S100A8-S100A9 Heterodimer Protein, Mouse (His)

S100A8, composed of calcium- and zinc-bound S100A8, plays a crucial regulatory role in inflammation and immune responses. As a calprotectin, it contributes to leukocyte function, regulates the cytoskeleton, and activates intracellular NADPH oxidase. The S100A8-S100A9 Heterodimer Protein, Mouse (His), is a recombinant protein dimer complex containing the S100A8-S100A9 heterodimer protein, expressed by E.coli and tagged with N-6*His^{[1][2][3][4][5][6]}.

S100A8, composed of calcium and zinc-bound S100A8, plays a crucial role in regulating inflammatory processes and immune responses. Normally existing as calprotectin (S100A8/A9), it possesses multiple intracellular functions, including promoting arachidonic acid transport and metabolism in leukocytes, regulating the tubulin-dependent cytoskeleton during phagocyte migration, and activating neutrophil NADPH oxidase. Extracellularly, it exhibits pro-inflammatory, antibacterial, oxidant-scavenging, and apoptosis-inducing activities. As an alarming or danger-associated molecular pattern (DAMP) molecule, S100A8 stimulates innate immune cells by binding to pattern recognition receptors such as Toll-like receptor 4 (TLR4) and the receptor for advanced glycation end products (AGER), thereby activating MAP kinase and the NF-kappa-B signaling pathway and amplifying the pro-inflammatory cascade. It possesses antibacterial activity against bacteria and fungi. Furthermore, S100A8/A9 induces cell death through autophagy and apoptosis, regulates neutrophil number and apoptosis, and acts as an oxidative scavenger to prevent tissue damage. In microbial infections (e.g., SARS-CoV-2), S100A8/A9 may induce the proliferation of abnormal immature neutrophils in a TLR4-dependent manner^{[1][2][3][4][5][6]}.

S100A8-S100A9 Heterodimer Protein, Mouse (1-20 μg/mL; 30 min) activates mouse platelets in a dose-dependent manner via GPIbα (CD36 acts as an auxiliary receptor), and induces P-selectin expression, GPIIb/IIIa activation and phosphatidylserine exposure on mouse platelets^[3].
S100A8-S100A9 Heterodimer Protein, Mouse (1 μg/mL; 24 h) activates NF-κB pathway and upregulates multiple chemokines and pro-inflammatory cytokines in mouse primary cardiac fibroblasts, and promotes the migration of monocytes and cardiac fibroblasts through RAGE receptor; it has no influence on the proliferation and differentiation of mouse cardiac fibroblasts^[4].
S100A8-S100A9 Heterodimer Protein, Mouse (0.2-5 μg/mL; 24 h) significantly increases the mRNA levels of MMP3, MMP9 and MMP13 in mouse bone marrow-derived macrophages^[5].
S100A8-S100A9 Heterodimer Protein, Mouse expressed by mouse tumor cells activates intratumoral NK cells and inhibits tumor growth in vivo^[6].

Mouse

E. coli

N-6*His

P27005 (P2-E89) (S100A8)&P31725 (A2-K113) (S100A9)

20201 (S100A8) & 20202 (S100A9)

S100A8:
PSELEKALSNLIDVYHNYSNIQGNHHALYKNDFKKMVTTECPQFVQNINIENLFRELDINSDNAINFEEFLAMVIKVGVASHKDSHKE
S100A9:
ANKAPSQMERSITTIIDTFHQYSRKEGHPDTLSKKEFRQMVEAQLATFMKKEKRNEALINDIMEDLDTNQDNQLSFEECMMLMAKLIFACHEKLHENNPRGHGHSHGKGCGK

Approximately 11&13kDa, based on SDS-PAGE under reducing conditions.

≥ 85%, as determined by reducing SDS-PAGE.

Lyophilized powder

Lyophilized from a 0.22 μm filtered solution of PBS, 6% Trehalose, pH 7.4.

<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]. Wang S, et al. S100A8/A9 in Inflammation. Front Immunol. 2018 Jun 11;9:1298.

  [2]. Chen Y, et al. S100A8 and S100A9 in Cancer. Biochim Biophys Acta Rev Cancer. 2023 May;1878(3):188891.

  [3]. Colicchia M, et al. S100A8/A9 drives the formation of procoagulant platelets through GPIbα. Blood. 2022 Dec 15;140(24):2626-2643.

  [4]. Wu Y, et al. S100a8/a9 Released by CD11b⁺Gr1⁺ Neutrophils Activates Cardiac Fibroblasts to Initiate Angiotensin II-Induced Cardiac Inflammation and Injury. Hypertension. 2014 Apr 7;63(6).

  [5]. van Lent PLEM, et al. Myeloid-related proteins S100A8/S100A9 regulate joint inflammation and cartilage destruction during antigen-induced arthritis. Ann Rheum Dis. 2008 Dec;67(12):1750-1758.

  [6]. Narumi K, et al. Proinflammatory Proteins S100A8/S100A9 Activate NK Cells via Interaction with RAGE. J Immunol. 2015 Jun 1;194(11):5539-5548.