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Lack of CSF1R-mediated signals impedes the differentiation of spleen macrophages of embryonic origin, and the resulted macrophage depletion during development.
CSF1R-dependent macrophages have roles in control of the intestinal stem-cell niche
Targeting MAMs by CSF1R blocking mAbs may be promising methods to (re)sensitize myeloma cells to chemotherapy.
Findings indicate that colony stimulating factor-1 receptor (CSF1R) signalling regulates inflammation in the central and peripheral nervous system in amyotrophic lateral sclerosis (ALS), suggesting therapeutic targeting of CSF1R in this disease.
Combining CSF1R inhibitor with a CXCR2 antagonist blocked granulocyte infiltration of tumors and showed strong anti-tumor effects.
These findings reveal a novel and functionally important role for EHD1 in governing CSF-1R signalling via regulation of anterograde transport of CSF-1R to the macrophage cell surface.
Our findings thus demonstrate that microenvironmental alteration by CSF-1R blockade renders tumor cells more susceptible to receptor tyrosine kinase inhibition in a preclinical glioblastoma model, which may have important translational relevance
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.
CSF-1R role in the development of erythro-myeloid progenitor cells in the developing fetal liver
analysis of CSF1R-deficient mice establishes a distinct role of CSF1R in fetal B-lymphopoiesis.
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.
this study shows that the iRhom2/ADAM17 pathway plays an important role in regulating CSF1R expression in the myeloid cell compartment at steady state, and in modulating development of monocytes/macrophages during their repopulation
this study shows that macrophage maturation is accompanied by colony-stimulating factor 1hypomethylation, and illustrates for the first time the ability of protein kinase A to increase Csf1r DNA methylation
Targeting of macrophages by either CSF1R signaling blockade or clodronate liposome-mediated cell killing has marked inhibitory effects on established leukemia.
Cav-1-dependent c-Fms stabilization contributes to efficient osteoclastogenesis.
these data indicate that CSF-1R signalling is critical for maintaining cardiac tissue resident M2-polarized macrophage population
Macropinosomes might be a central mechanism coupling CSF-1R signaling and macrophage growth.
Results indicate that prostaglandin E2 activates colony-stimulating factor-1 receptor (CSF-1R) and synergizes with its signaling at mitogen-activated protein kinase ERK1/2 level in promoting macrophage migration.
These findings indicate that PU.1-mediated upregulation of CSF-1R is a critical effector of MLL leukemogenesis.
miR-155 inhibits macrophage proliferation by suppressing Csf1r in early stages and decreased efferocytosis by targeting Bcl6 in advanced atherosclerosis.
M-CSFR inhibition suppressed programmed death-1 and -2 ligand in adult T-cell leukemia/lymphoma (ATLL) cells and macrophages stimulated with conditioned medium from ATL-T cells.
The detection of the CSF1R mutation outside of the region-encoding TKD may extend the genetic spectrum of adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP) with CSF1R mutations. Mutational analysis of all the coding exons of CSF1R should be considered for patients clinically suspected of having ALSP.
To verify its sensitivity and specificity, we retrospectively applied our criteria to 83 axonal spheroids and pigmented glia cases who had CSF1R mutations
Study find elevated expression of CSF1R 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 CSF1R in GC development, and a prognostic and predictive biomarker for GC.
Adult-onset Mendelian leukodystrophy genes are not common factors implicated in Alzheimer's disease, but there is a potential pathogenic link between NOTCH3, CSF1R, and sporadic late-onset Alzheimer's disease.
Adult-onset leukoencephalopathy with axonal spheroids and pigmented glia.(S39-S41) is a subtype of dominantly inherited leukoencephalopathy caused by CSF1R mutations.
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.
this is the first study to demonstrate CSF1R genetic variant regulates the CSF-1R signaling and sensitivity to CSF-1R inhibitors.
Hypoxia promotes glioma-associated macrophage infiltration via periostin and subsequent M2 polarization by upregulating TGF-beta and M-CSFR.
CSF-1R is a novel therapeutic target.
The phenotype of adult-onset leukoencephalopathy axonal spheroids and pigmented glia caused by CSF1R mutations is affected by sex
CSFIR mutation is associated with Metaplastic Breast Cancer.
Results suggest that TP63 rs7631358 G > A and CSF1R rs10079250 A > G may affect the risk and prognosis of lung cancer in never-smoking females.
findings suggest that expression of wild-type CSF1R in some cells, whether achieved by mosaicism or chimerism, may confer benefit in hereditary diffuse leukoencephalopathy with axonal spheroids.
This review showed that CSF1R mutation is related to Hereditary diffuse leukoencephalopathy with axonal spheroids.
High CSF-1R expression is associated with Clear Cell Renal Cell Carcinoma.
The aim of this study was to compare the expression of CSF-1R in nasopharyngeal carcinoma to nasopharyngitis.
CSF1R mutations account for 10% of idiopathic adult onset leukodystrophies.
The frequencies of the rare alleles of CCR2, ITGB3, and 3'UTR of c-fms in the Old Believers are lower than in the sample of Novosibirsk Russians, and the rare allele of DBH is more frequent
Data suggest that fms is not required for establishing a population of precursor cells during embryogenesis but is required for recruiting pigment cell precursors to xanthophore fates, with concomitant effects on melanophore organization.
The protein encoded by this gene is the receptor for colony stimulating factor 1, a cytokine which controls the production, differentiation, and function of macrophages. This receptor mediates most if not all of the biological effects of this cytokine. Ligand binding activates the receptor kinase through a process of oligomerization and transphosphorylation. The encoded protein is a tyrosine kinase transmembrane receptor and member of the CSF1/PDGF receptor family of tyrosine-protein kinases. Mutations in this gene have been associated with a predisposition to myeloid malignancy. The first intron of this gene contains a transcriptionally inactive ribosomal protein L7 processed pseudogene oriented in the opposite direction.
, macrophage colony-stimulating factor 1 receptor
, proto-oncogene c-Fms
, proto-oncogene fms
, CD115 antigen
, FMS proto-oncogene
, McDonough feline sarcoma viral (v-fms) oncogene homolog
, macrophage colony stimulating factor I receptor
, colony stimulating factor 1 receptor, formerly McDonough feline sarcoma viral (v-fms) oncogene homolog
, platelet-derived growth factor receptor, beta polypeptide
, protein-tyrosine kinase
, macrophage colony-stimulating factor receptor
, csf1r protein
, colony stimulating factor 1 receptor
, macrophage colony-stimulating factor 1 receptor-like
, fms proto-oncogene
, fms proto-oncogene homolog
, proto-oncogene c-Fms homolog
, proto-oncogene fms homolog