid
Vector pLenti-C-mGFP-P2A-Puro
Tag mGFP
Specie Reactivity Mouse
Type Expression Plasmid
Vector PCMV6-Kan/Neo
Specie Reactivity Mouse
Type Lentiviral Particle
Vector pLenti-C-Myc-DDK-P2A-Puro
Tag Myc-DDK
Specie Reactivity Mouse
Type Lentiviral Particle
Vector pLenti-C-mGFP-P2A-Puro
Tag GFP
Product List Background C1ra Functional Service

Background

C1ra (complement component 1, r subcomponent A), also known as mC1rA or C1r, serves as a serine protease. C1ra is found to be expressed in various structures such as the adrenal gland, small intestine, blood, and midbrain. In addition, C1ra is also found in the lymphatic system and the genitourinary system. As an integral component of the classical complement pathway, C1ra is closely linked to innate immune regulation.

Its Gene ID: 50909 and UniProtKB ID: Q8CG16.

Structure & Characteristics

The C1ra gene is orthologous to human C1R (complement C1r). However, unlike humans, the mouse C1r gene duplicates into C1ra and C1rb. In mice, the C1ra zymogen spans 691 amino acids (aa) and contains a CUB domain, an EGF-like motif, a second CUB domain, two CCP repeats, and a C-terminal peptidase S1 region. The data show that for AA 17-707, mouse C1ra is 91% identical to rat and 82% identical to human C1r. The aa sequence identity between full-length mouse C1ra and mouse C1rB is 96%.

Core Roles of C1ra

This component, encoded by the C1ra gene, works synergistically with C1rb to bind immune complexes or microbial pathogens. Completion of binding triggers a signal leading to activation of the C1 complex. In addition to facilitating the initiation of immune responses, activation of the classical complement pathway can also promote opsonization, inflammation, as well as pathogen clearance. Characterizing the function of complement C1ra in mice allows for a better understanding of the mechanisms by which the immune system recognizes and eliminates foreign invaders, which provides new horizons for the treatment of immune diseases.

Fig.1 C1ra gene. (Moreno-García, et al., 2020) Fig.1 Expression of inflammation-related genes in isolated microglia during experimental autoimmune encephalomyelitis.1,3

Products Available at Creative Biolabs

  • Assay Kits

Mouse C1ra ELISA kits are suitable for in vitro quantitative measurement of C1ra in a variety of samples, including plasma, cell lysates, and cell culture supernatants.

  • Antibodies

Our diverse antibodies are validated to be highly specific for mouse C1ra. Our C1ra antibodies are primarily derived from sheep and rats.

  • Proteins

Our cost-effective C1ra protein products are suitable for a variety of applications such as enzyme activity assays, WB, and ELISA.

For more complementary products, please contact our team.

C1ra Functional Service

Creative Biolabs provides a comprehensive range of C1ra related products, including anti-C1ra antibodies, ELISA kits, and C1ra proteins. These products can effectively carry out C1ra related experiments and thus play an important role in your research.

Fig. 2 The mRNA expression changes of C1q, C1s, and C1r in the cortex, striatum, thalamus, and hippocampus of TBI compared to sham-injured animals at different time points.Fig. 2 The changes in mRNA expression of C1q, C1s, and C1r in different brain area following TBI.2,3

The complement system plays a significant role in exacerbating secondary damage subsequent to traumatic brain injury (TBI). Researchers investigated how the brain activates the production of components associated with the classical and lectin complement pathways in response to TBI.2,3 In this study, researchers developed a traumatic brain injury (TBI) model in mice through the use of controlled cortical impact (CCI). To investigate the expression of components associated with the classical complement pathway, including C1q, C1r, and C1s, as well as elements of the lectin complement pathway, the team employed real-time quantitative polymerase chain reaction (RT-qPCR). The analysis was conducted across four brain regions: the cortex, striatum, thalamus, and hippocampus, allowing for a comprehensive understanding of the cellular markers involved in the response to TBI. These analyses were conducted on mice that had been exposed to CCI for periods ranging from 24 hours to 5 weeks. The results showed a long-lasting, time-dependent, and region-dependent significant increase in the mRNA levels of all classical complement components (C1q, C1r, and C1s), as well as some lectin pathway components, in all evaluated ipsilateral brain structures after TBI. In conclusion, the brain responds to TBI with a robust, widespread, and sustained upregulation of complement components, which may offer protective effects in the context of TBI.

Creative Biolabs offers C1ra functional services, including detection of C1ra binding and other tailored functional services for our esteemed clients engaged in clinical and scientific research.

References

  1. Moreno-García, Álvaro, et al. "Gene expression analysis of astrocyte and microglia endocannabinoid signaling during autoimmune demyelination." Biomolecules 10.9 (2020): 1228.
  2. Ciechanowska, Agata, et al. "Initiators of classical and lectin complement pathways are differently engaged after traumatic brain injury—time-dependent changes in the cortex, striatum, thalamus and hippocampus in a mouse model." International journal of molecular sciences 22.1 (2020): 45.
  3. Distributed under Open Access license CC BY 4.0, without modification.
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