Complement C3a Protein, Mouse

Complement C3/C3a protein activates the complement system, playing a central role in both classical and alternative pathways. C3b binds covalently to cell surface carbohydrates or immune aggregates, while C3a acts as an inflammatory mediator, inducing neutrophil chemoattraction and promoting smooth muscle contraction, increased vascular permeability, and histamine release. The shorter isoform of C3a stimulates B-cells. Complement C3a Protein, Mouse is the recombinant mouse-derived Complement C3/C3a protein, expressed by E. coli , with tag free.

Complement C3/C3a protein plays a pivotal role in the activation of the complement system, being the central reaction in both classical and alternative pathways. Following activation, C3b can bind covalently to cell surface carbohydrates or immune aggregates through its reactive thioester. C3a, derived from the proteolytic degradation of complement C3, acts as a local inflammatory mediator, inducing neutrophil chemoattraction and promoting smooth muscle contraction, increased vascular permeability, and histamine release from mast cells and basophilic leukocytes. Additionally, the shorter isoform of C3a exhibits B-cell stimulatory activity.

Complement C3/C3a Protein, Mouse (0-500 ng/mL, 48 h) enhances the expression of C3aR in Panc-02 cell, induces the activation of C3a/C3aR signaling pathway, thereby promoting the proliferation and migration ability of Panc-02 cell, and reducing its sensitivity to Gemcitabine (HY-17026)^[1].
Complement C3/C3a Protein, Mouse (10 µg/mL, 1 h) enhances the phagocytosis of mouse primary microglia cells^[2].
Complement C3/C3a Protein, Mouse (100 nM, 24-72 h) upregulates the expression of LC3B, downregulates the expression of p62, promotes podocyte autophagy under high glucose conditions in MPC-5 cell^[3].

Measured by its ability to enhance IL-6 secretion by THP-1 human acute monocytic leukemia cells. The ED₅₀ for this effect is 0.4-3.0 μg/mL.

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  Measured by its ability to enhance IL-6 secretion by THP-1 human acute monocytic leukemia cells. The ED₅₀ for this effect is 0.5190 μg/mL, corresponding to a specific activity is 1926.7823 U/mg.

Mouse

E. coli

Tag Free

P01027-1 (S671-R748)

12266  [NCBI]

Full Length of C3a anaphylatoxin

SVQLMERRMDKAGQYTDKGLRKCCEDGMRDIPMRYSCQRRARLITQGENCIKAFIDCCNHITKLREQHRRDHVLGLAR

Approximately 10 kDa

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  ≥ 95%, as determined by reducing SDS-PAGE.

Lyophilized powder

1.Lyophilized from a 0.22 μm filtered solution of PBS, pH 7.4.
2.Lyophilized from a 0.22 μm filtered solution of 20 mM PB, 150 mM NaCl, pH 7.4.
3.Lyophilized from a 0.22 μm filtered solution of PBS, pH 7.4, 8% trehalose.
Please refer to the lot-specific COA for specific buffer information.

<1 EU/μg, determined by LAL method.

It is not recommended to reconstitute to a concentration less than 100 μg/mL in ddH₂O. For long term storage it is recommended to add a carrier protein (0.1% BSA, 5% HSA, 10% FBS or 5% Trehalose).

Stored at -20°C for 2 years from date of receipt. After reconstitution, it is stable at 4°C for 1 week or -20°C for longer (with carrier protein). It is recommended to freeze aliquots at -20°C or -80°C for extended storage.

Room temperature in continental US; may vary elsewhere.

• [1]. Shi S, et al., The complement C3a/C3aR pathway is associated with treatment resistance to gemcitabine-based neoadjuvant therapy in pancreatic cancer. Comput Struct Biotechnol J. 2024 Oct 5;23:3634-3650.  [Content Brief]

  [2]. Li S, et al., Microglia mediate memory dysfunction via excitatory synaptic elimination in a fracture surgery mouse model. J Neuroinflammation. 2024 Sep 16;21(1):227.  [Content Brief]

  [3]. Zhang L, et al., C-reactive protein inhibits C3a/C3aR-dependent podocyte autophagy in favor of diabetic kidney disease. FASEB J. 2022 Jun;36(6):e22332.  [Content Brief]