Recombinant human M-CSF protein - Bioactive cytokine

Recombinant cytokine, source: CHO cells

SPECIFICATIONS

Specifications

Source
CHO cells
Species
Human
Synonyms
CSF-1
lanimostim
Proteoglycan macrophage colony-stimulating factor (PG-M-CSF)
Accession sequence

P09603

Protein size
224 a.a. (E33-R255)
Molecular weight
~35 kDa (SDS-PAGE)
Carrier
Carrier-free
Tag
Tag-free
Purity
≥ 95% (SDS-PAGE)
Solubility

100 μg/ml in water

Formulation buffer

Glycine phosphate buffer (pH 7), stabilizing agents, 5% saccharose

Appearance (form)
Lyophilized
Reconstitution buffer
Endotoxin-free water (provided)
Sterility

0.22 µm filtration

Endotoxin

The absence of bacterial contamination (e.g. lipoproteins and endotoxins) has been confirmed using HEK-Blue™ TLR2 and HEK‑Blue™ TLR4 cells.

Applications

Cellular assays (tested), ELISA

Quality control

Each lot is functionally tested and validated.

CONTENTS

Contents

  • Product: 
    Recombinant human M-CSF
  • Cat code: 
    rcyc-hmcsf
  • Quantity: 
    10 µg
Includes:

1.5 ml endotoxin-free water

Shipping & Storage

  • Shipping method:  Room temperature
  • Storage:

    • -20°C
    Stability: -20°C for up to 1 year

    Caution:

    • Avoid repeated freeze-thaw cycles

Details

Macrophage colony-stimulating factor (M-CSF, also known as CSF-1) is a key regulator of monocyte and macrophage biology [1–3]. M-CSF signals through the colony-stimulating factor-1 receptor (CSF-1R/CD115), a receptor also activated by interleukin-34 (IL-34). Unlike IL-34, which displays a more restricted tissue distribution, M-CSF is constitutively expressed in multiple tissues, where it maintains monocyte and macrophage homeostasis under physiological conditions [1–3].

Upon binding to CSF-1R, M-CSF induces receptor dimerization and activates downstream signaling pathways including JAK/STAT3, ERK1/2, PI3K/AKT, NF-κB, and Src-family kinases [2,3]. These pathways regulate macrophage proliferation, differentiation, migration, phagocytic activity, and polarization, and are frequently associated with tissue repair and M2-like phenotypes [1,2].

Dysregulation of the M-CSF/CSF-1R axis has been implicated in chronic inflammation, autoimmune diseases, atherosclerosis, fibrosis, and cancer [1,3–5]. Elevated M-CSF levels promote macrophage recruitment and accumulation at sites of chronic inflammation and within the tumor microenvironment. Sustained activation of CSF-1R signaling further contributes to fibrosis and the establishment of immunosuppressive macrophage populations. Consequently, the M-CSF/CSF-1R pathway has emerged as an attractive therapeutic target in inflammatory disorders and oncology [4,5].

​References:

1. Trus E et al., 2020.  Who's in charge here? Macrophage colony stimulating factor and granulocyte macrophage colony stimulating factor: Competing factors in macrophage polarization. Cytokine. 127:154939.
2. Ushach I, Zlotnik A, 2016. Biological role of granulocyte macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF) on cells of the myeloid lineage. J Leukoc Biol. 100:481–489.
3. Muñoz-Garcia J et al., 2021. The twin cytokines interleukin-34 and CSF-1: masterful conductors of macrophage homeostasis. Theranostics. 11(4):1568–1593.
4. Sinha SK et al., 2021. Local M-CSF (Macrophage Colony-Stimulating Factor) Expression Regulates Macrophage Proliferation and Apoptosis in Atherosclerosis. Arterioscler Thromb Vasc Biol. 41:220–233.
5. He K et al., 2022. G-CSF/GM-CSF-induced hematopoietic dysregulation in the progression of solid tumors. FEBS Open Bio. 12:1268–1285.
 

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