CSF-1R/M-CSF-R Antibody [P4B9] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IP1:200 IF1:100 FCM1:100 - 1:400

Application
WB, IP, IF, FCM

Reactivity
Human

Source
Rabbit Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW
140-200 kDa

Positive Control	Human peripheral blood mononuclear cells (preincubated with human Fc block, 2.5 µg/million cells, 10 min); THP-1 cells; Human CD14+ Monocytes
Negative Control	Raji cells

Datasheet & SDS

Biological Description

Specificity
CSF-1R/M-CSF-R Antibody [P4B9] detects endogenous levels of total CSF-1R/M-CSF-R protein.

Clone
P4B9

Synonym(s)
Macrophage colony-stimulating factor 1 receptor; CSF-1 receptor (CSF-1-R; CSF-1R; M-CSF-R); Proto-oncogene c-Fms; CD115; CSF1R; FMS

Background
CSF-1R, also known as M-CSF receptor or c-Fms (encoded by the c-fms proto-oncogene), is a class III transmembrane receptor tyrosine kinase primarily expressed on monocytes, macrophages, and their progenitors. It is the central regulator of mononuclear phagocyte lineage development, survival, and function. CSF-1R features five extracellular immunoglobulin-like domains (D1–D5) mediating ligand-induced dimerization, a single transmembrane helix, and a cytoplasmic region comprising a juxtamembrane domain, split kinase domains separated by a kinase insert, and a C-terminal tail. Key regulatory tyrosines include Y559 (juxtamembrane, binds Src and PI3K), Y721 (kinase insert, recruits PI3K and PLCγ2), and Y807 (activation loop, essential for kinase activity). Upon binding of homodimeric CSF-1 (M-CSF) or IL-34, CSF-1R dimerizes, undergoes juxtamembrane conformational changes that relieve autoinhibition, and trans-autophosphorylates at multiple tyrosines (including Y559, Y706, Y721, Y807, Y921, and Y974). These phosphorylation events create docking sites for downstream effectors, activating PI3K/Akt (promoting survival and proliferation), MAPK/ERK (driving differentiation), and PLCγ pathways. Collectively, these cascades drive monocyte-to-macrophage differentiation, osteoclastogenesis, tissue macrophage homeostasis, inflammatory responses, and cytokine production. CSF-1R is critical for embryonic development (macrophage and osteoclast ontogeny) and innate immunity (phagocytosis, antigen presentation). Dysregulation of CSF-1R is implicated in disease: overexpression or hyperactivation is associated with poor outcomes in ovarian and breast cancers due to increased tumor-associated macrophages, while genetic knockout impairs myelopoiesis.

Background

CSF-1R, also known as M-CSF receptor or c-Fms (encoded by the c-fms proto-oncogene), is a class III transmembrane receptor tyrosine kinase primarily expressed on monocytes, macrophages, and their progenitors. It is the central regulator of mononuclear phagocyte lineage development, survival, and function. CSF-1R features five extracellular immunoglobulin-like domains (D1–D5) mediating ligand-induced dimerization, a single transmembrane helix, and a cytoplasmic region comprising a juxtamembrane domain, split kinase domains separated by a kinase insert, and a C-terminal tail. Key regulatory tyrosines include Y559 (juxtamembrane, binds Src and PI3K), Y721 (kinase insert, recruits PI3K and PLCγ2), and Y807 (activation loop, essential for kinase activity). Upon binding of homodimeric CSF-1 (M-CSF) or IL-34, CSF-1R dimerizes, undergoes juxtamembrane conformational changes that relieve autoinhibition, and trans-autophosphorylates at multiple tyrosines (including Y559, Y706, Y721, Y807, Y921, and Y974). These phosphorylation events create docking sites for downstream effectors, activating PI3K/Akt (promoting survival and proliferation), MAPK/ERK (driving differentiation), and PLCγ pathways. Collectively, these cascades drive monocyte-to-macrophage differentiation, osteoclastogenesis, tissue macrophage homeostasis, inflammatory responses, and cytokine production. CSF-1R is critical for embryonic development (macrophage and osteoclast ontogeny) and innate immunity (phagocytosis, antigen presentation). Dysregulation of CSF-1R is implicated in disease: overexpression or hyperactivation is associated with poor outcomes in ovarian and breast cancers due to increased tumor-associated macrophages, while genetic knockout impairs myelopoiesis.

References
https://pubmed.ncbi.nlm.nih.gov/24890514/ https://pubmed.ncbi.nlm.nih.gov/34729112/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%