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anti-Human CSF1 Antibodies:
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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 - 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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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
Elevated CSF1 levels were identified as a causal risk factor for Coronary Artery Disease with consistent epidemiological results. Furthermore, genetically predicted CSF1 levels were associated with CAD in the UK Biobank
Data indicate a possible clinical applicability and a high diagnostic power for the combination of macrophage-colony stimulating factor (M-CSF), vascular endothelial growth factor (VEGF), CA 125 and SCC-Ag in the diagnosis of both studied types of cervical cancer.
data unveil a novel epigenetic mechanism whereby a BRG1-centered complex mediates transcriptional activation of CSF1 by Ang II in vascular endothelial cells.
CSF-1 mRNA decay can be regulated at an epigenetic level, and alteration of the N1methylation status leads to phenotypic changes in cancer cell behavior.
These results suggested that the interaction between CSF1 and its receptor served an important role in promoting macrophage infiltration and progression of EC.
at 3 months after cardiopulmonary bypass, monocytes continued to express a new macrophage-like milieu that was associated with the persistent activation of the PU.1/M-CSF pathway.
When monocytes are differentiated into macrophages with CSF-1, CSF-1R is redirected to transcription starting sites, colocalizes with H3K4me3, and interacts with ELK and YY1 transcription factors.
Expression of M-CSF is related to macrophage activity and tumor progression in sporadic vestibular schwannomas.
Cytoplasmic MCSF suppressed apoptosis in MCF7 human breast cancer cells by inhibiting the HIF1alpha/BNIP3/Bax signalling pathway, which potentiated the dissociation of Bcl2 from Bcl2BNIP3 compounds and the formation of Bcl2Bax compounds.
study found that age, smoking, periodontitis, manifest caries, and the presence of tumors are associated with the salivary levels of CSF-1.
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.
in ovarian follicles, following the luteinizing hormone surge, levels of MCSF and MCSF receptor decrease
We showed that 15-F2t-IsoP dose-dependently inhibited BAC1.2F5 macrophage spreading and adhesion but stimulated their migration towards CSF-1, with maximum effect at 10microM. Analysis of CSF-1 stimulated signalling pathways in BAC1.2F5 macrophages showed that phosphorylation of Akt, a key mediator of cell migration, and one of its regulators, the mTORC2 component, Rictor, was significantly decreased
this study demonstrates the role of CSF-1 in inflammatory and arthritic pain development
Cell surface CSF-1 (csCSF-1) is one of the substrates of ADAM17. We demonstrate that both infiltrated neutrophils and macrophages are major sources of csCSF-1.
The authors find that a soluble factor produced by tumor cells is responsible for macrophage RAE-1delta induction, and they identify tumor-derived colony-stimulating factor-1 (CSF-1) as necessary and sufficient for macrophage RAE-1delta induction in vitro and in vivo.
A dual-specific MCSF antagonist of c-FMS and integrin alpha5beta3 prevents the progression of osteoporosis.
CSF1 selectively upregulated the expression of the chemokine receptor CCR7 on the CSF1R(+) dendritic cell 2, but not the dendritic cell 1, population in response to allergen stimuli.
CSF1 levels were significantly higher in the spinal cords with acute and chronic experimental autoimmune encephalomyelitis (EAE) than those of normal and adjuvant-injected mice. CSF1 was expressed in astrocytes and neurons in normal mouse spinal cord. CSF1 upregulation in CNS may play an important role in the proliferation and activation of microglia in EAE, contributing to neuroinflammation and neurodegeneration.
DLK is required for mechanical allodynia and microgliosis after nerve injury by controling a transcriptional program in somatosensory neurons regulating the expression of numerous genes implicated in pain pathogenesis, including Csf1.
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, 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
study shows that PLCgamma1 controls osteoclast numbers via a CSF-1-dependent DAG/beta-catenin/cyclinD1 pathway.
the complete sequencing of M-CSF genes, gene organizaztion,splice varaiants, gene expression, and M-CSF role in the immune system
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 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
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