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anti-Human CSF1 Antibodies:
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Mouse (Murine) Monoclonal CSF1 Primary Antibody for Neut, ELISA - ABIN1177263
Nakoinz, Lee, Weaver, Ralph: Differentiation of the IL-3-dependent NFS-60 cell line and adaption to growth in macrophage colony-stimulating factor. in Journal of immunology (Baltimore, Md. : 1950) 1990
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Human Monoclonal CSF1 Primary Antibody for IHC, ELISA - ABIN965939
Price, Choi, Rosenberg, Stanley: The predominant form of secreted colony stimulating factor-1 is a proteoglycan. in The Journal of biological chemistry 1992
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Human Monoclonal CSF1 Primary Antibody for ELISA, WB - ABIN560496
Lawlor, Nazarian, Lacomis, Tempst, Villanueva: Pathway-based biomarker search by high-throughput proteomics profiling of secretomes. in Journal of proteome research 2009
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Mouse (Murine) Monoclonal CSF1 Primary Antibody for Neut, ELISA - ABIN2689477
Lokeshwar, Lin: A sandwich enzyme-linked immunoadsorbent assay for detection of murine macrophage colony-stimulating factor (CSF-1). in Journal of immunological methods 1989
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Mouse (Murine) Polyclonal CSF1 Primary Antibody for IHC (p), ELISA - ABIN3042763
Pei, Sun, Zhang, Wang, Ren: Interstitial tumor-associated macrophages combined with tumor-derived colony-stimulating factor-1 and interleukin-6, a novel prognostic biomarker in non-small cell lung cancer. in The Journal of thoracic and cardiovascular surgery 2015
the high level of colony-stimulating factor 1 expression during bovine pregnancy in uteroplacental tissues is consistent with its proposed role in placental physiology
results suggest that leukemia inhibitory factor and macrophage-colony stimulating factor are produced in the endometrium and may play different roles in early and mid-pregnancy
These results indicate that BARF1 blockade of CSF-1 signaling is an important immune evasion strategy for efficient acute EBV infection and a significant determinant for virus setpoint during persistent EBV infection.
the complete sequencing of M-CSF genes, gene organizaztion,splice varaiants, gene expression, and M-CSF role in the immune system
These results highlight heterogeneous effects of M-CSF isoforms on acute myeloid leukemia progression.
In glioblastoma, colony-stimulating factor-1 and angiocrine IL-6 induce robust arginase-1 expression and macrophage alternative activation, mediated through peroxisome proliferator-activated receptor-gamma-dependent transcriptional activation of hypoxia-inducible factor-2alpha.
Data showed that single expression of M-CSF or IL-34 can be observed in lung cancer tissues and correlated with poor survival. Additionally, their high co-expression correlates with disease stages and poor survival. Thus, evaluating the expression of both M-CSF and IL-34 may help to estimate disease progression and malignant degree in lung cancer patients.
The functional rs2050462 in CSF-1 might have a substantial influence on the renal cell carcinoma susceptibility and evolution in the Chinese population.
Study find elevated expression of CSF1 in primary gastric cancer tissue (GC) to be significantly associated with the presence of lymph node and peritoneal metastasis, advanced TNM stage, and poor survival. In vitro analysis also revealed a functional role for the CSF1 in GC development, and a prognostic and predictive biomarker for GC.
Results suggest that monocytes from Crohn's disease patients in remission produced high levels of CSF-1 that upregulate CCR5 expression. Consequently, monocytes differentiated in these conditions had a characteristic phenotype and lower production of inflammatory cytokines.
High M-CSF expression is associated with cervical cancer.
Concerning pigmented villonodular synovitis , clinical trials assessing CSF-1R inhibitors have revealed promising initial outcomes. Blocking CSF-1/CSF-1R signaling represents a promising immunotherapy approach and several new potential combination therapies for future clinical testing.
It was demonstrated that MCSF and folliclestimulating hormone stimulated the production of estradiol (E2) in luteinized granulosa cells. MCSF may be important in regulating the response of luteinized granulosa cells to gonadotropin and may have a promotive effect in the early phase of follicular development.
miR-1207-5p and CSF1 expression levels and their relationship with lung cancer survival and metastasis status were assayed by means of a lung cancer tissue microarray.
Upregulation of GM-CSF and M-CSF production by endothelial cells, an effect that appears to be mediated by NF-kappaB and to be independent of IL-1, may be an additional mechanism through which IL-33 contributes to inflammatory activation of the vessel wall.
High CSF-1 expression is associated with Breast Cancer.
Nucleolin both forms an mRNP complex with the eIF4G and CSF-1 mRNA, and is co-localized with the eIF4G in the cytoplasm further supporting nucleolin's role in translational regulation.
study, therefore, provided insights into the sequence-structure-function relationships of the M-CSF/c-FMS interaction and of ligand/receptor tyrosine kinase interactions in general.
Therefore, our findings indicate that CSF1 signaling is oncogenic during gliomagenesis through a mechanism distinct from modulating glioma-associated microglia/macrophage polarization status
High CSF1 expression is associated with breast cancer.
M-CSF has been shown to be comparable to CA15-3 and VEGF, specificity, and AUC values only in stages III and IV of BC.
M-CSF macrophage conversion into foam cells reduces their proinflammatory responses to classical M1-polarizing activation
This can be achieved by either blocking the EGF or CSF-1 receptors or supressing the EGF or CSF-1 signal.
findings demonstrated that M-CSF binds to IL-34; molecular docking studies predicted the formation of a heteromeric M-CSF/IL-34 cytokine
M-CSF serves as an intermediate signal, thus inducing a vital decrease in the NPR2 levels in cumulus cells, and regulates the process of LH-induced resumption of meiosis.
Findings revealed that stress-induced elevations in neuronal CSF1 provokes microglia-mediated neuronal remodeling in layer 1 medial prefrontal cortex, contributing to synaptic deficits and development of anxiety- and depressive-like behavior. Moreover, chronic stress exposure elicited divergent neuroimmune responses in male and female mice, demonstrating sex-dependent differences in neuron-microglia interactions.
PLEKHO2-deficient bone marrow-derived macrophages displayed increased apoptotic cell death in the absence of Macrophage-colony stimulating factor, although PLEKHO2 deficiency did not affect macrophage differentiation and proliferation.
lymphatic endothelial cells cause bone destruction in vivo in mice by secreting M-CSF, which promotes osteoclasts formation and activation.
NMB or NMBR silencing inhibited M-CSF/c-Fms-mediated downstream signaling pathways like activation of ERK and Akt and induction of D-type cyclins, cyclin D1 and D2.
address which CSF-1-activated pathways are involved in transmitting the lineage-instructive signal in primary bone marrow-derived GM progenitors.
study concludes that M-CSF is critical to host defenses against bacterial pneumonia by mediating survival and antimicrobial functions of mononuclear phagocytes in the lungs and liver.
study shows that PLCgamma1 controls osteoclast numbers via a CSF-1-dependent DAG/beta-catenin/cyclinD1 pathway.
study concludes that Langerhans cells require IL-34 when residing in fully differentiated and anatomically intact skin epidermis, but rely on neutrophil-derived CSF1 during inflamma
Proteomic Analysis Reveals Distinct Metabolic Differences Between Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) and Macrophage Colony Stimulating Factor (M-CSF) Grown Macrophages Derived from Murine Bone Marrow Cells
Hematopoietic cells can be induced by M-CSF to dedifferentiate to multipotent stem cells.
M-CSF promotes macrophagic over granulocytic differentiation by inducing ERK activation but also PKCd expression, which in turn, down-regulates Fli-1 expression and prevents granulocytic differentiation.
Results identify CSF-1-activated macrophages as crucial mediators of detrimental Schwann cell dedifferentiation in Cx32-deficient mice
Ceramide production in M-CSF-deprived macrophages arises from a combination of ASMase activity and de novo synthesis.
CSF-1 did not rescue the growth and lung defects associated with hyperoxia in this model; however, an increase in CSF-1R+ macrophages was not associated with an exacerbation of lung injury.
CSF-1 neutralization led to a relatively uniform reduction in all inflammatory cell populations; GM-CSF neutralization resulted in the preferential loss among the monocyte/macrophage populations.
The results of this study indicated that the CSF1 overexpression observed in CNS pathologies likely has pleiotropic influences on microglia.
The protein encoded by this gene is a cytokine that controls the production, differentiation, and function of macrophages. The active form of the protein is found extracellularly as a disulfide-linked homodimer, and is thought to be produced by proteolytic cleavage of membrane-bound precursors. The encoded protein may be involved in development of the placenta. Alternate splicing results in multiple transcript variants.
macrophage colony-stimulating factor 1
, colony stimulating factor 1 (macrophage)
, macrophage colony-stimulating factor 1-like
, colony-stimulating factor 1