PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 2807873-4 1989 The production of PGE2 was determined in macrophages representing various stages of activation (responsive, primed and fully activated) and various stages of differentiation (CSF-1-derived or GM-CSF-derived macrophages). Dinoprostone 18-22 colony stimulating factor 1 Homo sapiens 175-180 2817907-8 1989 Furthermore, GM-CSF and M-CSF were demonstrated to decrease serum cholesterol level in rabbits as well as in patients. Cholesterol 66-77 colony stimulating factor 1 Homo sapiens 14-19 2478497-5 1989 Pre-treatment of serum from DMN-exposed animals with anti-CSF-1 antibodies prior to in vitro culture had no affect on either cell number, cell phenotype or colony-stimulating activity, suggesting the presence of GM-CSF. Dimethylnitrosamine 28-31 colony stimulating factor 1 Homo sapiens 58-63 2546636-7 1989 The identity of EBV-B cell derived M-CSA with human urinary CSF-1 was confirmed by a complete neutralization of macrophage CSA by an antihuman urinary CSF-1 antiserum. m-csa 35-40 colony stimulating factor 1 Homo sapiens 60-65 2546636-7 1989 The identity of EBV-B cell derived M-CSA with human urinary CSF-1 was confirmed by a complete neutralization of macrophage CSA by an antihuman urinary CSF-1 antiserum. m-csa 35-40 colony stimulating factor 1 Homo sapiens 151-156 2546636-7 1989 The identity of EBV-B cell derived M-CSA with human urinary CSF-1 was confirmed by a complete neutralization of macrophage CSA by an antihuman urinary CSF-1 antiserum. Cyclosporine 37-40 colony stimulating factor 1 Homo sapiens 60-65 2649140-5 1989 The 3H-thymidine (3H-TdR) uptake studies revealed that IL-3, GM-CSF, G-CSF and M-CSF were efficient stimulators of DNA synthesis of AML cells in 19, 15, 13 and four of those cases, respectively. 3h-thymidine 4-16 colony stimulating factor 1 Homo sapiens 62-67 2649140-5 1989 The 3H-thymidine (3H-TdR) uptake studies revealed that IL-3, GM-CSF, G-CSF and M-CSF were efficient stimulators of DNA synthesis of AML cells in 19, 15, 13 and four of those cases, respectively. Tritium 4-6 colony stimulating factor 1 Homo sapiens 62-67 2784475-4 1989 Data obtained indicate that Pb potentiates the ability of CSF-1 to stimulate thymidine incorporation by BMDM; however, colony formation is inhibited reversibly, and the absolute number of cells in culture is adversely affected by Pb. Lead 28-30 colony stimulating factor 1 Homo sapiens 58-63 2784475-4 1989 Data obtained indicate that Pb potentiates the ability of CSF-1 to stimulate thymidine incorporation by BMDM; however, colony formation is inhibited reversibly, and the absolute number of cells in culture is adversely affected by Pb. Thymidine 77-86 colony stimulating factor 1 Homo sapiens 58-63 2784475-6 1989 The decrease in bone marrow cell responsiveness to CSF-1 in the presence of Pb observed in this system may contribute to the decrease in host resistance observed in Pb-exposed animals. Lead 76-78 colony stimulating factor 1 Homo sapiens 51-56 2784475-6 1989 The decrease in bone marrow cell responsiveness to CSF-1 in the presence of Pb observed in this system may contribute to the decrease in host resistance observed in Pb-exposed animals. Lead 165-167 colony stimulating factor 1 Homo sapiens 51-56 2521357-9 1989 Biological activity of IL-3 and CSF-1 was demonstrable in supernatant fluids of NK cells stimulated with PDBu/A23187 and CD16 ligands/rIL-2, respectively. Calcimycin 110-116 colony stimulating factor 1 Homo sapiens 32-37 2465043-5 1989 CSF-1 receptors on normal monocytes and myeloid leukemia cells could be induced to downmodulate by incubation with either human recombinant CSF-1 or phorbol esters, confirming that the receptors had functional ligand-binding sites and responded to transmodulation by inducers of protein kinase C. The numbers of receptors per cell and the percentage of positive cases were highest for leukemic blasts with cytochemical and morphological features of monocytes. Phorbol Esters 149-163 colony stimulating factor 1 Homo sapiens 0-5 2469691-0 1989 Identification of tyrosine-phosphorylated colony-stimulating factor 1 (CSF-1) receptor and a 56-kilodalton protein phosphorylated in intact human cells in response to CSF-1. Tyrosine 18-26 colony stimulating factor 1 Homo sapiens 42-69 2469691-0 1989 Identification of tyrosine-phosphorylated colony-stimulating factor 1 (CSF-1) receptor and a 56-kilodalton protein phosphorylated in intact human cells in response to CSF-1. Tyrosine 18-26 colony stimulating factor 1 Homo sapiens 71-76 2783371-3 1989 The presence of H-7 or staurosporine led to an inhibition of colony formation stimulated by crude colony-stimulating factor (CSF), interleukin-3 (IL-3), granulocyte-macrophage CSF (GM-CSF), granulocyte CSF (G-CSF), or macrophage CSF (M-CSF) in a dose-dependent manner. 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine 16-19 colony stimulating factor 1 Homo sapiens 182-187 2783371-3 1989 The presence of H-7 or staurosporine led to an inhibition of colony formation stimulated by crude colony-stimulating factor (CSF), interleukin-3 (IL-3), granulocyte-macrophage CSF (GM-CSF), granulocyte CSF (G-CSF), or macrophage CSF (M-CSF) in a dose-dependent manner. Staurosporine 23-36 colony stimulating factor 1 Homo sapiens 182-187 2974321-3 1988 Like the v-fms oncogene product, receptors bearing the activating mutation retained high-affinity binding sites for CSF-1 but were retarded in transport to the cell surface and were phosphorylated on tyrosine in the absence of ligand. Tyrosine 200-208 colony stimulating factor 1 Homo sapiens 116-121 2526035-7 1989 The isolated CSF-1 is a sialoglycoprotein with 41.5% of carbohydrate. Carbohydrates 56-68 colony stimulating factor 1 Homo sapiens 13-18 2526035-23 1989 The receptor alone, (labelled by cross-linking to [125I]CSF-1 with di-succinylimidyl-suberate), is a polypeptide with an approx. di-succinylimidyl-suberate 67-93 colony stimulating factor 1 Homo sapiens 56-61 2523989-7 1989 In contrast, the expression of c-fms, a cellular proto-oncogene which codes for the CSF-1 (monocyte-macrophage colony-stimulating factor) surface membrane receptor, is modified by Li in the presence of the differentiation induction agents DMSO and RA which promote the development of mature granulocytes from HL-60 cells. Dimethyl Sulfoxide 239-243 colony stimulating factor 1 Homo sapiens 84-163 2973787-5 1988 Furthermore, detection of CSF-1 transcripts was associated with secretion of CSF-1 protein that was increased after phorbol ester treatment. Phorbol Esters 116-129 colony stimulating factor 1 Homo sapiens 26-31 2460553-2 1988 Both granulocyte (G)-macrophage (M) CSF and IL-3 markedly enhanced histamine release upon stimulation with anti-IgE in a dose-dependent manner (maximal enhancement 25.5% by GM-CSF and 30.8% by IL-3 as expressed as percent increase against total cellular histamine content), whereas G-CSF, M-CSF, and IL-4 had no effect. Histamine 67-76 colony stimulating factor 1 Homo sapiens 174-179 2973787-5 1988 Furthermore, detection of CSF-1 transcripts was associated with secretion of CSF-1 protein that was increased after phorbol ester treatment. Phorbol Esters 116-129 colony stimulating factor 1 Homo sapiens 77-82 3264877-3 1988 The 4-kb CSF-1 cDNA product was synthesized as an integral transmembrane glycoprotein that was assembled into disulfide-linked dimers and rapidly underwent proteolytic cleavage to generate a soluble growth factor. Disulfides 110-119 colony stimulating factor 1 Homo sapiens 9-14 3264877-5 1988 Digestion with glycosidic enzymes indicated that soluble CSF-1 encoded by the 4-kb cDNA contained both asparagine(N)-linked and O-linked carbohydrate chains, whereas the product of the 1.6-kb clone had only N-linked oligosaccharides. Asparagine 103-113 colony stimulating factor 1 Homo sapiens 57-62 3264877-5 1988 Digestion with glycosidic enzymes indicated that soluble CSF-1 encoded by the 4-kb cDNA contained both asparagine(N)-linked and O-linked carbohydrate chains, whereas the product of the 1.6-kb clone had only N-linked oligosaccharides. o-linked carbohydrate 128-149 colony stimulating factor 1 Homo sapiens 57-62 3264877-5 1988 Digestion with glycosidic enzymes indicated that soluble CSF-1 encoded by the 4-kb cDNA contained both asparagine(N)-linked and O-linked carbohydrate chains, whereas the product of the 1.6-kb clone had only N-linked oligosaccharides. n-linked oligosaccharides 207-232 colony stimulating factor 1 Homo sapiens 57-62 2844756-0 1988 Colony-stimulating factor 1-induced Na+ influx into human monocytes involves activation of a pertussis toxin-sensitive GTP-binding protein. Guanosine Triphosphate 119-122 colony stimulating factor 1 Homo sapiens 0-27 2844756-2 1988 The present studies demonstrate that the interaction of CSF-1 with monocyte membranes is associated with a 2.4-fold increase in specific binding of the GTP analogue, GTP gamma S. Scatchard analysis of the GTP gamma S binding data indicated that CSF-1 stimulates GTP binding by increasing the affinity, rather than the number, of available sites. Guanosine Triphosphate 152-155 colony stimulating factor 1 Homo sapiens 56-61 2844756-2 1988 The present studies demonstrate that the interaction of CSF-1 with monocyte membranes is associated with a 2.4-fold increase in specific binding of the GTP analogue, GTP gamma S. Scatchard analysis of the GTP gamma S binding data indicated that CSF-1 stimulates GTP binding by increasing the affinity, rather than the number, of available sites. Guanosine Triphosphate 152-155 colony stimulating factor 1 Homo sapiens 245-250 2844756-2 1988 The present studies demonstrate that the interaction of CSF-1 with monocyte membranes is associated with a 2.4-fold increase in specific binding of the GTP analogue, GTP gamma S. Scatchard analysis of the GTP gamma S binding data indicated that CSF-1 stimulates GTP binding by increasing the affinity, rather than the number, of available sites. Guanosine Triphosphate 166-169 colony stimulating factor 1 Homo sapiens 56-61 2844756-2 1988 The present studies demonstrate that the interaction of CSF-1 with monocyte membranes is associated with a 2.4-fold increase in specific binding of the GTP analogue, GTP gamma S. Scatchard analysis of the GTP gamma S binding data indicated that CSF-1 stimulates GTP binding by increasing the affinity, rather than the number, of available sites. Guanosine Triphosphate 166-169 colony stimulating factor 1 Homo sapiens 245-250 2844756-2 1988 The present studies demonstrate that the interaction of CSF-1 with monocyte membranes is associated with a 2.4-fold increase in specific binding of the GTP analogue, GTP gamma S. Scatchard analysis of the GTP gamma S binding data indicated that CSF-1 stimulates GTP binding by increasing the affinity, rather than the number, of available sites. Guanosine Triphosphate 166-169 colony stimulating factor 1 Homo sapiens 56-61 2844756-2 1988 The present studies demonstrate that the interaction of CSF-1 with monocyte membranes is associated with a 2.4-fold increase in specific binding of the GTP analogue, GTP gamma S. Scatchard analysis of the GTP gamma S binding data indicated that CSF-1 stimulates GTP binding by increasing the affinity, rather than the number, of available sites. Guanosine Triphosphate 166-169 colony stimulating factor 1 Homo sapiens 245-250 2844756-2 1988 The present studies demonstrate that the interaction of CSF-1 with monocyte membranes is associated with a 2.4-fold increase in specific binding of the GTP analogue, GTP gamma S. Scatchard analysis of the GTP gamma S binding data indicated that CSF-1 stimulates GTP binding by increasing the affinity, rather than the number, of available sites. Guanosine Triphosphate 166-169 colony stimulating factor 1 Homo sapiens 56-61 2844756-2 1988 The present studies demonstrate that the interaction of CSF-1 with monocyte membranes is associated with a 2.4-fold increase in specific binding of the GTP analogue, GTP gamma S. Scatchard analysis of the GTP gamma S binding data indicated that CSF-1 stimulates GTP binding by increasing the affinity, rather than the number, of available sites. Guanosine Triphosphate 166-169 colony stimulating factor 1 Homo sapiens 245-250 2844756-3 1988 This stimulation of GTP binding by CSF-1 was also associated with an increase in GTPase activity. Guanosine Triphosphate 20-23 colony stimulating factor 1 Homo sapiens 35-40 2844756-5 1988 We also demonstrate that CSF-1 stimulates Na+ influx into monocytes by an amiloride-sensitive mechanism, presumably the Na+/H+ antiport. Amiloride 74-83 colony stimulating factor 1 Homo sapiens 25-30 2460758-8 1988 Analysis of the M-CSF proteins released by COS-7 cells revealed that monomer subunit proteins of 44 or 28 kDa were produced. carbonyl sulfide 43-46 colony stimulating factor 1 Homo sapiens 16-21 3265472-3 1988 However, in monocytes treated with 12-O-tetradecanoylphorbol-13-acetate (TPA), CSF-1 mRNA was increased by 3 h and reached maximal levels by 12 h of drug exposure. Tetradecanoylphorbol Acetate 35-71 colony stimulating factor 1 Homo sapiens 79-84 3265472-3 1988 However, in monocytes treated with 12-O-tetradecanoylphorbol-13-acetate (TPA), CSF-1 mRNA was increased by 3 h and reached maximal levels by 12 h of drug exposure. Tetradecanoylphorbol Acetate 73-76 colony stimulating factor 1 Homo sapiens 79-84 3265472-4 1988 When nuclear run-on assays were used, CSF-1 gene transcription was also at low or undetectable levels in resting monocytes but was activated after TPA exposure. Tetradecanoylphorbol Acetate 147-150 colony stimulating factor 1 Homo sapiens 38-43 3265472-5 1988 TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes. Tetradecanoylphorbol Acetate 0-3 colony stimulating factor 1 Homo sapiens 94-99 3265472-5 1988 TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes. Tetradecanoylphorbol Acetate 0-3 colony stimulating factor 1 Homo sapiens 214-219 3265472-5 1988 TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes. Dactinomycin 33-46 colony stimulating factor 1 Homo sapiens 94-99 3265472-5 1988 TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes. Dactinomycin 33-46 colony stimulating factor 1 Homo sapiens 214-219 3265472-5 1988 TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes. Cycloheximide 183-196 colony stimulating factor 1 Homo sapiens 94-99 3265472-5 1988 TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes. Cycloheximide 183-196 colony stimulating factor 1 Homo sapiens 214-219 3265472-5 1988 TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes. Cycloheximide 198-201 colony stimulating factor 1 Homo sapiens 94-99 3265472-5 1988 TPA-treated monocytes exposed to actinomycin D further demonstrated that the half-life of the CSF-1 mRNA is 0.9 h. The results also demonstrated that the protein synthesis inhibitor, cycloheximide (CHX), increases CSF-1 mRNA levels in both resting and TPA-treated monocytes. Tetradecanoylphorbol Acetate 252-255 colony stimulating factor 1 Homo sapiens 94-99 3265472-7 1988 Moreover, treatment of monocytes with CHX and actinomycin D demonstrated that inhibition of protein synthesis is associated with stabilization of the CSF-1 transcript. Cycloheximide 38-41 colony stimulating factor 1 Homo sapiens 150-155 3265472-7 1988 Moreover, treatment of monocytes with CHX and actinomycin D demonstrated that inhibition of protein synthesis is associated with stabilization of the CSF-1 transcript. Dactinomycin 46-59 colony stimulating factor 1 Homo sapiens 150-155 2456345-8 1988 In Northern blot analysis of enriched RNA, synthetic oligonucleotide probes complementary to human G-CSF and M-CSF coding sequence each hybridized with a single RNA species of 1.7 and 4.4 kb, respectively. Oligonucleotides 53-68 colony stimulating factor 1 Homo sapiens 109-114 2842754-2 1988 When expressed in mouse NIH 3T3 fibroblasts, the chimeric gene product was rapidly transported to the cell surface, was autophosphorylated on tyrosine only in response to human recombinant CSF-1, underwent ligand-induced but not phorbol ester-induced down-modulation, and stimulated CSF-1-dependent cell proliferation. Tyrosine 142-150 colony stimulating factor 1 Homo sapiens 189-194 2842754-2 1988 When expressed in mouse NIH 3T3 fibroblasts, the chimeric gene product was rapidly transported to the cell surface, was autophosphorylated on tyrosine only in response to human recombinant CSF-1, underwent ligand-induced but not phorbol ester-induced down-modulation, and stimulated CSF-1-dependent cell proliferation. Tyrosine 142-150 colony stimulating factor 1 Homo sapiens 283-288 2842754-2 1988 When expressed in mouse NIH 3T3 fibroblasts, the chimeric gene product was rapidly transported to the cell surface, was autophosphorylated on tyrosine only in response to human recombinant CSF-1, underwent ligand-induced but not phorbol ester-induced down-modulation, and stimulated CSF-1-dependent cell proliferation. Phorbol Esters 229-242 colony stimulating factor 1 Homo sapiens 189-194 2458149-8 1988 Poly(rI).poly(rC) appeared to be a better inducer for M-CSF than IL-1. poly(ri 0-7 colony stimulating factor 1 Homo sapiens 54-59 2458149-8 1988 Poly(rI).poly(rC) appeared to be a better inducer for M-CSF than IL-1. Poly C 9-17 colony stimulating factor 1 Homo sapiens 54-59 2832442-7 1988 The constitutive expression of CSF-1 transcripts was associated with production of CSF-1 protein, although detectable amounts of CSF-1 were not secreted unless the cells were exposed to phorbol ester. Phorbol Esters 186-199 colony stimulating factor 1 Homo sapiens 31-36 3125295-4 1988 CSF-1 production following mezerein activation was reduced by incubation in the presence of 10(3) and 10(4) units/ml rIFN gamma. mezerein 27-35 colony stimulating factor 1 Homo sapiens 0-5 2834139-6 1988 The isolated CSF-1 which exhibits a one band pattern on SDS-PAGE under non-reducing conditions after Coomassie Blue and silver stainings. Sodium Dodecyl Sulfate 56-59 colony stimulating factor 1 Homo sapiens 13-18 2834139-6 1988 The isolated CSF-1 which exhibits a one band pattern on SDS-PAGE under non-reducing conditions after Coomassie Blue and silver stainings. Coomassie blue 101-115 colony stimulating factor 1 Homo sapiens 13-18 2834139-6 1988 The isolated CSF-1 which exhibits a one band pattern on SDS-PAGE under non-reducing conditions after Coomassie Blue and silver stainings. Silver 120-126 colony stimulating factor 1 Homo sapiens 13-18 2834139-8 1988 Its apparent Mr is 57,000 with an isoelectric point pI = 5.8-6.0 CSF-1 is a glycoprotein with 40% of carbohydrate (w/w). Carbohydrates 101-113 colony stimulating factor 1 Homo sapiens 65-70 2834139-10 1988 An almost complete removal of the carbohydrate moiety from CSF-1 was obtained after treatment with trifluoromethanesulfonic (TFMS) acid followed by gel filtration on Sephadex G-25 (Fine). Carbohydrates 34-46 colony stimulating factor 1 Homo sapiens 59-64 2834139-10 1988 An almost complete removal of the carbohydrate moiety from CSF-1 was obtained after treatment with trifluoromethanesulfonic (TFMS) acid followed by gel filtration on Sephadex G-25 (Fine). trifluoromethanesulfonic 99-123 colony stimulating factor 1 Homo sapiens 59-64 2834139-10 1988 An almost complete removal of the carbohydrate moiety from CSF-1 was obtained after treatment with trifluoromethanesulfonic (TFMS) acid followed by gel filtration on Sephadex G-25 (Fine). sephadex 166-179 colony stimulating factor 1 Homo sapiens 59-64 3270454-3 1988 Both early progenitor cell growth factors, such as IL-3, and late acting factors such as CSF-1, stimulate tyrosine and serine-threonine substrate phosphorylations. Tyrosine 106-114 colony stimulating factor 1 Homo sapiens 89-94 3270454-3 1988 Both early progenitor cell growth factors, such as IL-3, and late acting factors such as CSF-1, stimulate tyrosine and serine-threonine substrate phosphorylations. Serine 119-125 colony stimulating factor 1 Homo sapiens 89-94 3270454-3 1988 Both early progenitor cell growth factors, such as IL-3, and late acting factors such as CSF-1, stimulate tyrosine and serine-threonine substrate phosphorylations. Threonine 126-135 colony stimulating factor 1 Homo sapiens 89-94 3039346-4 1987 CSF-1 was synthesized as an integral transmembrane glycoprotein that was rapidly dimerized through disulfide bonds. Disulfides 99-108 colony stimulating factor 1 Homo sapiens 0-5 2824612-6 1987 Superoxide production in response to phorbol myristic acetate was maintained in CSF-1 cultured monocytes, but declined with time in monocytes cultured in serum. Superoxides 0-10 colony stimulating factor 1 Homo sapiens 80-85 2824612-6 1987 Superoxide production in response to phorbol myristic acetate was maintained in CSF-1 cultured monocytes, but declined with time in monocytes cultured in serum. phorbol myristic acetate 37-61 colony stimulating factor 1 Homo sapiens 80-85 3498652-4 1987 The amino acid composition of the present preparation suggested that the M-CSF which we purified possessed a structure fitting the sequence 1-190 of TPA30-1 cell M-CSF deduced by Wong et al. tpa30 149-154 colony stimulating factor 1 Homo sapiens 73-78 3498652-4 1987 The amino acid composition of the present preparation suggested that the M-CSF which we purified possessed a structure fitting the sequence 1-190 of TPA30-1 cell M-CSF deduced by Wong et al. tpa30 149-154 colony stimulating factor 1 Homo sapiens 162-167 3498641-8 1987 Northern blots hybridized with an oligonucleotide probe based on the CSF-1 sequence showed a high-molecular weight band; however, low-molecular weight CSF-1 mRNAs, which are present in the CSF-1-producing cell line MIA-PaCa-2, were not detected in the LD-1 mRNA. Oligonucleotides 34-49 colony stimulating factor 1 Homo sapiens 69-74 3030467-2 1987 We have recently demonstrated that phorbol ester induces expression of CSF-1 in human monocytes. Phorbol Esters 35-48 colony stimulating factor 1 Homo sapiens 71-76 3105621-3 1987 Expression of the M-CSF gene was induced in blood mononuclear cells stimulated by phorbol myristate acetate (PMA) or gamma-interferon. Tetradecanoylphorbol Acetate 82-107 colony stimulating factor 1 Homo sapiens 18-23 3105621-3 1987 Expression of the M-CSF gene was induced in blood mononuclear cells stimulated by phorbol myristate acetate (PMA) or gamma-interferon. Tetradecanoylphorbol Acetate 109-112 colony stimulating factor 1 Homo sapiens 18-23 3496105-1 1987 CSF-1 was isolated from a large volume of human normal urine (10,000 l), using the following 5 stages of purification: concentration by dialysis, silica gel adsorption, hydrophobic chromatography on phenyl-Sepharose CL-6B, fast protein liquid chromatography (FPLC) and finally preparative electrophoresis on polyacrylamide gels. Silicon Dioxide 146-152 colony stimulating factor 1 Homo sapiens 0-5 3496105-1 1987 CSF-1 was isolated from a large volume of human normal urine (10,000 l), using the following 5 stages of purification: concentration by dialysis, silica gel adsorption, hydrophobic chromatography on phenyl-Sepharose CL-6B, fast protein liquid chromatography (FPLC) and finally preparative electrophoresis on polyacrylamide gels. sepharose CL 6B 206-221 colony stimulating factor 1 Homo sapiens 0-5 3496105-1 1987 CSF-1 was isolated from a large volume of human normal urine (10,000 l), using the following 5 stages of purification: concentration by dialysis, silica gel adsorption, hydrophobic chromatography on phenyl-Sepharose CL-6B, fast protein liquid chromatography (FPLC) and finally preparative electrophoresis on polyacrylamide gels. polyacrylamide 308-322 colony stimulating factor 1 Homo sapiens 0-5 3496105-2 1987 We have isolated 8 mg of purified CSF-1 which migrated as a single band under non-reducing conditions in SDS-PAGE (staining with Coomassie Blue and the sensitive silver techniques). Sodium Dodecyl Sulfate 105-108 colony stimulating factor 1 Homo sapiens 34-39 3496105-2 1987 We have isolated 8 mg of purified CSF-1 which migrated as a single band under non-reducing conditions in SDS-PAGE (staining with Coomassie Blue and the sensitive silver techniques). Coomassie blue 129-143 colony stimulating factor 1 Homo sapiens 34-39 3545083-2 1987 The purity of human CSF-1 was demonstrated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) with a diffuse single band of Mr 42,000-50,000 and by N-terminal amino acid analysis of glutamate residue. Sodium Dodecyl Sulfate 46-68 colony stimulating factor 1 Homo sapiens 20-25 3545083-9 1987 When treated with neuraminidase and endo-beta-D-N-acetylglucosaminidase D, the molecular weight of CSF-1 was reduced to 36,000-40,000, and to 18,000-20,000 in the presence of mercaptoethanol. Mercaptoethanol 175-190 colony stimulating factor 1 Homo sapiens 99-104 3545083-2 1987 The purity of human CSF-1 was demonstrated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) with a diffuse single band of Mr 42,000-50,000 and by N-terminal amino acid analysis of glutamate residue. polyacrylamide 69-83 colony stimulating factor 1 Homo sapiens 20-25 3545083-2 1987 The purity of human CSF-1 was demonstrated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) with a diffuse single band of Mr 42,000-50,000 and by N-terminal amino acid analysis of glutamate residue. Sodium Dodecyl Sulfate 105-108 colony stimulating factor 1 Homo sapiens 20-25 3545083-2 1987 The purity of human CSF-1 was demonstrated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) with a diffuse single band of Mr 42,000-50,000 and by N-terminal amino acid analysis of glutamate residue. Glutamic Acid 203-212 colony stimulating factor 1 Homo sapiens 20-25 3545083-7 1987 However, CSF-1 activity was inhibited totally by the combination of 10 mM DTT and 1 mM SDS. Dithiothreitol 74-77 colony stimulating factor 1 Homo sapiens 9-14 3545083-7 1987 However, CSF-1 activity was inhibited totally by the combination of 10 mM DTT and 1 mM SDS. Sodium Dodecyl Sulfate 87-90 colony stimulating factor 1 Homo sapiens 9-14 3545083-8 1987 Under denaturing and reducing conditions, CSF-1 appeared on SDS-PAGE as a single protein band of Mr 21,000-25,000 and concurrently lost its activity, indicating that human CSF-1 possibly consists of two similar subunits and that the intact quaternary structure is essential for the biological activity. Sodium Dodecyl Sulfate 60-63 colony stimulating factor 1 Homo sapiens 42-47 2434085-4 1986 The results further demonstrate that normal human monocytes express CSF-1 RNA and that the level of these transcripts increases upon treatment with phorbol ester. Phorbol Esters 148-161 colony stimulating factor 1 Homo sapiens 68-73 3027579-3 1987 We show that the human c-fms gene stimulates growth of mouse NIH 3T3 cells in agar in response to human recombinant CSF-1, indicating that receptor transduction is sufficient to induce a CSF-1 responsive phenotype. Agar 78-82 colony stimulating factor 1 Homo sapiens 116-121 3011859-5 1986 Like peripheral blood mononuclear cells and phorbol ester-treated HL-60 cells, the choriocarcinoma cells expressed high affinity binding sites for human CSF-1. Phorbol Esters 44-57 colony stimulating factor 1 Homo sapiens 153-158 3489636-1 1986 Bone marrow cells taken from mice treated eight days previously with 5-fluorouracil, formed colonies consisting of 10-100 cells after four days of incubation in methylcellulose cultures containing only 500 cells/dish, in the presence of partially purified synergistic factor from human placental-conditioned medium (SFHPlac) and macrophage colony-stimulating factor (CSF-1). Fluorouracil 69-83 colony stimulating factor 1 Homo sapiens 367-372 2428865-9 1986 When monocytes were induced with poly-I.C, 22-fold higher levels of interferon were produced by the cells exposed to CSF-1. Poly I 33-39 colony stimulating factor 1 Homo sapiens 117-122 2428865-9 1986 When monocytes were induced with poly-I.C, 22-fold higher levels of interferon were produced by the cells exposed to CSF-1. Carbon 40-41 colony stimulating factor 1 Homo sapiens 117-122 3020426-3 1986 The PDGF and CSF-1 receptors also share a characteristic distribution of extracellular cysteine residues. Cysteine 87-95 colony stimulating factor 1 Homo sapiens 13-18 3488735-1 1986 Colony Stimulating Factor-1 has been purified to apparent homogeneity from the serum-free medium conditioned by cultured human pancreatic carcinoma cells which had been induced with phorbol myristate acetate. Tetradecanoylphorbol Acetate 182-207 colony stimulating factor 1 Homo sapiens 0-27 3488774-9 1986 Northern analysis of mRNA from induced-MIA PaCa cells, using a human CSF-1 oligonucleotide probe, revealed multiple species of CSF-1 mRNA ranging from 1.5 to 4.5 kilobases (kb). Oligonucleotides 75-90 colony stimulating factor 1 Homo sapiens 69-74 3488774-9 1986 Northern analysis of mRNA from induced-MIA PaCa cells, using a human CSF-1 oligonucleotide probe, revealed multiple species of CSF-1 mRNA ranging from 1.5 to 4.5 kilobases (kb). Oligonucleotides 75-90 colony stimulating factor 1 Homo sapiens 127-132 3487387-2 1986 Partial purification of TPA-LCM demonstrated the presence of human-active granulocyte-macrophage colony-stimulating factor (GM-CSF; Mr 50-70Kd), macrophage-CSF (M-CSF; Mr greater than 100Kd) and possibly a third protein (Mr 24-26Kd) supporting survival and growth of hematopoietic stem cells in vitro. Tetradecanoylphorbol Acetate 24-27 colony stimulating factor 1 Homo sapiens 145-159 3487387-2 1986 Partial purification of TPA-LCM demonstrated the presence of human-active granulocyte-macrophage colony-stimulating factor (GM-CSF; Mr 50-70Kd), macrophage-CSF (M-CSF; Mr greater than 100Kd) and possibly a third protein (Mr 24-26Kd) supporting survival and growth of hematopoietic stem cells in vitro. Tetradecanoylphorbol Acetate 24-27 colony stimulating factor 1 Homo sapiens 125-130 3958493-1 1986 In the presence of the hemopoietic growth factor CSF-1, the later committed cells of the macrophage lineage can be detected by their ability to form small colonies in clonal agar culture (CFCCSF-1). Agar 174-178 colony stimulating factor 1 Homo sapiens 49-54 2941289-4 1986 every 12 h. In patients receiving only ciprofloxacin clinical cure with eradication of bacteria was obtained in 15 patients (75%) with infections of bone and joint (6), skin and soft tissue (4), lung (2), middle ear (2) and CSF (1). Ciprofloxacin 39-52 colony stimulating factor 1 Homo sapiens 224-231 3332553-5 1986 The subsequent addition of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) to cultures initially treated with CSF-GM or CSF-1 further increased multinucleated cell formation. Calcitriol 27-51 colony stimulating factor 1 Homo sapiens 112-117 3332553-5 1986 The subsequent addition of 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) to cultures initially treated with CSF-GM or CSF-1 further increased multinucleated cell formation. Calcitriol 53-65 colony stimulating factor 1 Homo sapiens 112-117 3015514-2 1986 The purified receptor is a single glycosylated polypeptide, Mr 165 000, which exhibits CSF-1-dependent autophosphorylation in tyrosine. Tyrosine 126-134 colony stimulating factor 1 Homo sapiens 87-92 3085095-4 1986 A sixth cytokine, colony-stimulating factor 1, has an alanine followed by a similar pattern of five amino acids at the end of the putative signal peptide. Alanine 54-61 colony stimulating factor 1 Homo sapiens 18-45 3022923-11 1986 In membrane preparations, tyrosine-specific phosphorylation of the v-fms product appears to be constitutive, whereas in vitro phosphorylation of the c-fms-coded glycoprotein on tyrosine is enhanced in the presence of CSF-1. Tyrosine 26-34 colony stimulating factor 1 Homo sapiens 217-222 6610703-0 1984 Feedback regulation of colony-stimulating factor (CSF-1)-induced macrophage proliferation by endogenous E prostaglandins and interferon-alpha/beta. e prostaglandins 104-120 colony stimulating factor 1 Homo sapiens 50-55 6102677-7 1980 The concentrations of gentamicin in ventricular and lumbar CSF 1--6 h after an intraventricular dose of 2.5 mg gentamicin were 10--130 microgram/ml and 8--85 microgram/ml, respectively. Gentamicins 22-32 colony stimulating factor 1 Homo sapiens 59-64 6982897-6 1982 Whereas the parent molecule bound concanavalin A, the product did not, indicating that heterogeneity in the saccharide component could explain the observed variation in the molecular weight of CSF-1. Carbohydrates 108-118 colony stimulating factor 1 Homo sapiens 193-198 6982897-10 1982 Treatment of native CSF-1 with endo-beta-N-acetylglucosaminidase D was almost as efficient in removing carbohydrate as in the case of the reduced and alkylated subunits. Carbohydrates 103-115 colony stimulating factor 1 Homo sapiens 20-25 6609780-5 1984 The M-CSF had an apparent molecular weight of 77,000 in the absence of 0.1% SDS and 49,000 in its presence. Sodium Dodecyl Sulfate 76-79 colony stimulating factor 1 Homo sapiens 4-9 6606982-1 1984 A variety of growth factors and lectins were tested; only colony-stimulating factors CSF-1, Interleukin 3, and a T-lymphocyte GM CSF induced colony formation in semisolid medium and stimulated thymidine incorporation in liquid culture. Thymidine 193-202 colony stimulating factor 1 Homo sapiens 85-90 33143617-6 2021 METHODS: A comprehensive literature search was conducted in the relevant databases to identify studies published in this field during recent years Conclusion: Pexidartinib acts by inhibiting the colony-stimulating factor (CSF1)/CSF1 receptor pathway which leads to inhibition of the cell lines proliferation and promotes the autophosphorylation process of ligand-induced CSF1 receptor. pexidartinib 159-171 colony stimulating factor 1 Homo sapiens 222-226 34058245-11 2021 Detection of CSF1 mRNA expression may also have predictive significance in cases where use of the CSF1 inhibitor pexidartinib is considered. pexidartinib 113-125 colony stimulating factor 1 Homo sapiens 13-17 34058245-11 2021 Detection of CSF1 mRNA expression may also have predictive significance in cases where use of the CSF1 inhibitor pexidartinib is considered. pexidartinib 113-125 colony stimulating factor 1 Homo sapiens 98-102 33852104-1 2021 Background LY3022855 is a recombinant, immunoglobulin, human monoclonal antibody targeting the colony-stimulating factor-1 receptor. ly3022855 11-20 colony stimulating factor 1 Homo sapiens 95-122 33545279-14 2021 This work is scientifically relevant as we demonstrate for the first time that local administration of a CSF-1Ri to the lungs leads to a shift in balance of TAMs in the TME of a model of lung tumor, adding to the sparse literature of CSF-1Ris related to lung cancers. tams 157-161 colony stimulating factor 1 Homo sapiens 105-110 33245731-8 2020 TMPRSS2, inflammatory cytokines G-CSF, M-CSF, IL-1alpha, IL-6 and MCP-1 are suppressed by MEKi alone or with remdesivir. remdesivir 109-119 colony stimulating factor 1 Homo sapiens 39-44 33166408-6 2020 We analyzed the transcriptomes of human monocyte-derived macrophages stimulated in the presence of Ado or PGE2 and demonstrated that, in macrophages differentiated in M-CSF, Ado and PGE2 induce a shared transcriptional program involving the downregulation of inflammatory mediators and the upregulation of growth factors. Adenosine 99-102 colony stimulating factor 1 Homo sapiens 167-172 33166408-6 2020 We analyzed the transcriptomes of human monocyte-derived macrophages stimulated in the presence of Ado or PGE2 and demonstrated that, in macrophages differentiated in M-CSF, Ado and PGE2 induce a shared transcriptional program involving the downregulation of inflammatory mediators and the upregulation of growth factors. Dinoprostone 106-110 colony stimulating factor 1 Homo sapiens 167-172 33166408-6 2020 We analyzed the transcriptomes of human monocyte-derived macrophages stimulated in the presence of Ado or PGE2 and demonstrated that, in macrophages differentiated in M-CSF, Ado and PGE2 induce a shared transcriptional program involving the downregulation of inflammatory mediators and the upregulation of growth factors. Adenosine 174-177 colony stimulating factor 1 Homo sapiens 167-172 33166408-6 2020 We analyzed the transcriptomes of human monocyte-derived macrophages stimulated in the presence of Ado or PGE2 and demonstrated that, in macrophages differentiated in M-CSF, Ado and PGE2 induce a shared transcriptional program involving the downregulation of inflammatory mediators and the upregulation of growth factors. Dinoprostone 182-186 colony stimulating factor 1 Homo sapiens 167-172 33977320-8 2021 DMEK-ME eyes had a significantly thicker CSF 1 month after surgery (432.0 +- 97.6 mum) compared with non-DMEK-ME eyes (283.7 +- 22.2 mum; P = 0.01). dmek-me 0-7 colony stimulating factor 1 Homo sapiens 41-46 34012800-9 2021 There are several strategies for TAM targeting and utilizing them for therapeutic purposes including limiting monocyte recruitment and localization through various pathways such as CCL2-CCR2, CSF1-CSF1R, and CXCL12-CXCR4, targeting the activation of TAMs, genetic and epigenetic reprogramming of TAMs to antitumor phenotype, and utilizing TAMs as the carrier for anti-cancer drugs. tam 33-36 colony stimulating factor 1 Homo sapiens 192-196 32916415-8 2020 Associations of PFAS and hepatocyte growth factor (HGF) and macrophage colony-stimulating factor 1 (CSF-1) remained significant (p-value <0.05) following full covariate adjustment for smoking, exercise habits, education, energy, and alcohol intake, body mass index (BMI), glomular filtration rate (GFR) as well as corticoid- and COX-inhibitor treatment. Alcohols 233-240 colony stimulating factor 1 Homo sapiens 100-105 32787110-4 2020 The CSF1-CSF1R signaling pathway modulates the production, differentiation and function of TAMs; however, the discovery of selective CSF1R inhibitors devoid of Type III kinase activity has proven to be challenging. tams 91-95 colony stimulating factor 1 Homo sapiens 4-8 32673666-4 2020 Phorbol-12-myristate-13-acetate (PMA) was used to induce THP-1 cells to differentiate into macrophages, followed by induction to osteoclasts using macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-kappaB ligand (RANKL). Tetradecanoylphorbol Acetate 0-31 colony stimulating factor 1 Homo sapiens 147-183 32673666-4 2020 Phorbol-12-myristate-13-acetate (PMA) was used to induce THP-1 cells to differentiate into macrophages, followed by induction to osteoclasts using macrophage colony-stimulating factor (M-CSF) and receptor activator of NF-kappaB ligand (RANKL). Tetradecanoylphorbol Acetate 0-31 colony stimulating factor 1 Homo sapiens 185-190 33194026-0 2020 Upregulation of CSF-1 is correlated with elevated TAM infiltration and poor prognosis in oral squamous cell carcinoma. tam 50-53 colony stimulating factor 1 Homo sapiens 16-21 33194026-4 2020 Meanwhile, the correlation between CSF-1 expression and TAM infiltration was also explored. tam 56-59 colony stimulating factor 1 Homo sapiens 35-40 33194026-7 2020 Additionally, there was a positive correlation between a high CSF-1 level and elevated TAM infiltration. tam 87-90 colony stimulating factor 1 Homo sapiens 62-67 33194026-8 2020 The xenograft model study showed that CSF-1 signal blockade inhibited tumor growth, with a significant synchronous decrease in CSF-1 expression and TAM infiltration. tam 148-151 colony stimulating factor 1 Homo sapiens 38-43 33194026-9 2020 Overall, our findings indicated that CSF-1 plays a crucial role in TAMs-mediated OSCC tumor progression and invasion. Tamoxifen 67-71 colony stimulating factor 1 Homo sapiens 37-42 33101590-10 2020 Rh-CSF1 treatment significantly attenuated neurological deficits, infarct volume, OS, neuronal apoptosis, and degeneration at 48 h after HI. Histidine 137-139 colony stimulating factor 1 Homo sapiens 3-7 33101590-12 2020 The neuroprotective effects of rh-CSF1 were abolished by BLZ945 or U73122. 4-(2-(2-hydroxycyclohexylamino)benzothiazol-6-yloxy)pyridine-2-carboxylic acid methylamide 57-63 colony stimulating factor 1 Homo sapiens 34-38 33101590-12 2020 The neuroprotective effects of rh-CSF1 were abolished by BLZ945 or U73122. 1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione 67-73 colony stimulating factor 1 Homo sapiens 34-38 33101590-13 2020 These results suggested that rh-CSF1 treatment attenuated OS-induced neuronal degeneration and apoptosis after HI, at least in part, through the CSF1R/PLCG2/PKA/UCP2 signaling pathway. Histidine 111-113 colony stimulating factor 1 Homo sapiens 32-36 32973322-8 2020 We show that a specific CSF-1R kinase inhibitor, GW2580, abolishes CSF-1 induced trophoblast cell proliferation and migration and can be cytotoxic. 5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine 49-55 colony stimulating factor 1 Homo sapiens 24-29 31624866-6 2020 Phenolic acid extracts contained in 10 mg biofortified bread downregulated the LPS-induced expression of chemokines MCP-1, M-CSF, and CXCL-10 as well as pro-inflammatory cytokines TNF-alpha and IL-1beta, in endothelial cells and monocytes, with CXCL-10 as the most reduced inflammatory mediator. phenolic acid 0-13 colony stimulating factor 1 Homo sapiens 123-128 32793908-8 2020 TMPRSS2, inflammatory cytokines G-CSF, M- CSF, IL-1a, IL-6 and MCP-1 are suppressed by MEKi alone or in combination with remdesivir. remdesivir 121-131 colony stimulating factor 1 Homo sapiens 39-45 32861994-4 2020 Mechanistically, LY500307 treatment reduced tumor-derived CSF1 and decreased infiltration of CSF1R+ MDSCs in the tumor bed. erteberel 17-25 colony stimulating factor 1 Homo sapiens 58-62 31972592-7 2020 Interestingly, triptolide treatment could reduce colony-stimulating factor 1 level and expression of Sorcin in both SKOV3 and SKOV3/DDP cell lines. triptolide 15-25 colony stimulating factor 1 Homo sapiens 49-76 32255741-5 2020 Interestingly, in M-CSF MPhi, LCMV-ARM induced more IL-10 production than Cl13. cl13 74-78 colony stimulating factor 1 Homo sapiens 18-23 32522286-12 2020 Rh-CSF1 significantly improved the neurological deficits at 48 h and 4 weeks after HI, which was accompanied by a reduction in the brain infarct area, brain edema, brain atrophy, and neuroinflammation. Histidine 83-85 colony stimulating factor 1 Homo sapiens 3-7 32522286-14 2020 Inhibition of CSF1R and PLCG2 abolished these neuroprotective effects of rh-CSF1 after HI. Histidine 87-89 colony stimulating factor 1 Homo sapiens 14-18 32522286-15 2020 CONCLUSIONS: Our findings demonstrated that the activation of CSF1R by rh-CSF1 attenuated neuroinflammation and improved neurological deficits after HI. Histidine 149-151 colony stimulating factor 1 Homo sapiens 62-66 31896762-3 2020 Higher DMPA levels were associated with reduced CVL concentrations of GCSF, MCSF, IL-16, CTACK, LIF, IL-1alpha, and SCGF-beta in adjusted linear mixed models. N,N-dimethyl-4-anisidine 7-11 colony stimulating factor 1 Homo sapiens 76-80 32435453-11 2020 Conclusion: The present study reveals that the alterations of GNAQ activate NF-kappaB pathway in cancers, which increase RANKL and M-CSF expression and induce osteoclastogenesis in cancers.Cite this article: Bone Joint Res. gnaq 62-66 colony stimulating factor 1 Homo sapiens 131-136 32264887-0 2020 MiR-423-5p may regulate ovarian response to ovulation induction via CSF1. mir-423-5p 0-10 colony stimulating factor 1 Homo sapiens 68-72 32410856-6 2020 In ECs and monocytes, three carotenoids, i.e., beta-cryptoxanthin, lutein, and lycopene, suppressed the fructose-induced expression of chemokines MCP-1, M-CSF, and CXCL-10 and inflammatory cytokines TNF-alpha and IL-1beta, with CXCL-10 being the most repressed inflammatory mediator. Carotenoids 28-39 colony stimulating factor 1 Homo sapiens 153-158 32410856-6 2020 In ECs and monocytes, three carotenoids, i.e., beta-cryptoxanthin, lutein, and lycopene, suppressed the fructose-induced expression of chemokines MCP-1, M-CSF, and CXCL-10 and inflammatory cytokines TNF-alpha and IL-1beta, with CXCL-10 being the most repressed inflammatory mediator. Beta-Cryptoxanthin 47-65 colony stimulating factor 1 Homo sapiens 153-158 32410856-6 2020 In ECs and monocytes, three carotenoids, i.e., beta-cryptoxanthin, lutein, and lycopene, suppressed the fructose-induced expression of chemokines MCP-1, M-CSF, and CXCL-10 and inflammatory cytokines TNF-alpha and IL-1beta, with CXCL-10 being the most repressed inflammatory mediator. Lutein 67-73 colony stimulating factor 1 Homo sapiens 153-158 32410856-6 2020 In ECs and monocytes, three carotenoids, i.e., beta-cryptoxanthin, lutein, and lycopene, suppressed the fructose-induced expression of chemokines MCP-1, M-CSF, and CXCL-10 and inflammatory cytokines TNF-alpha and IL-1beta, with CXCL-10 being the most repressed inflammatory mediator. Lycopene 79-87 colony stimulating factor 1 Homo sapiens 153-158 32410856-6 2020 In ECs and monocytes, three carotenoids, i.e., beta-cryptoxanthin, lutein, and lycopene, suppressed the fructose-induced expression of chemokines MCP-1, M-CSF, and CXCL-10 and inflammatory cytokines TNF-alpha and IL-1beta, with CXCL-10 being the most repressed inflammatory mediator. Fructose 104-112 colony stimulating factor 1 Homo sapiens 153-158 32050752-5 2020 Mechanistically, OEA inhibits Rac activation in response to macrophage colony-stimulating factor (M-CSF), but not RANKL. oleoylethanolamide 17-20 colony stimulating factor 1 Homo sapiens 60-96 32050752-5 2020 Mechanistically, OEA inhibits Rac activation in response to macrophage colony-stimulating factor (M-CSF), but not RANKL. oleoylethanolamide 17-20 colony stimulating factor 1 Homo sapiens 98-103 32150886-7 2020 The release of IL-1beta, IL-8, MCP-1 and M-CSF proteins was mainly affected in macrophages after metal ion exposure (100 microM), indicating a higher impact on pro-inflammatory activity. Metals 97-102 colony stimulating factor 1 Homo sapiens 41-46 32220976-5 2020 Unlike AMs, the development of NAMs requires CSF1 but not GM-CSF. NAMS 31-35 colony stimulating factor 1 Homo sapiens 45-49 32075617-6 2020 RESULTS: RANKL + M-CSF significantly increased TRAP activity, number of osteoclasts, number and area of lacunae, intracellular content of ROS, protein levels of Nox1, TRAF6, c-Src and p-PI3K, as well as the content of activated GTP-Rac1, which were significantly blocked by polyphyllin VII in a concentration-dependent manner. Reactive Oxygen Species 138-141 colony stimulating factor 1 Homo sapiens 17-22 31924656-8 2020 The expression of some lactate-induced genes is dependent on autocrine M-CSF consumption. Lactic Acid 23-30 colony stimulating factor 1 Homo sapiens 71-76 32075617-6 2020 RESULTS: RANKL + M-CSF significantly increased TRAP activity, number of osteoclasts, number and area of lacunae, intracellular content of ROS, protein levels of Nox1, TRAF6, c-Src and p-PI3K, as well as the content of activated GTP-Rac1, which were significantly blocked by polyphyllin VII in a concentration-dependent manner. polyphyllin VII 274-289 colony stimulating factor 1 Homo sapiens 17-22 32009119-3 2020 JTE-952 potently inhibited human CSF1R kinase activity, with a half maximal inhibitory concentration of 11.1 nmol/L, and inhibited the phosphorylation of CSF1R in human macrophages and the CSF1-induced proliferation of human macrophages. CHEMBL4474690 0-7 colony stimulating factor 1 Homo sapiens 33-37 31670078-2 2020 TAMs are predominantly polarized to a pro-tumorigenic M2-phenotype through macrophage colony stimulating factor 1 (MCSF) cytokines that bind to the colony-stimulating factor 1 receptor (CSF1R), a class III receptor tyrosine kinase. Tyrosine 215-223 colony stimulating factor 1 Homo sapiens 75-113 31670078-2 2020 TAMs are predominantly polarized to a pro-tumorigenic M2-phenotype through macrophage colony stimulating factor 1 (MCSF) cytokines that bind to the colony-stimulating factor 1 receptor (CSF1R), a class III receptor tyrosine kinase. Tyrosine 215-223 colony stimulating factor 1 Homo sapiens 115-119 31654098-10 2020 At the end of the culture period of M-CSF + RANKL-stimulated CD14+ PBMCs, there was a correlation between the secretion of TRAP 5a and 5b proteins with CTX-I. ciguatoxin 1B (CTX 1B) 152-157 colony stimulating factor 1 Homo sapiens 36-41 30825104-8 2020 Pexidartinib exposure and plasma levels of adiponectin and colony-stimulating factor 1 increased following multiple daily pexidartinib administrations. pexidartinib 122-134 colony stimulating factor 1 Homo sapiens 59-86 31862249-12 2019 The study met its primary efficacy endpoint, with fenfluramine 0 7 mg/kg per day showing a 62 3% greater reduction in mean MCSF compared with placebo (95% CI 47 7-72 8, p<0 0001); fenfluramine 0 2 mg/kg per day showed a 32 4% reduction in mean MCSF compared with placebo (95% CI 6 2-52 3, p=0 0209). Fenfluramine 50-62 colony stimulating factor 1 Homo sapiens 123-127 31862249-12 2019 The study met its primary efficacy endpoint, with fenfluramine 0 7 mg/kg per day showing a 62 3% greater reduction in mean MCSF compared with placebo (95% CI 47 7-72 8, p<0 0001); fenfluramine 0 2 mg/kg per day showed a 32 4% reduction in mean MCSF compared with placebo (95% CI 6 2-52 3, p=0 0209). Fenfluramine 50-62 colony stimulating factor 1 Homo sapiens 247-251 31732480-2 2019 Nintedanib, a tyrosine kinase inhibitor targeting the PDGF, FGF, VEGF and M-CSF pathways, has shown comparable efficacy in idiopathic pulmonary fibrosis (IPF) and systemic sclerosis-associated ILD (SSc-ILD). nintedanib 0-10 colony stimulating factor 1 Homo sapiens 74-79 31655310-11 2019 These results were supported by the negative relationship between miR-148b and CSF1 expression and TAM infiltration in HCC patients. tam 99-102 colony stimulating factor 1 Homo sapiens 79-83 31655310-13 2019 CONCLUSION: MiR-148b-CSF1 signaling-induced TAM infiltration promotes HCC metastasis. tam 44-47 colony stimulating factor 1 Homo sapiens 21-25 30940906-8 2019 Further analyses of serial samples from ibrutinib-treated patients (n = 8) highlighted a rapid decrease of CSF1, IL-10, and CD163 in responsive patients. ibrutinib 40-49 colony stimulating factor 1 Homo sapiens 107-111 31602563-1 2019 Pexidartinib (TURALIO ) is an orally administered small molecule tyrosine kinase inhibitor with selective activity against the colony-stimulating factor 1 (CSF1) receptor, KIT proto-oncogene receptor tyrosine kinase (KIT) and FMS-like tyrosine kinase 3 harboring an internal tandem duplication mutation (FLT3-ITD). pexidartinib 0-12 colony stimulating factor 1 Homo sapiens 127-154 31602563-1 2019 Pexidartinib (TURALIO ) is an orally administered small molecule tyrosine kinase inhibitor with selective activity against the colony-stimulating factor 1 (CSF1) receptor, KIT proto-oncogene receptor tyrosine kinase (KIT) and FMS-like tyrosine kinase 3 harboring an internal tandem duplication mutation (FLT3-ITD). pexidartinib 0-12 colony stimulating factor 1 Homo sapiens 156-160 31618941-0 2019 ATP-Evoked Intracellular Ca2+ Responses in M-CSF Differentiated Human Monocyte-Derived Macrophage are Mediated by P2X4 and P2Y11 Receptor Activation. Adenosine Triphosphate 0-3 colony stimulating factor 1 Homo sapiens 43-48 31618941-2 2019 Here, we investigated ATP-evoked intracellular Ca2+ responses in human macrophage differentiated with macrophage colony-stimulating factor (M-CSF). Adenosine Triphosphate 22-25 colony stimulating factor 1 Homo sapiens 102-138 31618941-2 2019 Here, we investigated ATP-evoked intracellular Ca2+ responses in human macrophage differentiated with macrophage colony-stimulating factor (M-CSF). Adenosine Triphosphate 22-25 colony stimulating factor 1 Homo sapiens 140-145 31469844-4 2019 RESULTS: AL tissues had elevated levels of TNF-family members sTNFR2, TNFSF14, sFasL, sBAFF, cytokines/chemokines IL8, CCL2, IL1RA/IL36, sIL6R, and growth factors sAREG, CSF1, comparing to non-AL. Aluminum 9-11 colony stimulating factor 1 Homo sapiens 170-174 31569368-5 2019 Subsequently, the cultures of human osteoblasts with PhIP-stimulated condition medium of 786-O increased the expression of the macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL), and decreased the expression of osteoprotegerin (OPG). 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine 53-57 colony stimulating factor 1 Homo sapiens 127-163 31569368-5 2019 Subsequently, the cultures of human osteoblasts with PhIP-stimulated condition medium of 786-O increased the expression of the macrophage colony-stimulating factor (M-CSF) and receptor activator of nuclear factor kappa-B ligand (RANKL), and decreased the expression of osteoprotegerin (OPG). 2-amino-1-methyl-6-phenylimidazo(4,5-b)pyridine 53-57 colony stimulating factor 1 Homo sapiens 165-170 31012882-0 2019 Intratumoral delivery of M-CSF by calcium crosslinked polymer micelles enhances cancer immunotherapy. Calcium 34-41 colony stimulating factor 1 Homo sapiens 25-30 31229240-3 2019 We aimed to evaluate pexidartinib, a CSF1 receptor inhibitor, in patients with TGCT to provide them with a viable systemic treatment option, especially in cases that are not amenable to surgical resection. pexidartinib 21-33 colony stimulating factor 1 Homo sapiens 37-41 31012882-5 2019 This nanoparticle was prepared by introducing CaCO3 as a crosslinker to form an M-CSF-loaded stable micelle (NP/M-CSF/CaCO3). Calcium Carbonate 46-51 colony stimulating factor 1 Homo sapiens 80-85 31012882-6 2019 Administration of NP/M-CSF/CaCO3 significantly inhibited tumor growth by enhancing T cell-mediated anti-tumor immune responses and reversing the TAM-mediated immunosuppression. Tamoxifen 145-148 colony stimulating factor 1 Homo sapiens 21-26 31012882-5 2019 This nanoparticle was prepared by introducing CaCO3 as a crosslinker to form an M-CSF-loaded stable micelle (NP/M-CSF/CaCO3). Calcium Carbonate 118-123 colony stimulating factor 1 Homo sapiens 80-85 31217507-0 2019 A Selective FGFR inhibitor AZD4547 suppresses RANKL/M-CSF/OPG-dependent ostoclastogenesis and breast cancer growth in the metastatic bone microenvironment. AZD4547 27-34 colony stimulating factor 1 Homo sapiens 52-57 31138333-3 2019 METHODS: In this study, an in vitro method to generate monocyte- derived TAM using tumor- conditioned media (TCM) and a cytokine cocktail containing IL-4, IL-10, and M-CSF was utilized to study the phenotype, morphology, and function of TAM across multiple cancer types. tam 73-76 colony stimulating factor 1 Homo sapiens 166-171 31138333-11 2019 Our data confirm that monocyte-derived TAM can be generated reliably using TCM plus the cytokine cocktail of IL-4, IL-10, and M-CSF. tam 39-42 colony stimulating factor 1 Homo sapiens 126-131 30389911-6 2018 The inhibitory effects of syndecan ectodomains, heparan sulfate, and N-desulfated heparin derivatives on osteoclast differentiation were attributed to their direct binding to the macrophage-colony stimulating factor (M-CSF), resulting in the blocking of M-CSF-mediated downstream signals such as extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK), p38, and Akt. Heparin 82-89 colony stimulating factor 1 Homo sapiens 179-215 30859335-5 2019 PLX3397, an inhibitor of the colony stimulating factor-1 (CSF-1)/CSF-1 receptor (CSF-1R) pathway and macrophage survival, was delivered to B16F10 tumors via M2pep-modified PLGA nanoparticles. pexidartinib 0-7 colony stimulating factor 1 Homo sapiens 29-56 30859335-5 2019 PLX3397, an inhibitor of the colony stimulating factor-1 (CSF-1)/CSF-1 receptor (CSF-1R) pathway and macrophage survival, was delivered to B16F10 tumors via M2pep-modified PLGA nanoparticles. pexidartinib 0-7 colony stimulating factor 1 Homo sapiens 58-63 30592292-7 2019 Hoechst 33342 staining and flow cytometry were utilized to evaluate the effect of M-CSF on apoptosis in MCF-7 cells treated with ADM. Doxorubicin 129-132 colony stimulating factor 1 Homo sapiens 82-87 30696910-0 2019 Imaging endogenous macrophage iron deposits reveals a metabolic biomarker of polarized tumor macrophage infiltration and response to CSF1R breast cancer immunotherapy. Iron 30-34 colony stimulating factor 1 Homo sapiens 133-137 30400004-5 2019 Prostate cancer cells treated with docetaxel released more macrophage colony-stimulating factor (M-CSF-1 or CSF-1), IL-10 and other factors, which can recruit and modulate circulating monocytes to promote their protumorigenic functions. Docetaxel 35-44 colony stimulating factor 1 Homo sapiens 99-104 30400004-5 2019 Prostate cancer cells treated with docetaxel released more macrophage colony-stimulating factor (M-CSF-1 or CSF-1), IL-10 and other factors, which can recruit and modulate circulating monocytes to promote their protumorigenic functions. Docetaxel 35-44 colony stimulating factor 1 Homo sapiens 108-113 30616794-4 2019 Several approaches to block TAMs have been investigated, including TAMs inactivation by means of the colony stimulating factor 1 (CSF-1)/CSF-1 receptor (CSF-1R) inhibitors or strategies to reprogram TAMs from M2 protumoral phenotype toward M1 antitumoral phenotype. tams 67-71 colony stimulating factor 1 Homo sapiens 101-128 30616794-4 2019 Several approaches to block TAMs have been investigated, including TAMs inactivation by means of the colony stimulating factor 1 (CSF-1)/CSF-1 receptor (CSF-1R) inhibitors or strategies to reprogram TAMs from M2 protumoral phenotype toward M1 antitumoral phenotype. tams 67-71 colony stimulating factor 1 Homo sapiens 101-128 30519664-0 2018 Fungal metabolite (+)-terrein suppresses IL-6/sIL-6R-induced CSF1 secretion by inhibiting JAK1 phosphorylation in human gingival fibroblasts. terrein 18-29 colony stimulating factor 1 Homo sapiens 61-65 30519664-7 2018 Treatment with (+)-terrein suppressed expression of mRNA and protein of CSF1 and VEGF by IL-6/sIL-6R stimulation. terrein 15-26 colony stimulating factor 1 Homo sapiens 72-76 30519664-10 2018 Therefore, (+)-terrein suppresses IL-6/sIL-6R-induced expression of CSF1 and VEGF via inhibition of JAK1, Akt, and SHP-2. terrein 11-22 colony stimulating factor 1 Homo sapiens 68-72 30596089-7 2018 FA and Dex also inhibited inflammatory cytokine (CD14, M-CSF, MIP-3alpha, and TNF-alpha) secretion. Dexamethasone 7-10 colony stimulating factor 1 Homo sapiens 55-60 30389911-0 2018 Suppressive effect of syndecan ectodomains and N-desulfated heparins on osteoclastogenesis via direct binding to macrophage-colony stimulating factor. Heparin 60-68 colony stimulating factor 1 Homo sapiens 113-149 30389911-6 2018 The inhibitory effects of syndecan ectodomains, heparan sulfate, and N-desulfated heparin derivatives on osteoclast differentiation were attributed to their direct binding to the macrophage-colony stimulating factor (M-CSF), resulting in the blocking of M-CSF-mediated downstream signals such as extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK), p38, and Akt. Heparitin Sulfate 48-63 colony stimulating factor 1 Homo sapiens 179-215 30389911-6 2018 The inhibitory effects of syndecan ectodomains, heparan sulfate, and N-desulfated heparin derivatives on osteoclast differentiation were attributed to their direct binding to the macrophage-colony stimulating factor (M-CSF), resulting in the blocking of M-CSF-mediated downstream signals such as extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK), p38, and Akt. Heparitin Sulfate 48-63 colony stimulating factor 1 Homo sapiens 217-222 30516070-2 2019 Monocyte chemoattractant protein (MCP)-1 and macrophage colony-stimulating factor (MCSF) stimulate monocyte migration and transition into macrophages with subsequent release of neopterin. Neopterin 177-186 colony stimulating factor 1 Homo sapiens 45-81 30516070-2 2019 Monocyte chemoattractant protein (MCP)-1 and macrophage colony-stimulating factor (MCSF) stimulate monocyte migration and transition into macrophages with subsequent release of neopterin. Neopterin 177-186 colony stimulating factor 1 Homo sapiens 83-87 30769285-8 2019 The mechanical study revealed that tumoral NOX4-induced reactive oxygen species (ROS) stimulated various cytokine production, including CCL7, IL8, CSF-1 and VEGF-C, via PI3K/Akt signaling-dependent manner. Reactive Oxygen Species 56-79 colony stimulating factor 1 Homo sapiens 147-152 30769285-8 2019 The mechanical study revealed that tumoral NOX4-induced reactive oxygen species (ROS) stimulated various cytokine production, including CCL7, IL8, CSF-1 and VEGF-C, via PI3K/Akt signaling-dependent manner. Reactive Oxygen Species 81-84 colony stimulating factor 1 Homo sapiens 147-152 30813507-7 2019 On nanofunctionalized titanium specimens, the osteoclast-specific TRAP5b protein was monitored and showed a significantly decreased amount on cDMAB-titanium in PBMCs + RANKL/MCSF. Titanium 148-156 colony stimulating factor 1 Homo sapiens 174-178 30389911-6 2018 The inhibitory effects of syndecan ectodomains, heparan sulfate, and N-desulfated heparin derivatives on osteoclast differentiation were attributed to their direct binding to the macrophage-colony stimulating factor (M-CSF), resulting in the blocking of M-CSF-mediated downstream signals such as extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK), p38, and Akt. Heparin 82-89 colony stimulating factor 1 Homo sapiens 217-222 30237497-8 2018 By RNA profiling, Western blot and luciferase reporter assay, we further observed that miR-125b directly regulated tumor cell-derived chemokine CSF1 and CX3CL1, which are known to control the recruitment of TAMs to tumor sites. mir-125b 87-95 colony stimulating factor 1 Homo sapiens 144-148 30075184-10 2018 Moreover, multi-kinase inhibitor, cabozantinib, suppressed CSF-1R activation and drastically reduced cell growth when combined with gefitinib. cabozantinib 34-46 colony stimulating factor 1 Homo sapiens 59-64 30322928-7 2018 Cytokine profiling of CRPC tumor grafts exposed to GSNO revealed a significant decrease in expression of G-CSF and M-CSF compared with grafts not exposed to GSNO. S-Nitrosoglutathione 51-55 colony stimulating factor 1 Homo sapiens 115-120 29061766-2 2017 Because tissue homeostasis is maintained through an adequate balance of pro- and anti-inflammatory macrophages, we assessed the transcriptional and functional profile of M-CSF-dependent monocyte-derived human macrophages exposed to concentrations of saturated fatty acids found in obese individuals. Fatty Acids 250-271 colony stimulating factor 1 Homo sapiens 170-175 29314558-4 2018 Inhibiting neutrophil production of CSF1 or preventing macrophage proliferation, using targeted nanoparticles loaded with the cell cycle inhibitor simvastatin, abrogates the induction of tolerance. Simvastatin 147-158 colony stimulating factor 1 Homo sapiens 36-40 29796177-7 2018 In vitro experiments showed that tyrosine phosphorylation of CSF-1R, ERK, and FAK and cell migration are differentially regulated by IL-34 and CSF-1 in breast cancer cell lines. Tyrosine 33-41 colony stimulating factor 1 Homo sapiens 61-66 29449600-5 2018 We report here that the GC, dexamethasone, induces apoptosis in GM-CSF-treated human monocytes while having no impact on M-CSF-induced monocyte survival. Dexamethasone 28-41 colony stimulating factor 1 Homo sapiens 65-70 29449600-7 2018 Transcriptomic and Ingenuity pathway analyses found that dexamethasone differentially modulated dendritic cell maturation and TREM1 signaling pathways in GM-CSF-treated and M-CSF-treated monocytes, two pathways known to be regulated by ERK1/2 activity. Dexamethasone 57-70 colony stimulating factor 1 Homo sapiens 155-160 29358859-6 2017 The action mechanism of astragaloside IV was investigated by detecting the expression of microRNAs and the expression and secretion of the oncogenic factor, macrophage colony-stimulating factor (M-CSF), and the tumor suppressive factor, tissue inhibitor of metalloproteinase 2 (TIMP2), in different groups of GCAFs. astragaloside 24-37 colony stimulating factor 1 Homo sapiens 195-200 30031388-11 2018 The IPA of "diseases and functions" regulators (85) were involved with cAMP, STAT2, 26S proteasome, CSF1, IFNgamma, LDL, TGFA, and microRNA-155-5p, miR-223, miR-21-5p. Cyclic AMP 71-75 colony stimulating factor 1 Homo sapiens 100-104 29875321-4 2018 This reduction in CSF1-dependent TAMs resulted in increased CD8+ T cell attack on tumors, but its effect on tumor growth was limited by a compensatory increase in Foxp3+ Treg cells. tams 33-37 colony stimulating factor 1 Homo sapiens 18-22 29174801-8 2018 Cabozantinib (60 mg/kg, 3 weeks) suppressed tumor growth in bone and reduced expression of RANKL and M-CSF and subsequent tumor-induced osteolysis. cabozantinib 0-12 colony stimulating factor 1 Homo sapiens 101-106 28407244-5 2018 It was observed that nicotine at low concentrations elicit an increase in osteoclast differentiation, but only in the presence of M-CSF and RANKL it was also able to significantly increase the resorbing ability of osteoclasts. Nicotine 21-29 colony stimulating factor 1 Homo sapiens 130-135 28724665-4 2017 Tumor-associated macrophages in surgical specimens and sensitivity to CSF-1R inhibitors were used to determine macrophage function.Results: A CSF1R c.1085A>G genetic variant causing the change of histidine to arginine in the domain of receptor dimerization was identified as a high allele frequency in Eastern Asian population. Histidine 199-208 colony stimulating factor 1 Homo sapiens 142-146 28724665-4 2017 Tumor-associated macrophages in surgical specimens and sensitivity to CSF-1R inhibitors were used to determine macrophage function.Results: A CSF1R c.1085A>G genetic variant causing the change of histidine to arginine in the domain of receptor dimerization was identified as a high allele frequency in Eastern Asian population. Arginine 212-220 colony stimulating factor 1 Homo sapiens 142-146 29245915-10 2017 Multiplex analyses of plasma taken after drug exposure at animal nadir indicated that the levels of M-CSF, CXCL-9, PDGF and G-CSF were significantly increased by [curcumin + sildenafil] and that expression of CXCL1 and CCL5 were significantly reduced. Curcumin 163-171 colony stimulating factor 1 Homo sapiens 100-105 28861734-2 2017 Here, the effect of sesamin on human osteoclasts was investigated in terms of differentiation and function in M-CSF and RANKL induced human PBMCs. sesamin 20-27 colony stimulating factor 1 Homo sapiens 110-115 28637652-6 2017 A striking shift toward proinflammatory eicosanoids was observed when the same cells were exposed (30 min) to bacterial stimuli: M-CSF Mphis produced considerably more 5-lipoxygenase products, particularly leukotriene C4, potentially linked to M2 functions in asthma. Eicosanoids 40-51 colony stimulating factor 1 Homo sapiens 129-134 28637652-6 2017 A striking shift toward proinflammatory eicosanoids was observed when the same cells were exposed (30 min) to bacterial stimuli: M-CSF Mphis produced considerably more 5-lipoxygenase products, particularly leukotriene C4, potentially linked to M2 functions in asthma. Leukotriene C4 206-220 colony stimulating factor 1 Homo sapiens 129-134 28637652-8 2017 In the M-CSF cells, there was also an enhanced release of arachidonic acid and activation of cytosolic phospholipase A2 However, GM-CSF cells expressed higher levels of 5-lipoxygenase and 5-lipoxygenase-activating protein, and in ionophore incubations these cells also produced the highest levels of 5-hydroxyeicosatetraenoic acid. Arachidonic Acid 58-74 colony stimulating factor 1 Homo sapiens 7-12 28637652-8 2017 In the M-CSF cells, there was also an enhanced release of arachidonic acid and activation of cytosolic phospholipase A2 However, GM-CSF cells expressed higher levels of 5-lipoxygenase and 5-lipoxygenase-activating protein, and in ionophore incubations these cells also produced the highest levels of 5-hydroxyeicosatetraenoic acid. 5-hydroxy-6,8,11,14-eicosatetraenoic acid 300-330 colony stimulating factor 1 Homo sapiens 7-12 28637652-9 2017 In summary, GM-CSF and M-CSF Mphis displayed similar proresolving lipid mediator formation in resting conditions but shifted toward different proinflammatory eicosanoids upon bacterial stimuli. Eicosanoids 158-169 colony stimulating factor 1 Homo sapiens 13-18 28656272-1 2017 Our previous demonstrated that macrophage colony-stimulating factor (M-CSF) stimulated the production of estradiol (E2) and progesterone (P) in luteinized granulosa cells (GCs), and that its secretion may be regulated by follicle-stimulating hormone (FSH). Estradiol 105-114 colony stimulating factor 1 Homo sapiens 31-67 28656272-1 2017 Our previous demonstrated that macrophage colony-stimulating factor (M-CSF) stimulated the production of estradiol (E2) and progesterone (P) in luteinized granulosa cells (GCs), and that its secretion may be regulated by follicle-stimulating hormone (FSH). Estradiol 105-114 colony stimulating factor 1 Homo sapiens 69-74 28656272-1 2017 Our previous demonstrated that macrophage colony-stimulating factor (M-CSF) stimulated the production of estradiol (E2) and progesterone (P) in luteinized granulosa cells (GCs), and that its secretion may be regulated by follicle-stimulating hormone (FSH). Progesterone 124-136 colony stimulating factor 1 Homo sapiens 31-67 28656272-1 2017 Our previous demonstrated that macrophage colony-stimulating factor (M-CSF) stimulated the production of estradiol (E2) and progesterone (P) in luteinized granulosa cells (GCs), and that its secretion may be regulated by follicle-stimulating hormone (FSH). Progesterone 124-136 colony stimulating factor 1 Homo sapiens 69-74 28656272-12 2017 Furthermore, M-CSF induced the phosphorylation of c-Jun N-terminal kinase (JNK) and p38; however, the level of E2 in the medium was not altered when the cells were pretreated with the JNK inhibitor SP600125 or the p38 inhibitor SB203580. pyrazolanthrone 198-206 colony stimulating factor 1 Homo sapiens 13-18 28656272-12 2017 Furthermore, M-CSF induced the phosphorylation of c-Jun N-terminal kinase (JNK) and p38; however, the level of E2 in the medium was not altered when the cells were pretreated with the JNK inhibitor SP600125 or the p38 inhibitor SB203580. SB 203580 228-236 colony stimulating factor 1 Homo sapiens 13-18 29245915-10 2017 Multiplex analyses of plasma taken after drug exposure at animal nadir indicated that the levels of M-CSF, CXCL-9, PDGF and G-CSF were significantly increased by [curcumin + sildenafil] and that expression of CXCL1 and CCL5 were significantly reduced. Sildenafil Citrate 174-184 colony stimulating factor 1 Homo sapiens 100-105 28052488-7 2017 LEC-mediated OC formation and bone resorption were blocked by an M-CSF neutralizing antibody or Ki20227, an inhibitor of the M-CSF receptor, c-Fms. N-(4-((6,7-dimethoxy-4-quinolyl)oxy)-2-methoxyphenyl)-N'-(1-(1,3-thiazole-2-yl)ethyl)urea 96-103 colony stimulating factor 1 Homo sapiens 125-130 29059867-5 2017 The extracellularly released BLZ-945 could be taken up by TAMs, which locate preferentially in the perivascular region [4], to directly disturb CSF-1/CSF-1R signaling pathway to suppress TAMs and modulate the tumor immune microenvironment, while the released small particles carrying Pt-prodrug could penetrate deeply into bulk tumor to kill more cancer cells [5], realizing synergistic antitumor effect of chemo- and immunotherapy (Fig. tams 58-62 colony stimulating factor 1 Homo sapiens 144-149 28629162-6 2017 CSF-1 also regulates macrophage survival, proliferation and differentiation, and its many effects are transduced by its receptor, the CSF-1R, via phosphotyrosine motif-activated signals. Phosphotyrosine 146-161 colony stimulating factor 1 Homo sapiens 0-5 28159742-7 2017 Here, we address which CSF-1-activated pathways are involved in transmitting the lineage-instructive signal in primary bone marrow-derived GM progenitors. gm 139-141 colony stimulating factor 1 Homo sapiens 23-28 28273887-7 2017 When we analyzed clinical parameters, patients treated with azathioprine had the highest CSF-1 levels and CCR5 expression. Azathioprine 60-72 colony stimulating factor 1 Homo sapiens 89-94 28273064-5 2017 We previously reported that a first-in-class selective class IIa histone deacetylase (HDAC) inhibitor, TMP195, influenced human monocyte responses to the colony-stimulating factors CSF-1 and CSF-2 in vitro. TMP195 103-109 colony stimulating factor 1 Homo sapiens 181-186 28063981-9 2017 GM-CSF-stimulated macrophages expressed higher levels of the mannose receptor CD206 compared to M-CSF-stimulated cells, and uptake of AMS6, but not AMS8, was reduced following the downregulation of CD206 in GM-CSF-stimulated cells; particle uptake was also suppressed by mannan, a competitive ligand. ams6 134-138 colony stimulating factor 1 Homo sapiens 1-6 28063981-9 2017 GM-CSF-stimulated macrophages expressed higher levels of the mannose receptor CD206 compared to M-CSF-stimulated cells, and uptake of AMS6, but not AMS8, was reduced following the downregulation of CD206 in GM-CSF-stimulated cells; particle uptake was also suppressed by mannan, a competitive ligand. Mannans 271-277 colony stimulating factor 1 Homo sapiens 1-6 28377874-14 2017 In cultured muscle cells, EPS promoted a significant increase in the expression and secretion of CSF1. eps 26-29 colony stimulating factor 1 Homo sapiens 97-101 28004478-6 2017 Furthermore, CS2164 demonstrated the inhibitory effect on CSF-1R phosphorylation that led to the suppression of ligand-stimulated monocyte-to-macrophage differentiation and reduced CSF-1R+ cells in tumor tissues. chiauranib 13-19 colony stimulating factor 1 Homo sapiens 58-63 28097809-7 2017 Upon treatment of M-CSF neutralizing antibody, the ROS generation and M2 polarization of CAFs CM-stimulated monocytes were significantly inhibited (P < 0.05). Reactive Oxygen Species 51-54 colony stimulating factor 1 Homo sapiens 18-23 28808355-6 2017 FE MCSF rose significantly since CKD stages 1-2, FE neopterin since CKD stages 3-5. Iron 0-2 colony stimulating factor 1 Homo sapiens 3-7 29953775-3 2017 Resistence of ovarian cancer cells to paclitaxel and cisplatin is associated with a reduced expression of miR-30c, miR-130, and miR335, which results in activation of M-CSF, the known factor of resistance to cytostatic drugs. Cisplatin 53-62 colony stimulating factor 1 Homo sapiens 167-172 27741434-3 2017 Notably M-CSF macrophages exhibited a timely dependent PGD2 production upon niacin challenge. Niacin 76-82 colony stimulating factor 1 Homo sapiens 8-13 29953775-3 2017 Resistence of ovarian cancer cells to paclitaxel and cisplatin is associated with a reduced expression of miR-30c, miR-130, and miR335, which results in activation of M-CSF, the known factor of resistance to cytostatic drugs. Paclitaxel 38-48 colony stimulating factor 1 Homo sapiens 167-172 27741434-4 2017 Short pretreatment of M-CSF macrophages with autologous postprandial TRLs induced the down-regulation of HCA2 gene and up-regulation of genes encoding COX1 and COX2 enzymes in a fatty acid-dependent manner. Fatty Acids 178-188 colony stimulating factor 1 Homo sapiens 22-27 26920997-3 2016 As a means to identify MTX response markers, we have explored its transcriptional effect on macrophages polarised by GM-CSF (GM-MO) or M-CSF (M-MO), which resemble proinflammatory and anti-inflammatory macrophages found in RA and normal joints, respectively. Methotrexate 23-26 colony stimulating factor 1 Homo sapiens 118-123 28101209-7 2016 Stratified analysis demonstrated that, in AIS/MIA patients, there was a statistically significant difference between the number of TAMs (TAMs <=25 and TAMs >25) in the CD68+CSF-1+IL-6+ group compared with other groups (including CD68+CSF-1-IL-6-, CD68+CSF-1+IL-6-, CD68+CSF-1-IL-6+ and CD68- groups). tams 131-135 colony stimulating factor 1 Homo sapiens 179-184 27677742-9 2016 Most advanced strategies aim at depleting macrophages by targeting the CSF1/CSF1R pathway, which is fundamental for TAM survival. tam 116-119 colony stimulating factor 1 Homo sapiens 71-75 27622030-5 2016 We report here that CD14(+) CD163(+) TAM isolated from ovarian cancer patients and macrophages generated in vitro with M-CSF, express high levels of the membrane ectonucleotidase CD39 compared to classically activated macrophages. tam 37-40 colony stimulating factor 1 Homo sapiens 119-124 27736957-9 2016 In vitro studies demonstrated that TAS-115 inhibited HGF-, VEGF-, and macrophage-colony stimulating factor (M-CSF)-induced signaling pathways in osteoclasts. 4-(2-fluoro-4-((((2-phenylacetyl)amino)thioxomethyl)amino)phenoxy)-7-methoxy-N-methyl-6-quinolinecarboxamide 35-42 colony stimulating factor 1 Homo sapiens 70-106 27736957-9 2016 In vitro studies demonstrated that TAS-115 inhibited HGF-, VEGF-, and macrophage-colony stimulating factor (M-CSF)-induced signaling pathways in osteoclasts. 4-(2-fluoro-4-((((2-phenylacetyl)amino)thioxomethyl)amino)phenoxy)-7-methoxy-N-methyl-6-quinolinecarboxamide 35-42 colony stimulating factor 1 Homo sapiens 108-113 27736957-10 2016 Moreover, TAS-115 inhibited Feline McDonough Sarcoma oncogene (FMS) kinase, as well as M-CSF and receptor activator of NF-kappaB ligand (RANKL)-induced osteoclast differentiation. 4-(2-fluoro-4-((((2-phenylacetyl)amino)thioxomethyl)amino)phenoxy)-7-methoxy-N-methyl-6-quinolinecarboxamide 10-17 colony stimulating factor 1 Homo sapiens 87-92 27605608-8 2016 Independently of AGER, methylglyoxal reduced the release of endothelial CSF-1 (M-CSF), which stimulates polarization of macrophages to a noninflammatory phenotype in the microenvironment of the ischemic brain. Pyruvaldehyde 23-36 colony stimulating factor 1 Homo sapiens 72-77 27605608-8 2016 Independently of AGER, methylglyoxal reduced the release of endothelial CSF-1 (M-CSF), which stimulates polarization of macrophages to a noninflammatory phenotype in the microenvironment of the ischemic brain. Pyruvaldehyde 23-36 colony stimulating factor 1 Homo sapiens 79-84 27173404-6 2016 The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor fluvastatin could also be shown to moderately reduce the IL-33-mediated effect on M-CSF, but not on GM-CSF expression. Fluvastatin 72-83 colony stimulating factor 1 Homo sapiens 154-159 27135205-8 2016 M-CSF stimulated incorporation of [(3)H] thymidine in human aortic smooth muscle cells in a concentration-dependent manner. [(3)h] thymidine 34-50 colony stimulating factor 1 Homo sapiens 0-5 27995121-10 2016 The expressions of OPG, RANKL, and M-CSF have decreased via the alendronate. Alendronate 64-75 colony stimulating factor 1 Homo sapiens 35-40 26538356-9 2016 Furthermore M-CSF levels tended to be low in preterm deliveries, placental insufficiency and nicotine consumption. Nicotine 93-101 colony stimulating factor 1 Homo sapiens 12-17 26908330-8 2016 Everolimus-specific biomarkers (CSF1, ICAM1, IL-18BP, KIM1, TNFRII) with hazard ratio >= 1.8 were integrated into a CBS (range 0-5). Everolimus 0-10 colony stimulating factor 1 Homo sapiens 32-36 25724173-7 2016 Flavonols and resveratrol significantly reduced also the endothelial expression and release of M-CSF. Flavonols 0-9 colony stimulating factor 1 Homo sapiens 95-100 25724173-7 2016 Flavonols and resveratrol significantly reduced also the endothelial expression and release of M-CSF. Resveratrol 14-25 colony stimulating factor 1 Homo sapiens 95-100 28219867-0 2016 [Effects of retinol on expressions of epidermal growth factor, stem cell factor, colony-stimulating factor 1 and leukemia inhibitory factor in human umbilical cord-derived mesenchymal stem cells]. Vitamin A 12-19 colony stimulating factor 1 Homo sapiens 81-108 28219867-1 2016 OBJECTIVE: To investigate effects of retinol on the expressions of epidermal growth factor (EGF), stem cell factor (SCF), colony-stimulating factor 1 (CSF1) and leukemia inhibitory factor (LIF) in cultured human umbilical-derived mesenchymal stem cells (UCMSCs). Vitamin A 37-44 colony stimulating factor 1 Homo sapiens 122-149 28219867-1 2016 OBJECTIVE: To investigate effects of retinol on the expressions of epidermal growth factor (EGF), stem cell factor (SCF), colony-stimulating factor 1 (CSF1) and leukemia inhibitory factor (LIF) in cultured human umbilical-derived mesenchymal stem cells (UCMSCs). Vitamin A 37-44 colony stimulating factor 1 Homo sapiens 151-155 28219867-6 2016 Retinol (1 micromol/L) significantly promoted the expressions of SCF and CSF1 at both mRNA and protein levels but did not result in changes of EGF and LIF expressions in human UCMSCs. Vitamin A 0-7 colony stimulating factor 1 Homo sapiens 73-77 28219867-7 2016 CONCLUSION: Retinol at the concentration of 1 micromol/L can promote expression of SCF and CSF1 in human UCMSCs in vitro. Vitamin A 12-19 colony stimulating factor 1 Homo sapiens 91-95 26098772-2 2015 During breast cancer progression the colony stimulating factor 1 (CSF-1) can reprogram MCs into tumor-promoting macrophages in the primary tumor. mcs 87-90 colony stimulating factor 1 Homo sapiens 37-64 26811453-5 2016 Here, we report that the mitogenic stimulus, colony-stimulating factor 1 (CSF-1), engages a myelocytomatosis viral oncogen (Myc)-dependent transcriptional program that is responsible for cell cycle entry and the up-regulation of glucose and glutamine catabolism in bone marrow-derived macrophages (BMDMs). Glucose 229-236 colony stimulating factor 1 Homo sapiens 45-72 26811453-5 2016 Here, we report that the mitogenic stimulus, colony-stimulating factor 1 (CSF-1), engages a myelocytomatosis viral oncogen (Myc)-dependent transcriptional program that is responsible for cell cycle entry and the up-regulation of glucose and glutamine catabolism in bone marrow-derived macrophages (BMDMs). Glucose 229-236 colony stimulating factor 1 Homo sapiens 74-79 26811453-5 2016 Here, we report that the mitogenic stimulus, colony-stimulating factor 1 (CSF-1), engages a myelocytomatosis viral oncogen (Myc)-dependent transcriptional program that is responsible for cell cycle entry and the up-regulation of glucose and glutamine catabolism in bone marrow-derived macrophages (BMDMs). Glutamine 241-250 colony stimulating factor 1 Homo sapiens 45-72 26811453-5 2016 Here, we report that the mitogenic stimulus, colony-stimulating factor 1 (CSF-1), engages a myelocytomatosis viral oncogen (Myc)-dependent transcriptional program that is responsible for cell cycle entry and the up-regulation of glucose and glutamine catabolism in bone marrow-derived macrophages (BMDMs). Glutamine 241-250 colony stimulating factor 1 Homo sapiens 74-79 26336156-7 2016 Finally, we studied the connection between ERK and PKCd and showed that in the presence of the MEK inhibitor U0126, PKCd expression is decreased, and Fli-1 expression is increased in response to M-CSF. U 0126 109-114 colony stimulating factor 1 Homo sapiens 195-200 26095744-4 2015 We demonstrate that simultaneous addition of M-CSF and IL-34 led to a specific activation pattern on the M-CSFR, with higher phosphorylation of the tyrosine residues at low concentrations. Tyrosine 148-156 colony stimulating factor 1 Homo sapiens 45-50 26344055-8 2015 In patients with acetaminophen-induced acute liver failure, a low serum level of CSF1 was associated with increased mortality. Acetaminophen 17-30 colony stimulating factor 1 Homo sapiens 81-85 26468083-7 2015 RESULTS: We found that Everolimus significantly inhibited the differentiation of OCs and their in vitro bone-resorbing activity, and also found decreases of both mRNA and secreted pro-OC factors such as M-CSF, IL-6, and IL-1beta, whose lower ELISA levels paralleled the defective phosphorylation of NFkB pathway effectors. Everolimus 23-33 colony stimulating factor 1 Homo sapiens 203-208 26233509-1 2015 OBJECTIVE: To assess the efficacy and safety of JNJ-40346527, a selective inhibitor of colony-stimulating factor-1 (CSF-1) receptor kinase that acts to inhibit macrophage survival, proliferation, and differentiation in patients with active rheumatoid arthritis (RA) despite disease-modifying antirheumatic drug (DMARD) therapy. JNJ-40346527 48-60 colony stimulating factor 1 Homo sapiens 87-114 26233509-1 2015 OBJECTIVE: To assess the efficacy and safety of JNJ-40346527, a selective inhibitor of colony-stimulating factor-1 (CSF-1) receptor kinase that acts to inhibit macrophage survival, proliferation, and differentiation in patients with active rheumatoid arthritis (RA) despite disease-modifying antirheumatic drug (DMARD) therapy. JNJ-40346527 48-60 colony stimulating factor 1 Homo sapiens 116-121 26085050-2 2015 In ACS, aspirin at antiplatelet doses exhibits anti-inflammatory effects as seen from the decrease in inflammation markers such as CRP, M-CSF, MCP-1 and others. Aspirin 8-15 colony stimulating factor 1 Homo sapiens 136-141 26179200-2 2015 CSF1 receptor (CSF1R) activation leads to the recruitment of CSF1R-expressing cells of the mononuclear phagocyte lineage that constitute the tumor mass in dt-GCT. Thymidine 155-157 colony stimulating factor 1 Homo sapiens 0-4 26798359-10 2016 Further, an indirect effect of Si on osteoclastogenesis may also occur, through a downregulation of M-CSF and RANKL expression by osteoblasts. Silicon 31-33 colony stimulating factor 1 Homo sapiens 100-105 26098772-2 2015 During breast cancer progression the colony stimulating factor 1 (CSF-1) can reprogram MCs into tumor-promoting macrophages in the primary tumor. mcs 87-90 colony stimulating factor 1 Homo sapiens 66-71 26098772-5 2015 Our results underline the addiction of MCs to CSF-1 while surprisingly, microglia were not affected. mcs 39-42 colony stimulating factor 1 Homo sapiens 46-51 26098772-7 2015 Yet treatment with IL-34 and co-culture with carcinoma cells partially rescued the anti-CSF-1 effects on MCs. mcs 105-108 colony stimulating factor 1 Homo sapiens 88-93 26098772-8 2015 Further, MC-induced invasion was significantly reduced by anti-CSF-1 treatment while microglia-induced invasion was reduced to a lower extend. Methylcholanthrene 9-11 colony stimulating factor 1 Homo sapiens 63-68 26098772-10 2015 Taken together, our findings demonstrate not only differences of anti-CSF-1 treatment on MCs and microglia but also in the CSF-1 receptor and ligand expression in brain and bone marrow as well as in brain metastasis. mcs 89-92 colony stimulating factor 1 Homo sapiens 70-75 25551094-10 2014 OPG, RANKL, and M-CSF expression were all decreased by alendronate treatment. Alendronate 55-66 colony stimulating factor 1 Homo sapiens 16-21 25887296-8 2015 In addition, LLDT-8 decreased the number of TRAP-positive cells derived from RAW264.7 in the presence of RANKL and M-CSF. 5alpha-Hydroxytriptolide 13-19 colony stimulating factor 1 Homo sapiens 115-120 25611090-5 2015 Furthermore, the cell-intrinsic and -extrinsic factors (namely, Spi-C, IRF8/4, heme oxygenase-1, and M-CSF) that regulate the development and survival of RPMs have been identified. rpms 154-158 colony stimulating factor 1 Homo sapiens 101-106 25413299-4 2015 We demonstrated that coculture in collagen scaffolds of BM-MSC with Mf derived from monocytes polarized with M-CSF (M-Mf), but not with GM-CSF (GM-Mf) resulted in significantly higher glycosaminoglycan (GAG) content than what would be expected from an equal number of BM-MSC alone (defined as chondro-induction). Glycosaminoglycans 184-201 colony stimulating factor 1 Homo sapiens 109-114 25886134-9 2015 Through in vitro studies, we show that M-CSF and IL-34 upregulate CD163, a marker for type 2 activation of MPhis (M2), by primary monocytes, which is attenuated by the addition of GW2580. 5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine 180-186 colony stimulating factor 1 Homo sapiens 39-44 25736687-3 2015 ABT induced the tumor cells to express macrophage colony-stimulating factor 1 (M-CSF1 or CSF1) and other cytokines that recruit and modulate macrophages, causing a significant increase in TAM infiltration. abt 0-3 colony stimulating factor 1 Homo sapiens 39-77 25736687-3 2015 ABT induced the tumor cells to express macrophage colony-stimulating factor 1 (M-CSF1 or CSF1) and other cytokines that recruit and modulate macrophages, causing a significant increase in TAM infiltration. abt 0-3 colony stimulating factor 1 Homo sapiens 81-85 25736687-3 2015 ABT induced the tumor cells to express macrophage colony-stimulating factor 1 (M-CSF1 or CSF1) and other cytokines that recruit and modulate macrophages, causing a significant increase in TAM infiltration. abt 0-3 colony stimulating factor 1 Homo sapiens 89-93 25736687-4 2015 Inhibitors of CSF1 signaling through its receptor, CSF1R, were tested in combination with ABT, demonstrating that blockade of TAM influx in this setting disrupts tumor promotion and sustains a more durable therapeutic response compared with ABT alone. tam 126-129 colony stimulating factor 1 Homo sapiens 14-18 25736687-4 2015 Inhibitors of CSF1 signaling through its receptor, CSF1R, were tested in combination with ABT, demonstrating that blockade of TAM influx in this setting disrupts tumor promotion and sustains a more durable therapeutic response compared with ABT alone. abt 241-244 colony stimulating factor 1 Homo sapiens 14-18 25688212-3 2015 In cells stimulated with M-CSF, microscopic imaging of fluorescent probes for intracellular lipids indicated that the PI3K product phosphatidylinositol (3,4,5)-trisphosphate (PIP3) appeared in cups just prior to DAG. phosphatidylinositol 3,4,5-triphosphate 131-173 colony stimulating factor 1 Homo sapiens 25-30 25688212-3 2015 In cells stimulated with M-CSF, microscopic imaging of fluorescent probes for intracellular lipids indicated that the PI3K product phosphatidylinositol (3,4,5)-trisphosphate (PIP3) appeared in cups just prior to DAG. PIP3 175-179 colony stimulating factor 1 Homo sapiens 25-30 25688212-3 2015 In cells stimulated with M-CSF, microscopic imaging of fluorescent probes for intracellular lipids indicated that the PI3K product phosphatidylinositol (3,4,5)-trisphosphate (PIP3) appeared in cups just prior to DAG. Diglycerides 212-215 colony stimulating factor 1 Homo sapiens 25-30 25688212-6 2015 The phospholipase C (PLC) inhibitor U73122 blocked macropinocytosis by M-CSF but not PMA. 1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione 36-42 colony stimulating factor 1 Homo sapiens 71-76 25688212-7 2015 Macropinocytosis in response to M-CSF and PMA was inhibited by the Ras inhibitor farnesyl thiosalicylate (FTS), by the PKC inhibitor Calphostin C and by the broad specificity inhibitor rottlerin. farnesylthiosalicylic acid 81-104 colony stimulating factor 1 Homo sapiens 32-37 25688212-7 2015 Macropinocytosis in response to M-CSF and PMA was inhibited by the Ras inhibitor farnesyl thiosalicylate (FTS), by the PKC inhibitor Calphostin C and by the broad specificity inhibitor rottlerin. farnesylthiosalicylic acid 106-109 colony stimulating factor 1 Homo sapiens 32-37 25688212-7 2015 Macropinocytosis in response to M-CSF and PMA was inhibited by the Ras inhibitor farnesyl thiosalicylate (FTS), by the PKC inhibitor Calphostin C and by the broad specificity inhibitor rottlerin. calphostin C 133-145 colony stimulating factor 1 Homo sapiens 32-37 25688212-7 2015 Macropinocytosis in response to M-CSF and PMA was inhibited by the Ras inhibitor farnesyl thiosalicylate (FTS), by the PKC inhibitor Calphostin C and by the broad specificity inhibitor rottlerin. rottlerin 185-194 colony stimulating factor 1 Homo sapiens 32-37 25688212-8 2015 These studies support a model in which M-CSF stimulates PI3K in macropinocytic cups, and the resulting increase in PIP3 activates PLC, which in turn generates DAG necessary for activation of PKC, Ras and the late stages of macropinosome closure. Diglycerides 159-162 colony stimulating factor 1 Homo sapiens 39-44 25226391-6 2014 These monocytes are then cultured in fluorinated ethylene propylene (FEP) Teflon-coated cell culture bags in the presence of macrophage colony-stimulating factor (M-CSF). 1-Propene, polymer with ethene 49-67 colony stimulating factor 1 Homo sapiens 163-168 24424564-1 2014 Sunitinib is a tyrosine kinase inhibitor with direct anti-tumor and anti-angiogenesis activity targeting VEGFR 1-2, PDGFR alpha-beta, c-kit, bFGF, (CSF-1), FLT3 and RET. Sunitinib 0-9 colony stimulating factor 1 Homo sapiens 148-153 25375896-6 2014 ED71 was significantly less effective in inhibiting M-CSF and RANKL-stimulated osteoclastogenesis than was 1,25(OH)2D3 in vitro. eldecalcitol 0-4 colony stimulating factor 1 Homo sapiens 52-57 24950779-5 2014 Flutamide decreased the levels, notably, of CSF-1 and ErbB4 in ovarian stroma (P <= 0.0006) and ovarian endosalpingiosis (P <= 0.01), ErbB4 in ovarian epithelium (P = 0.006), and CSF-1R in ovarian endosalpingiosis (P = 0.009). Flutamide 0-9 colony stimulating factor 1 Homo sapiens 44-49 24956020-3 2014 We also tested the ability of zoledronate, denosumab and 5H4, an antibody directed against CSF-1, to interfere with the osteoclastogenic potential of breast cancer. CHEMBL3125049 57-60 colony stimulating factor 1 Homo sapiens 91-96 24950779-8 2014 Thus, our data suggest that a short 6-week exposure of flutamide reversed elevated levels of CSF-1 and ErbB4 (both of which we had previously found correlated with high risk status). Flutamide 55-64 colony stimulating factor 1 Homo sapiens 93-98 24950779-9 2014 CSF-1 and ErbB4 in ovarian stroma led to a model with high predictive value for flutamide sensitivity. Flutamide 80-89 colony stimulating factor 1 Homo sapiens 0-5 25134536-3 2014 In this study, we investigated the impact of a medium-chain fatty acid, capric acid, on the osteoclast differentiation, function, and survival induced by receptor activator of NF-kappaB ligand (RANKL) and macrophage colony-stimulating factor (MCSF). medium-chain fatty acid 47-70 colony stimulating factor 1 Homo sapiens 205-241 24796276-4 2014 TAM differentiation and expansion is regulated by CSF1, whose expression is directly controlled by STAT1 at the gene promoter level. tam 0-3 colony stimulating factor 1 Homo sapiens 50-54 25134536-3 2014 In this study, we investigated the impact of a medium-chain fatty acid, capric acid, on the osteoclast differentiation, function, and survival induced by receptor activator of NF-kappaB ligand (RANKL) and macrophage colony-stimulating factor (MCSF). decanoic acid 72-83 colony stimulating factor 1 Homo sapiens 205-241 25134536-7 2014 In addition, capric acid abrogated M-CSF and RANKL-mediated cytoskeleton reorganization, which is crucial for the efficient bone resorption of osteoclasts. decanoic acid 13-24 colony stimulating factor 1 Homo sapiens 35-40 25134536-8 2014 Capric acid also increased apoptosis in mature osteoclasts through the induction of Bim expression and the suppression of ERK activation by M-CSF. decanoic acid 0-11 colony stimulating factor 1 Homo sapiens 140-145 24360989-3 2014 Exposing the BMCs to 3%, 5%, or 10% O2 in the presence of receptor activator of NF-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) generated tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cells, consistent with OCs. Oxygen 36-38 colony stimulating factor 1 Homo sapiens 109-145 24736562-3 2014 We found that primary human corneal epithelial cells (PHCEC), fibroblasts (PHKF) and allogeneic macrophages (M1, GM-CSF; M2, M-CSF) were capable of generating cortisol (M1>PHKF>M2>PHCEC) but in corneal cells, this was independent of Toll-like receptor (TLR) activation. Hydrocortisone 159-167 colony stimulating factor 1 Homo sapiens 114-119 24038146-2 2014 In this study, we explored the role of the Ca(2+)i signaling transduction pathway in the commitment of hematopoietic stem/progenitor cells to either the monocytic or granulocytic lineage in response to macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF). ca(2+)i 43-50 colony stimulating factor 1 Homo sapiens 202-238 24473090-9 2014 Under oxidative stress, M-CSF may produce signals that are cumulative/synergistic with host mediators (e.g., low levels of histamine), facilitating tumor-directed expression of decoy receptors and immune suppressive factors (e.g., dTNFR, IL-5, IL-10, TGF-b, PGE2). Histamine 123-132 colony stimulating factor 1 Homo sapiens 24-29 24473090-9 2014 Under oxidative stress, M-CSF may produce signals that are cumulative/synergistic with host mediators (e.g., low levels of histamine), facilitating tumor-directed expression of decoy receptors and immune suppressive factors (e.g., dTNFR, IL-5, IL-10, TGF-b, PGE2). Dinoprostone 258-262 colony stimulating factor 1 Homo sapiens 24-29 24038146-2 2014 In this study, we explored the role of the Ca(2+)i signaling transduction pathway in the commitment of hematopoietic stem/progenitor cells to either the monocytic or granulocytic lineage in response to macrophage colony-stimulating factor (M-CSF) and granulocyte colony-stimulating factor (G-CSF). ca(2+)i 43-50 colony stimulating factor 1 Homo sapiens 240-245 21938481-0 2012 Bisphosphonates modulate the expression of OPG and M-CSF in hMSC-derived osteoblasts. Diphosphonates 0-15 colony stimulating factor 1 Homo sapiens 51-56 24382441-13 2013 It was found that most significant addition markers of tumor progression with presence of DTC in BM are the levels of cytokines such as TNF in BM and PB, CSF-1 and IL-6 in PB and endogenous IFN in BM and PB of BC patients. dtc 90-93 colony stimulating factor 1 Homo sapiens 154-159 23648053-4 2013 Here we show that pY721-based signaling is necessary for CSF-1-stimulated PtdIns(3,4,5)P production. ptdins(3,4,5)p 74-88 colony stimulating factor 1 Homo sapiens 57-62 23443487-0 2013 A crucial role for reactive oxygen species in macrophage colony-stimulating factor-induced RANK expression in osteoclastic differentiation. Reactive Oxygen Species 19-42 colony stimulating factor 1 Homo sapiens 46-82 23443487-2 2013 M-CSF transiently increased the intracellular level of reactive oxygen species (ROS) through an NADPH oxidase (Nox) and induced the expression of receptor for activation of nuclear factor-kappaB (RANK) in early-stage osteoclast precursor cells (c-fms+RANK-). Reactive Oxygen Species 55-78 colony stimulating factor 1 Homo sapiens 0-5 23443487-2 2013 M-CSF transiently increased the intracellular level of reactive oxygen species (ROS) through an NADPH oxidase (Nox) and induced the expression of receptor for activation of nuclear factor-kappaB (RANK) in early-stage osteoclast precursor cells (c-fms+RANK-). Reactive Oxygen Species 80-83 colony stimulating factor 1 Homo sapiens 0-5 22773056-7 2013 RESULTS: RAF265 significantly impaired in vitro differentiation of PBMCs to OCs induced by receptor activator of NF-kB ligand (RANKL) and M-CSF (IC(50) 160 nM). RAF265 9-15 colony stimulating factor 1 Homo sapiens 138-143 22909061-0 2012 Regulation of colony stimulating factor-1 expression and ovarian cancer cell behavior in vitro by miR-128 and miR-152. mir-128 98-105 colony stimulating factor 1 Homo sapiens 14-41 24391839-0 2013 Amelioration of cancer stem cells in macrophage colony stimulating factor-expressing U87MG-human glioblastoma upon 5-fluorouracil therapy. Fluorouracil 115-129 colony stimulating factor 1 Homo sapiens 37-73 24391839-4 2013 Cytotoxicity of anti-cancer drug 5-fluorouracil (5-FU) was evaluated on both U87MG and U87-MCSF cells. Fluorouracil 33-47 colony stimulating factor 1 Homo sapiens 91-95 24391839-4 2013 Cytotoxicity of anti-cancer drug 5-fluorouracil (5-FU) was evaluated on both U87MG and U87-MCSF cells. Fluorouracil 49-53 colony stimulating factor 1 Homo sapiens 91-95 24391839-5 2013 Interestingly, the proliferation of U87-MCSF cells was less (p<0.001) than that of U87MG cells alone, after treatment with 5-FU. Fluorouracil 126-130 colony stimulating factor 1 Homo sapiens 40-44 24391839-6 2013 Significant decrease in expression levels of cyclin E and A2 quantified by real time PCR analysis corroborated the reduced proliferation of 5-FU treated U87-MCSF cells. Fluorouracil 140-144 colony stimulating factor 1 Homo sapiens 157-161 24391839-8 2013 Notch-1 upregulation induced a possible epithelial-mesenchymal transition in U87-MCSF cells, which accounted for an increase in the proportion of CD24(high)/CD44(less) cancer stem cells in U87-MCSF cells after 5-FU treatment. Fluorouracil 210-214 colony stimulating factor 1 Homo sapiens 81-85 24391839-9 2013 The elevated resistance of U87-MCSF cells towards 5-FU was due to the increase in the expressions (10.2 and 6 fold) of ABCB1 and mdm2, respectively. Fluorouracil 50-54 colony stimulating factor 1 Homo sapiens 31-35 24391839-11 2013 Our studies provided mechanistic insights into drug resistance of U87MG cells and also described the pivotal role played by MCSF in augmenting the resistance of U87MG cells to 5-FU. Fluorouracil 176-180 colony stimulating factor 1 Homo sapiens 124-128 23183906-11 2013 Indomethacin also enhanced the production of tumor necrosis factor-alpha (TNF-alpha), macrophage colony-stimulating factor (M-CSF), and matrix metalloproteinase-9 (MMP-9) under periodic hypoxia compared to normoxia. Indomethacin 0-12 colony stimulating factor 1 Homo sapiens 86-122 23183906-11 2013 Indomethacin also enhanced the production of tumor necrosis factor-alpha (TNF-alpha), macrophage colony-stimulating factor (M-CSF), and matrix metalloproteinase-9 (MMP-9) under periodic hypoxia compared to normoxia. Indomethacin 0-12 colony stimulating factor 1 Homo sapiens 124-129 24083094-6 2013 Butyric acid suppressed HIV expression while succinic acid significantly increased expression in macrophages differentiated with either GM-CSF or M-CSF. Succinic Acid 45-58 colony stimulating factor 1 Homo sapiens 137-142 24019961-2 2013 We previously reported that the proline 72 polymorphic variant of p53 (P72) demonstrates increased ability to transactivate a subset of genes, relative to arginine 72 (R72); one of these genes is macrophage colony stimulating factor (CSF1). Proline 32-39 colony stimulating factor 1 Homo sapiens 234-238 23570706-2 2013 To date, limited data regarding the influence of age, gender, diabetes, smoking, and alcohol consumption on the systemic expression of M-CSF and VEGF after long bone fracture exist. Alcohols 85-92 colony stimulating factor 1 Homo sapiens 135-140 23668619-3 2013 Imatinib is a tirosin-kinase inhibitors (TKI) active against CSF1-receptor whose activity in naive PVNS was already described. Imatinib Mesylate 0-8 colony stimulating factor 1 Homo sapiens 61-65 23668619-4 2013 We report on two PVNS patients who responded to imatinib after failure to nilotinib, another CSF1-receptor inhibitor. Imatinib Mesylate 48-56 colony stimulating factor 1 Homo sapiens 93-97 23443487-5 2013 These results suggested that ROS produced in response to M-CSF via a process mediated by Nox2 acted as an intracellular signaling mediator for RANK expression through the activation of ERK and the expression of PU.1 and MITF in early-stage osteoclast precursor cells. Reactive Oxygen Species 29-32 colony stimulating factor 1 Homo sapiens 57-62 23042575-5 2013 Furthermore, although low severity (CSF ~ 1.94) dilute acid pretreatment of a xylan-Avicel mixture hydrolyzed most of the xylan (98%) and produced negligible amounts of pseudo-lignin, enzymatic conversion of cellulose dropped significantly (>25%) compared to cellulose pretreated alone at the same conditions. xylan-avicel 78-90 colony stimulating factor 1 Homo sapiens 36-43 23042575-5 2013 Furthermore, although low severity (CSF ~ 1.94) dilute acid pretreatment of a xylan-Avicel mixture hydrolyzed most of the xylan (98%) and produced negligible amounts of pseudo-lignin, enzymatic conversion of cellulose dropped significantly (>25%) compared to cellulose pretreated alone at the same conditions. Xylans 78-83 colony stimulating factor 1 Homo sapiens 36-43 21938481-6 2012 Treatment of differentiating cells with alendronate or pamidronate, nitrogen-containing BPs increase the expression of OPG, which suppresses osteoclastogenesis, whereas it decreases the expression of M-CSF, which enhances preosteoclast formation. Alendronate 40-51 colony stimulating factor 1 Homo sapiens 200-205 21938481-6 2012 Treatment of differentiating cells with alendronate or pamidronate, nitrogen-containing BPs increase the expression of OPG, which suppresses osteoclastogenesis, whereas it decreases the expression of M-CSF, which enhances preosteoclast formation. Pamidronate 55-66 colony stimulating factor 1 Homo sapiens 200-205 21938481-6 2012 Treatment of differentiating cells with alendronate or pamidronate, nitrogen-containing BPs increase the expression of OPG, which suppresses osteoclastogenesis, whereas it decreases the expression of M-CSF, which enhances preosteoclast formation. Nitrogen 68-76 colony stimulating factor 1 Homo sapiens 200-205 21895511-8 2012 TNF-alpha treatment promoted NF-kappaB p65 binding to the M-CSF promoter in phorbol 12-myristate 13-acetate (PMA) treated U937 cells chronically infected with HIV-1 (U1 cells), but not in PMA treated uninfected U937 cells, suggesting that the presence of HIV-1 increases the NF-kappaB response. Tetradecanoylphorbol Acetate 76-107 colony stimulating factor 1 Homo sapiens 58-63 22572726-4 2012 RECENT FINDINGS: Imatinib, a tyrosine kinase inhibitor, blocks expression of colony stimulating factor 1 (CSF1) by a small subpopulation of tumor cells that recruit CSF1-bearing nonneoplastic cells. Imatinib Mesylate 17-25 colony stimulating factor 1 Homo sapiens 77-104 22572726-4 2012 RECENT FINDINGS: Imatinib, a tyrosine kinase inhibitor, blocks expression of colony stimulating factor 1 (CSF1) by a small subpopulation of tumor cells that recruit CSF1-bearing nonneoplastic cells. Imatinib Mesylate 17-25 colony stimulating factor 1 Homo sapiens 106-110 22572726-4 2012 RECENT FINDINGS: Imatinib, a tyrosine kinase inhibitor, blocks expression of colony stimulating factor 1 (CSF1) by a small subpopulation of tumor cells that recruit CSF1-bearing nonneoplastic cells. Imatinib Mesylate 17-25 colony stimulating factor 1 Homo sapiens 165-169 22554285-7 2012 RESULTS: In univariate analyses increased expression of M-CSF (P = 0.034), Ki67 (P < 0.001) and TGF-beta (P = 0.003) in tumor correlated with shorter disease-specific survival (DSS). dss 180-183 colony stimulating factor 1 Homo sapiens 56-61 22038446-3 2012 The aim of this study was therefore to analyse alterations in the expression of M-CSF, VEGF and TGF-ss1 after treatment with enoxaparin in patients with long bone fracture to investigate the effect of LMWH on human fracture healing. Enoxaparin 125-135 colony stimulating factor 1 Homo sapiens 80-85 22038446-7 2012 RESULTS: M-CSF serum concentrations were found to be significantly higher only at 48 weeks after surgery in enoxaparin. Enoxaparin 108-118 colony stimulating factor 1 Homo sapiens 9-14 22038446-10 2012 CONCLUSION: This is the first comparative systemic measurement of M-CSF, VEGF and TGF-ss1 serum levels in patients with and without enoxaparin after long bone fracture. Enoxaparin 132-142 colony stimulating factor 1 Homo sapiens 66-71 22038446-11 2012 Significant differences of the expression of the growth factors after enoxaparin therapy were only observed at week 48 after surgery for M-CSF and TGF-ss1. Enoxaparin 70-80 colony stimulating factor 1 Homo sapiens 137-142 22468857-0 2012 CSF-1 signaling in macrophages: pleiotrophy through phosphotyrosine-based signaling pathways. Phosphotyrosine 52-67 colony stimulating factor 1 Homo sapiens 0-5 22468857-5 2012 CSF-1-induced CSF-1R activation triggers autophosphorylation of several intracellular tyrosine residues, leading to initiation of an array of phosphotyrosine-based signaling cascades that mediate the wide variety of cellular responses to CSF-1. Tyrosine 86-94 colony stimulating factor 1 Homo sapiens 0-5 22468857-5 2012 CSF-1-induced CSF-1R activation triggers autophosphorylation of several intracellular tyrosine residues, leading to initiation of an array of phosphotyrosine-based signaling cascades that mediate the wide variety of cellular responses to CSF-1. Tyrosine 86-94 colony stimulating factor 1 Homo sapiens 14-19 22468857-5 2012 CSF-1-induced CSF-1R activation triggers autophosphorylation of several intracellular tyrosine residues, leading to initiation of an array of phosphotyrosine-based signaling cascades that mediate the wide variety of cellular responses to CSF-1. Tyrosine 86-94 colony stimulating factor 1 Homo sapiens 14-19 22468857-5 2012 CSF-1-induced CSF-1R activation triggers autophosphorylation of several intracellular tyrosine residues, leading to initiation of an array of phosphotyrosine-based signaling cascades that mediate the wide variety of cellular responses to CSF-1. Phosphotyrosine 142-157 colony stimulating factor 1 Homo sapiens 0-5 22468857-5 2012 CSF-1-induced CSF-1R activation triggers autophosphorylation of several intracellular tyrosine residues, leading to initiation of an array of phosphotyrosine-based signaling cascades that mediate the wide variety of cellular responses to CSF-1. Phosphotyrosine 142-157 colony stimulating factor 1 Homo sapiens 14-19 22468857-5 2012 CSF-1-induced CSF-1R activation triggers autophosphorylation of several intracellular tyrosine residues, leading to initiation of an array of phosphotyrosine-based signaling cascades that mediate the wide variety of cellular responses to CSF-1. Phosphotyrosine 142-157 colony stimulating factor 1 Homo sapiens 14-19 22780915-8 2012 The profiles of cytokine gene expression in peripheral blood were set: a positive correlation between glucose and MCSF, HMOX1 or TNFalpha were found. Glucose 102-109 colony stimulating factor 1 Homo sapiens 114-118 22466005-3 2012 Based on this knowledge, this study aimed to define the effects of the TLR3 ligand polyriboinosinic:polyribocytidylic acid (poly(I:C)) on the expression of adhesion molecules and macrophage colony-stimulating factor (M-CSF) on resident glomerular cells. polyriboinosinic 83-99 colony stimulating factor 1 Homo sapiens 179-215 22466005-3 2012 Based on this knowledge, this study aimed to define the effects of the TLR3 ligand polyriboinosinic:polyribocytidylic acid (poly(I:C)) on the expression of adhesion molecules and macrophage colony-stimulating factor (M-CSF) on resident glomerular cells. polyriboinosinic 83-99 colony stimulating factor 1 Homo sapiens 217-222 22466005-3 2012 Based on this knowledge, this study aimed to define the effects of the TLR3 ligand polyriboinosinic:polyribocytidylic acid (poly(I:C)) on the expression of adhesion molecules and macrophage colony-stimulating factor (M-CSF) on resident glomerular cells. Poly C 100-122 colony stimulating factor 1 Homo sapiens 179-215 22466005-3 2012 Based on this knowledge, this study aimed to define the effects of the TLR3 ligand polyriboinosinic:polyribocytidylic acid (poly(I:C)) on the expression of adhesion molecules and macrophage colony-stimulating factor (M-CSF) on resident glomerular cells. Poly C 100-122 colony stimulating factor 1 Homo sapiens 217-222 22466005-3 2012 Based on this knowledge, this study aimed to define the effects of the TLR3 ligand polyriboinosinic:polyribocytidylic acid (poly(I:C)) on the expression of adhesion molecules and macrophage colony-stimulating factor (M-CSF) on resident glomerular cells. poly 83-87 colony stimulating factor 1 Homo sapiens 179-215 22466005-3 2012 Based on this knowledge, this study aimed to define the effects of the TLR3 ligand polyriboinosinic:polyribocytidylic acid (poly(I:C)) on the expression of adhesion molecules and macrophage colony-stimulating factor (M-CSF) on resident glomerular cells. poly 83-87 colony stimulating factor 1 Homo sapiens 217-222 22375015-1 2012 Colony-stimulating factor-1 (CSF-1)-stimulated CSF-1 receptor (CSF-1R) tyrosine phosphorylation initiates survival, proliferation, and differentiation signaling pathways in macrophages. Tyrosine 71-79 colony stimulating factor 1 Homo sapiens 0-27 22375015-1 2012 Colony-stimulating factor-1 (CSF-1)-stimulated CSF-1 receptor (CSF-1R) tyrosine phosphorylation initiates survival, proliferation, and differentiation signaling pathways in macrophages. Tyrosine 71-79 colony stimulating factor 1 Homo sapiens 29-34 22375015-3 2012 YEF, a CSF-1R in which all eight tyrosines phosphorylated in the activated receptor were mutated to phenylalanine, lacks in vitro kinase activity and in vivo CSF-1-regulated tyrosine phosphorylation. Tyrosine 33-42 colony stimulating factor 1 Homo sapiens 7-12 22375015-3 2012 YEF, a CSF-1R in which all eight tyrosines phosphorylated in the activated receptor were mutated to phenylalanine, lacks in vitro kinase activity and in vivo CSF-1-regulated tyrosine phosphorylation. Phenylalanine 100-113 colony stimulating factor 1 Homo sapiens 7-12 22375015-3 2012 YEF, a CSF-1R in which all eight tyrosines phosphorylated in the activated receptor were mutated to phenylalanine, lacks in vitro kinase activity and in vivo CSF-1-regulated tyrosine phosphorylation. Tyrosine 33-41 colony stimulating factor 1 Homo sapiens 7-12 22375015-4 2012 The addition of Tyr-807 alone to the YEF backbone (Y807AB) led to CSF-1-independent but receptor kinase-dependent proliferation, without detectable activation loop Tyr-807 phosphorylation. Tyrosine 16-19 colony stimulating factor 1 Homo sapiens 66-71 22375015-5 2012 The addition of Tyr-559 alone (Y559AB) supported a low level of CSF-1-independent proliferation that was slightly enhanced by CSF-1, indicating that Tyr-559 has a positive Tyr-807-independent effect. Tyrosine 16-19 colony stimulating factor 1 Homo sapiens 64-69 22375015-5 2012 The addition of Tyr-559 alone (Y559AB) supported a low level of CSF-1-independent proliferation that was slightly enhanced by CSF-1, indicating that Tyr-559 has a positive Tyr-807-independent effect. Tyrosine 16-19 colony stimulating factor 1 Homo sapiens 126-131 22375015-5 2012 The addition of Tyr-559 alone (Y559AB) supported a low level of CSF-1-independent proliferation that was slightly enhanced by CSF-1, indicating that Tyr-559 has a positive Tyr-807-independent effect. Tyrosine 149-152 colony stimulating factor 1 Homo sapiens 64-69 22375015-5 2012 The addition of Tyr-559 alone (Y559AB) supported a low level of CSF-1-independent proliferation that was slightly enhanced by CSF-1, indicating that Tyr-559 has a positive Tyr-807-independent effect. Tyrosine 149-152 colony stimulating factor 1 Homo sapiens 126-131 22375015-5 2012 The addition of Tyr-559 alone (Y559AB) supported a low level of CSF-1-independent proliferation that was slightly enhanced by CSF-1, indicating that Tyr-559 has a positive Tyr-807-independent effect. Tyrosine 149-152 colony stimulating factor 1 Homo sapiens 64-69 22375015-5 2012 The addition of Tyr-559 alone (Y559AB) supported a low level of CSF-1-independent proliferation that was slightly enhanced by CSF-1, indicating that Tyr-559 has a positive Tyr-807-independent effect. Tyrosine 149-152 colony stimulating factor 1 Homo sapiens 126-131 22375015-9 2012 Thus Tyr-807 confers sufficient kinase activity for strong CSF-1-independent proliferation, whereas Tyr-559 maintains the receptor in an inactive state. Tyrosine 5-8 colony stimulating factor 1 Homo sapiens 59-64 22375015-10 2012 Tyr-559 phosphorylation releases this restraint and may also contribute to the CSF-1-regulated proliferative response by activating Src family kinase. Tyrosine 0-3 colony stimulating factor 1 Homo sapiens 79-84 21895511-8 2012 TNF-alpha treatment promoted NF-kappaB p65 binding to the M-CSF promoter in phorbol 12-myristate 13-acetate (PMA) treated U937 cells chronically infected with HIV-1 (U1 cells), but not in PMA treated uninfected U937 cells, suggesting that the presence of HIV-1 increases the NF-kappaB response. Tetradecanoylphorbol Acetate 109-112 colony stimulating factor 1 Homo sapiens 58-63 22479263-9 2012 These effects of thrombin were significantly reduced by the addition of argatroban (M-CSF, p < 0.01; GM-CSF, p < 0.01; G-CSF, p < 0.05). argatroban 72-82 colony stimulating factor 1 Homo sapiens 84-89 22212249-9 2012 The conditioned media from these cultures activates macrophages, which promote caspase 3/7-dependent EVT apoptosis with antibodies against GM-CSF or M-CSF blocking this effect. EVT 101-104 colony stimulating factor 1 Homo sapiens 140-145 22212249-11 2012 Both GM-CSF and M-CSF activate macrophages, which initiate caspase-dependent EVT apoptosis. EVT 77-80 colony stimulating factor 1 Homo sapiens 6-11 21664461-0 2011 Reactive oxygen species regulate M-CSF-induced monocyte/macrophage proliferation through SHP1 oxidation. Reactive Oxygen Species 0-23 colony stimulating factor 1 Homo sapiens 33-38 22197934-5 2011 In vitro, CSF-1 stimulation resulted in rapid autophosphorylation of selected tyrosine residues in the kinase domain of wild-type but not mutant CSF1R, suggesting that HDLS may result from partial loss of CSF1R function. Tyrosine 78-86 colony stimulating factor 1 Homo sapiens 10-15 22027642-6 2011 Sunitinib is a multikinase inhibitor that targets the PDGF-alpha- and ?beta-, VEGF-1-3-, KIT-, FLT3-, CSF-1- and RET-receptor, thereby impairing tumour proliferation, pathological angiogenesis and metastasation. Sunitinib 0-9 colony stimulating factor 1 Homo sapiens 102-125 21664461-1 2011 Macrophage colony-stimulating factor (M-CSF) stimulation results in the production of reactive oxygen species (ROS) that participate in the proliferation of monocyte/macrophage. Reactive Oxygen Species 86-109 colony stimulating factor 1 Homo sapiens 0-36 21664461-1 2011 Macrophage colony-stimulating factor (M-CSF) stimulation results in the production of reactive oxygen species (ROS) that participate in the proliferation of monocyte/macrophage. Reactive Oxygen Species 86-109 colony stimulating factor 1 Homo sapiens 38-43 21664461-1 2011 Macrophage colony-stimulating factor (M-CSF) stimulation results in the production of reactive oxygen species (ROS) that participate in the proliferation of monocyte/macrophage. Reactive Oxygen Species 111-114 colony stimulating factor 1 Homo sapiens 0-36 21664461-1 2011 Macrophage colony-stimulating factor (M-CSF) stimulation results in the production of reactive oxygen species (ROS) that participate in the proliferation of monocyte/macrophage. Reactive Oxygen Species 111-114 colony stimulating factor 1 Homo sapiens 38-43 21664461-2 2011 However, the molecular mechanisms whereby ROS modulate the signaling processes of M-CSF remain poorly defined. Reactive Oxygen Species 42-45 colony stimulating factor 1 Homo sapiens 82-87 21664461-4 2011 Application of diphenylene iodonium (DPI) inhibited the responses of BMMs to M-CSF, including ROS production, cell proliferation, and phosphorylation of c-Fms as well as Akt kinase, but not of MAP kinases such as ERK, p38, and JNK. diphenyleneiodonium 15-35 colony stimulating factor 1 Homo sapiens 77-82 21664461-4 2011 Application of diphenylene iodonium (DPI) inhibited the responses of BMMs to M-CSF, including ROS production, cell proliferation, and phosphorylation of c-Fms as well as Akt kinase, but not of MAP kinases such as ERK, p38, and JNK. diphenyleneiodonium 37-40 colony stimulating factor 1 Homo sapiens 77-82 21664461-4 2011 Application of diphenylene iodonium (DPI) inhibited the responses of BMMs to M-CSF, including ROS production, cell proliferation, and phosphorylation of c-Fms as well as Akt kinase, but not of MAP kinases such as ERK, p38, and JNK. Reactive Oxygen Species 94-97 colony stimulating factor 1 Homo sapiens 77-82 21664461-6 2011 These findings demonstrate that M-CSF-mediated ROS generation leads to SHP1 oxidation, which promotes cell proliferation through the PI3K/Akt-dependent signaling pathway. Reactive Oxygen Species 47-50 colony stimulating factor 1 Homo sapiens 32-37 21294864-11 2011 On the other hand, IL-17 enhanced pannus-like tissue growth, the production of TNF-alpha and M-CSF and the development of osteoclastic activity in the presence of indomethacin, an inhibitor of endogenous prostanoid production, while exogenous addition of PGE1 suppressed their activities. Indomethacin 163-175 colony stimulating factor 1 Homo sapiens 93-98 21792394-2 2011 As a consequence of the conversion of chondroitin sulfate (CS) to dermatan sulfate (DS), the glycosaminoglycans become more flexible and enable DS to perform more sophisticated signaling functions. Chondroitin Sulfates 38-57 colony stimulating factor 1 Homo sapiens 59-61 21792394-2 2011 As a consequence of the conversion of chondroitin sulfate (CS) to dermatan sulfate (DS), the glycosaminoglycans become more flexible and enable DS to perform more sophisticated signaling functions. Dermatan Sulfate 66-82 colony stimulating factor 1 Homo sapiens 59-61 21792394-2 2011 As a consequence of the conversion of chondroitin sulfate (CS) to dermatan sulfate (DS), the glycosaminoglycans become more flexible and enable DS to perform more sophisticated signaling functions. Glycosaminoglycans 93-111 colony stimulating factor 1 Homo sapiens 59-61 21792394-2 2011 As a consequence of the conversion of chondroitin sulfate (CS) to dermatan sulfate (DS), the glycosaminoglycans become more flexible and enable DS to perform more sophisticated signaling functions. Dermatan Sulfate 144-146 colony stimulating factor 1 Homo sapiens 59-61 21792394-4 2011 C-terminal truncation constructs from S222A enabled us to identify an amino acid segment that lies within the CSF-1 part which prevents DS synthesis. Dermatan Sulfate 136-138 colony stimulating factor 1 Homo sapiens 110-115 21389328-4 2011 Moreover, an inhibitor of activin receptor-like kinase 4/5/7 (ALK4/5/7 or SB431542) promoted M2 (M-CSF) marker expression but limited the acquisition of M1 (GM-CSF) polarization markers, suggesting a role for Smad2/3 activation in macrophage polarization. 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide 74-82 colony stimulating factor 1 Homo sapiens 97-102 21377872-10 2011 In subsequent fermentations with pretreated biomass, the ethanol concentration was maximal at 19.2g/l at CSF 1.9 when maleic acid was used as the pretreatment catalyst. Ethanol 57-64 colony stimulating factor 1 Homo sapiens 105-110 21377872-10 2011 In subsequent fermentations with pretreated biomass, the ethanol concentration was maximal at 19.2g/l at CSF 1.9 when maleic acid was used as the pretreatment catalyst. maleic acid 118-129 colony stimulating factor 1 Homo sapiens 105-110 20876703-7 2010 Neutralization of CSF-1 in MDA-CM using CSF-1 antibody inhibited MDA-CM-induced iNOS protein expression and migration of macrophages, and CSF-1-induced iNOS protein and migration was blocked by adding JNK inhibitor SP and NF-kappaB inhibitor BAY. TFF2 protein, human 215-217 colony stimulating factor 1 Homo sapiens 18-23 20619482-4 2011 In this study we investigated the regulation of M-CSF production by Th1 and Th2 cytokines (IFN-gamma and IL-4) and tolerogenic stimuli - glucocorticoid dexamethasone in primary human monocyte derived macrophages. Dexamethasone 152-165 colony stimulating factor 1 Homo sapiens 48-53 20619482-9 2011 Analyzing the mechanism of this responsiveness, we showed that dexamethasone up-regulates surface expression of M-CSF receptor - CSF-1R. Dexamethasone 63-76 colony stimulating factor 1 Homo sapiens 112-117 22216091-3 2011 The general protein kinase C (PKC) inhibitor Ro-31-8220, the conventional PKCalpha/beta inhibitor Go-6976, overexpression of dominant negative PKCalpha constructs and PKCalpha siRNA reduced NF-kappaB activity in response to M-CSF. Ro 31-8220 45-55 colony stimulating factor 1 Homo sapiens 224-229 22096574-7 2011 Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation. Imatinib Mesylate 74-82 colony stimulating factor 1 Homo sapiens 31-36 22096574-7 2011 Furthermore, the inhibition of CSF-1/CSF-1R signaling, by CSF-1R siRNA or imatinib treatment, impaired CSF-1 induced ERK1/2 activation and cell proliferation. Imatinib Mesylate 74-82 colony stimulating factor 1 Homo sapiens 37-42 21738673-8 2011 The mitogen-activated protein kinase kinase (MEK) 1 inhibitor PD98059 partially blocked augmentation of resorption by M-CSF. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 62-69 colony stimulating factor 1 Homo sapiens 118-123 20829061-6 2010 Furthermore, GW2580, a c-FMS kinase inhibitor, inhibited the induction of MCP-1 by M-CSF or IL-34 in a concentration dependent manner. 5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine 13-19 colony stimulating factor 1 Homo sapiens 83-88 20876703-7 2010 Neutralization of CSF-1 in MDA-CM using CSF-1 antibody inhibited MDA-CM-induced iNOS protein expression and migration of macrophages, and CSF-1-induced iNOS protein and migration was blocked by adding JNK inhibitor SP and NF-kappaB inhibitor BAY. TFF2 protein, human 215-217 colony stimulating factor 1 Homo sapiens 40-45 20876703-7 2010 Neutralization of CSF-1 in MDA-CM using CSF-1 antibody inhibited MDA-CM-induced iNOS protein expression and migration of macrophages, and CSF-1-induced iNOS protein and migration was blocked by adding JNK inhibitor SP and NF-kappaB inhibitor BAY. TFF2 protein, human 215-217 colony stimulating factor 1 Homo sapiens 40-45 20613670-2 2010 The aim of this study was to investigate the effect of raloxifene, a selective estrogen receptor modulator, on serum M-CSF and IL-18 levels, cytokines that are presumably involved in the pathogenesis of atherosclerosis. Raloxifene Hydrochloride 55-65 colony stimulating factor 1 Homo sapiens 117-122 20613670-7 2010 M-CSF levels were reduced by 5.94% in the raloxifene group, but the difference was not statistically significant. Raloxifene Hydrochloride 42-52 colony stimulating factor 1 Homo sapiens 0-5 20579763-6 2010 Analysis of PL species profiles revealed that GM-CSF/IL-4 differentiated cells have increased amounts of longer and more desaturated phospatidylethanolamine (PE) and phosphatidylserine (PS) species, but lower amounts of shorter and less desaturated PE and PS species than M-CSF differentiated cells. phospatidylethanolamine 133-156 colony stimulating factor 1 Homo sapiens 47-52 20580464-6 2010 In contrast to the HO-1 inhibitor tin protoporphyrin (SnPP), the administration of cobalt protoporphyrin (CoPP), a potent inducer of HO-1 resulted in increased LPS-triggered IL-10 release from M2 (M-CSF) macrophages. cobaltiprotoporphyrin 83-104 colony stimulating factor 1 Homo sapiens 197-202 21049007-4 2010 Here, we conducted quantitative mass spectrometry utilizing stable isotope labeling (SILAC) analysis to profile candidate SRC-substrates induced by the CSF-1R tyrosine kinase by comparing the phosphotyrosine-containing peptides from cells expressing either CSF-1R or a mutant form of this RTK that is unable to bind to SFKs. Phosphotyrosine 192-207 colony stimulating factor 1 Homo sapiens 152-157 21049007-4 2010 Here, we conducted quantitative mass spectrometry utilizing stable isotope labeling (SILAC) analysis to profile candidate SRC-substrates induced by the CSF-1R tyrosine kinase by comparing the phosphotyrosine-containing peptides from cells expressing either CSF-1R or a mutant form of this RTK that is unable to bind to SFKs. Peptides 219-227 colony stimulating factor 1 Homo sapiens 152-157 20614110-11 2010 RT-PCR showed that H2O2 stimulated the expression of M-CSF and RANKL and increased the RANKL/OPG ratio. Hydrogen Peroxide 19-23 colony stimulating factor 1 Homo sapiens 53-58 20580464-6 2010 In contrast to the HO-1 inhibitor tin protoporphyrin (SnPP), the administration of cobalt protoporphyrin (CoPP), a potent inducer of HO-1 resulted in increased LPS-triggered IL-10 release from M2 (M-CSF) macrophages. cobaltiprotoporphyrin 106-110 colony stimulating factor 1 Homo sapiens 197-202 20579763-6 2010 Analysis of PL species profiles revealed that GM-CSF/IL-4 differentiated cells have increased amounts of longer and more desaturated phospatidylethanolamine (PE) and phosphatidylserine (PS) species, but lower amounts of shorter and less desaturated PE and PS species than M-CSF differentiated cells. pe 158-160 colony stimulating factor 1 Homo sapiens 47-52 20579763-6 2010 Analysis of PL species profiles revealed that GM-CSF/IL-4 differentiated cells have increased amounts of longer and more desaturated phospatidylethanolamine (PE) and phosphatidylserine (PS) species, but lower amounts of shorter and less desaturated PE and PS species than M-CSF differentiated cells. Phosphatidylserines 166-184 colony stimulating factor 1 Homo sapiens 47-52 20579763-6 2010 Analysis of PL species profiles revealed that GM-CSF/IL-4 differentiated cells have increased amounts of longer and more desaturated phospatidylethanolamine (PE) and phosphatidylserine (PS) species, but lower amounts of shorter and less desaturated PE and PS species than M-CSF differentiated cells. Phosphatidylserines 186-188 colony stimulating factor 1 Homo sapiens 47-52 20579763-6 2010 Analysis of PL species profiles revealed that GM-CSF/IL-4 differentiated cells have increased amounts of longer and more desaturated phospatidylethanolamine (PE) and phosphatidylserine (PS) species, but lower amounts of shorter and less desaturated PE and PS species than M-CSF differentiated cells. pe 249-251 colony stimulating factor 1 Homo sapiens 47-52 20579763-8 2010 Taken together, our results show that GM-CSF/IL-4 compared to M-CSF differentiated monocytes have less mono-unsaturated FA and PL species, which are due to lower SCD activity observed in DCs. Phospholipids 127-129 colony stimulating factor 1 Homo sapiens 39-44 20580464-3 2010 A different iron metabolism gene signature was detected in both macrophage types, with the heme regulatory molecules CD163 and Heme Oxygenase-1 (HO-1) being preferentially expressed by M2 (M-CSF) macrophages. Iron 12-16 colony stimulating factor 1 Homo sapiens 189-194 20580464-3 2010 A different iron metabolism gene signature was detected in both macrophage types, with the heme regulatory molecules CD163 and Heme Oxygenase-1 (HO-1) being preferentially expressed by M2 (M-CSF) macrophages. Heme 91-95 colony stimulating factor 1 Homo sapiens 189-194 20570927-5 2010 RESULTS: Although sorafenib significantly inhibited tumor growth and lung metastasis, it induced a significant increase in peripheral recruitment and intratumoral infiltration of F4/80- and CD11b-positive cells, which was accompanied with elevation of colony-stimulating factor-1, stromal-derived factor 1alpha, and vascular endothelial growth factor in the tumor and elevation of plasma colony-stimulating factor-1 and mouse vascular endothelial growth factor in peripheral blood, suggesting the role of macrophages in tumor progression under sorafenib treatment. Sorafenib 18-27 colony stimulating factor 1 Homo sapiens 252-279 20570927-5 2010 RESULTS: Although sorafenib significantly inhibited tumor growth and lung metastasis, it induced a significant increase in peripheral recruitment and intratumoral infiltration of F4/80- and CD11b-positive cells, which was accompanied with elevation of colony-stimulating factor-1, stromal-derived factor 1alpha, and vascular endothelial growth factor in the tumor and elevation of plasma colony-stimulating factor-1 and mouse vascular endothelial growth factor in peripheral blood, suggesting the role of macrophages in tumor progression under sorafenib treatment. Sorafenib 18-27 colony stimulating factor 1 Homo sapiens 388-415 20385828-2 2010 Here we demonstrate that macrophage colony-stimulating factor (M-CSF)-dependent differentiation of primary human monocytes from healthy volunteers induces transcription of SREBP-1c target genes required for fatty acid (FA) biosynthesis and impairs transcription of SREBP-2 target genes required for cholesterol synthesis. Cholesterol 299-310 colony stimulating factor 1 Homo sapiens 63-68 20497911-5 2010 Imatinib is used in the treatment of DFSP, characterized by a translocation of the gene PDGF, or in pigmented villonodular synovitis (PVNS), a tumor of soft part also locally aggressive, caused by an abnormality of the gene coding for the M-CSF. Imatinib Mesylate 0-8 colony stimulating factor 1 Homo sapiens 239-244 20346376-12 2010 Simvastatin also activated ERK pathways and inactivated Src phosphorylation in human osteoclasts differentiated by M-CSF and RANKL treatments. Simvastatin 0-11 colony stimulating factor 1 Homo sapiens 115-120 20385828-2 2010 Here we demonstrate that macrophage colony-stimulating factor (M-CSF)-dependent differentiation of primary human monocytes from healthy volunteers induces transcription of SREBP-1c target genes required for fatty acid (FA) biosynthesis and impairs transcription of SREBP-2 target genes required for cholesterol synthesis. Fatty Acids 207-217 colony stimulating factor 1 Homo sapiens 25-61 20045402-7 2010 beta-CTX inversely correlated with vascular endothelial growth factor (VEGF) and albumin, and directly correlated with serum macrophage colony-stimulating factor (M-CSF). beta-ctx 0-8 colony stimulating factor 1 Homo sapiens 125-161 20385828-2 2010 Here we demonstrate that macrophage colony-stimulating factor (M-CSF)-dependent differentiation of primary human monocytes from healthy volunteers induces transcription of SREBP-1c target genes required for fatty acid (FA) biosynthesis and impairs transcription of SREBP-2 target genes required for cholesterol synthesis. Fatty Acids 207-217 colony stimulating factor 1 Homo sapiens 63-68 20385828-2 2010 Here we demonstrate that macrophage colony-stimulating factor (M-CSF)-dependent differentiation of primary human monocytes from healthy volunteers induces transcription of SREBP-1c target genes required for fatty acid (FA) biosynthesis and impairs transcription of SREBP-2 target genes required for cholesterol synthesis. Cholesterol 299-310 colony stimulating factor 1 Homo sapiens 25-61 20045402-7 2010 beta-CTX inversely correlated with vascular endothelial growth factor (VEGF) and albumin, and directly correlated with serum macrophage colony-stimulating factor (M-CSF). beta-ctx 0-8 colony stimulating factor 1 Homo sapiens 163-168 19711348-4 2010 To examine this interaction in NB in vivo, mice bearing human CSF-1-expressing SK-N-AS and CSF-1-negative SK-N-DZ NB xenografts were treated with intratumoral injections of small interfering RNAs directed against mouse CSF-1. sk-n-as 79-86 colony stimulating factor 1 Homo sapiens 62-67 19911374-5 2010 It was observed that the conditioned medium from dexamethasone osteogenic-induced bone marrow cell cultures displayed the highest osteoclastogenic potential, with similar behaviour to that observed in the presence of both M-CSF and RANKL. Dexamethasone 49-62 colony stimulating factor 1 Homo sapiens 222-227 20008303-5 2010 Here, we use the selective pharmacologic inhibitor of CSF1R signaling, GW2580, to demonstrate that CSF-1 regulates the tumor recruitment of CD11b(+)Gr-1(lo)Ly6C(hi) mononuclear MDSCs. 5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine 71-77 colony stimulating factor 1 Homo sapiens 99-104 20008303-5 2010 Here, we use the selective pharmacologic inhibitor of CSF1R signaling, GW2580, to demonstrate that CSF-1 regulates the tumor recruitment of CD11b(+)Gr-1(lo)Ly6C(hi) mononuclear MDSCs. ly6c 156-160 colony stimulating factor 1 Homo sapiens 99-104 19416641-1 2009 We previously reported that incubation of bone-marrow derived macrophages in the absence of macrophage-colony stimulating factor (M-CSF), a cytokine that is essential for their growth and survival, resulted in stimulation of acid sphingomyelinase, accumulation of ceramides, and induction of apoptosis [A. Gomez-Munoz et al. Ceramides 264-273 colony stimulating factor 1 Homo sapiens 130-135 19880194-5 2009 At high concentrations, progesterone is a potent inducer of Th2-type cytokines as well as of LIF and M-CSF production by T cells. Progesterone 24-36 colony stimulating factor 1 Homo sapiens 101-106 19376223-0 2009 Phosphatidylinostitol-3 kinase and phospholipase C enhance CSF-1-dependent macrophage survival by controlling glucose uptake. Glucose 110-117 colony stimulating factor 1 Homo sapiens 59-64 19376223-3 2009 Since we had previously shown that CSF-1 stimulates glucose uptake by macrophages, we have now investigated whether glucose metabolism is required for the survival of CSF-1-dependent macrophages as well as examined the mechanism by which CSF-1 stimulates glucose uptake. Glucose 52-59 colony stimulating factor 1 Homo sapiens 35-40 19376223-4 2009 Importantly, we found that CSF-1-induced macrophage survival required metabolism of the glucose taken up in response to CSF-1 stimulation. Glucose 88-95 colony stimulating factor 1 Homo sapiens 27-32 19376223-4 2009 Importantly, we found that CSF-1-induced macrophage survival required metabolism of the glucose taken up in response to CSF-1 stimulation. Glucose 88-95 colony stimulating factor 1 Homo sapiens 120-125 19376223-6 2009 The uptake of glucose induced by CSF-1 required intact PI3K and PLC signalling pathways, as well as the downstream effectors Akt and PKC, together with a dynamic actin cytoskeleton. Glucose 14-21 colony stimulating factor 1 Homo sapiens 33-38 19376223-8 2009 Taken together, these results suggest that CSF-1 regulates macrophage survival, in part, by stimulating glucose uptake via Glut1, and PI3K and PLC signalling pathways. Glucose 104-111 colony stimulating factor 1 Homo sapiens 43-48 19349075-6 2009 NHBC responded to PE particles by increasing the mRNA expression of several genes associated with osteoclast formation and activity (RANKL, IL-8 and M-CSF) and decreased the expression of the osteoclast antagonist, OPG. Polyethylene 18-20 colony stimulating factor 1 Homo sapiens 149-154 19453268-3 2009 Sunitinib is a multi-kinase inhibitor of VEGFR-2, PDGFR (alpha,beta), FLT-3, KIT, CSF-1 and RET. Sunitinib 0-9 colony stimulating factor 1 Homo sapiens 82-87 19951991-3 2009 We report that folate receptor beta (FRbeta), encoded by the FOLR2 gene, is a marker for macrophages generated in the presence of M-CSF (M2), but not GM-CSF (M1), and whose expression correlates with increased folate uptake ability. Folic Acid 15-21 colony stimulating factor 1 Homo sapiens 130-135 19951991-4 2009 The acquisition of folate uptake ability by macrophages is promoted by M-CSF, maintained by IL-4, prevented by GM-CSF, and reduced by IFNgamma, indicating a link between FRbeta expression and M2 polarization. Folic Acid 19-25 colony stimulating factor 1 Homo sapiens 71-76 19721010-1 2009 The differentiation of human peripheral blood monocytes into resident macrophages is driven by colony-stimulating factor-1 (CSF-1), which upon interaction with CSF-1 receptor (CSF-1R) induces within minutes the phosphorylation of its cytoplasmic tyrosine residues and the activation of multiple signaling complexes. Tyrosine 246-254 colony stimulating factor 1 Homo sapiens 95-122 19721010-1 2009 The differentiation of human peripheral blood monocytes into resident macrophages is driven by colony-stimulating factor-1 (CSF-1), which upon interaction with CSF-1 receptor (CSF-1R) induces within minutes the phosphorylation of its cytoplasmic tyrosine residues and the activation of multiple signaling complexes. Tyrosine 246-254 colony stimulating factor 1 Homo sapiens 124-129 19648688-1 2009 OBJECTIVE: To observe the influence of technetium 99Tc methylenediphosphonate (99Tc-MDP) on osteoclastogenesis induced by receptor activator of NF-kappaB ligand (RANKL) and macrophage-colony stimulating factor (M-CSF) in peripheral blood mononuclear cells in patients with rheumatoid arthritis, and to study the mechanism of 99Tc-MDP in osteoclast differentiation. technetium 99tc methylenediphosphonate 39-77 colony stimulating factor 1 Homo sapiens 173-209 19648688-1 2009 OBJECTIVE: To observe the influence of technetium 99Tc methylenediphosphonate (99Tc-MDP) on osteoclastogenesis induced by receptor activator of NF-kappaB ligand (RANKL) and macrophage-colony stimulating factor (M-CSF) in peripheral blood mononuclear cells in patients with rheumatoid arthritis, and to study the mechanism of 99Tc-MDP in osteoclast differentiation. 99mTc-Methylene diphosphonate 79-87 colony stimulating factor 1 Homo sapiens 173-209 19648688-1 2009 OBJECTIVE: To observe the influence of technetium 99Tc methylenediphosphonate (99Tc-MDP) on osteoclastogenesis induced by receptor activator of NF-kappaB ligand (RANKL) and macrophage-colony stimulating factor (M-CSF) in peripheral blood mononuclear cells in patients with rheumatoid arthritis, and to study the mechanism of 99Tc-MDP in osteoclast differentiation. 99mTc-Methylene diphosphonate 79-87 colony stimulating factor 1 Homo sapiens 211-216 19432671-9 2009 Macrophage colony-stimulating factor (also known as colony-stimulating factor; CSF-1), which is one of the cytokines considered to induce TAM to polarize toward an M2 phenotype, was then evaluated. tam 138-141 colony stimulating factor 1 Homo sapiens 79-84 19047067-8 2009 Tumors from the prenatally choline-supplemented rats overexpressed genes that confer favorable prognosis in human cancers (Klf6, Klf9, Nid2, Ntn4, Per1, and Txnip) and underexpressed those associated with aggressive disease (Bcar3, Cldn12, Csf1, Jag1, Lgals3, Lypd3, Nme1, Ptges2, Ptgs1, and Smarcb1). Choline 27-34 colony stimulating factor 1 Homo sapiens 240-244 18705650-3 2009 MATERIAL AND METHODS: Naringenin was tested in a human osteoclastogenesis model using primary osteoclast precursor cells activated by receptor activator of nuclear factor-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) for 6 days. naringenin 22-32 colony stimulating factor 1 Homo sapiens 197-233 18705650-3 2009 MATERIAL AND METHODS: Naringenin was tested in a human osteoclastogenesis model using primary osteoclast precursor cells activated by receptor activator of nuclear factor-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) for 6 days. naringenin 22-32 colony stimulating factor 1 Homo sapiens 235-240 19287193-3 2009 Using in vitro M-CSF predifferentiated macrophages and TaqMan low density arrays we could show that linoleic acid, palmitic acid, and high glucose levels have a major impact on ABCA1 and ABCG1 expression but do not strongly affect most other human ABC transporters. Linoleic Acid 100-113 colony stimulating factor 1 Homo sapiens 15-20 19287193-3 2009 Using in vitro M-CSF predifferentiated macrophages and TaqMan low density arrays we could show that linoleic acid, palmitic acid, and high glucose levels have a major impact on ABCA1 and ABCG1 expression but do not strongly affect most other human ABC transporters. Palmitic Acid 115-128 colony stimulating factor 1 Homo sapiens 15-20 19287193-3 2009 Using in vitro M-CSF predifferentiated macrophages and TaqMan low density arrays we could show that linoleic acid, palmitic acid, and high glucose levels have a major impact on ABCA1 and ABCG1 expression but do not strongly affect most other human ABC transporters. Glucose 139-146 colony stimulating factor 1 Homo sapiens 15-20 18971950-0 2009 Imatinib sensitivity as a consequence of a CSF1R-Y571D mutation and CSF1/CSF1R signaling abnormalities in the cell line GDM1. Imatinib Mesylate 0-8 colony stimulating factor 1 Homo sapiens 43-47 19004987-6 2009 CSF-1 also up-regulated genes encoding enzymes of the cholesterol biosynthetic pathway (HMGCR, MVD, IDI1, FDPS, SQLE, CYP51A1, EBP, NSDHL, DHCR7, and DHCR24), and expression of ABCG1, encoding a cholesterol efflux transporter, was repressed. Cholesterol 54-65 colony stimulating factor 1 Homo sapiens 0-5 19004987-7 2009 Consistent with these effects, CSF-1 increased levels of free cholesterol in HMDM, and the selective CSF-1R kinase inhibitor GW2580 ablated this response. Cholesterol 62-73 colony stimulating factor 1 Homo sapiens 31-36 18523268-5 2008 Elucidation of M-CSF receptor (M-CSFR) signaling pathways revealed that the total tyrosine phosphorylation pattern upon M-CSF stimulation was altered in Tec(-/-)Btk(-/-) macrophages despite normal expression and phosphorylation of the M-CSFR. Tyrosine 82-90 colony stimulating factor 1 Homo sapiens 15-20 19144181-8 2009 Transcript regulation of the cartilage-selective matrix genes Col2a1, Agc1 and Hapln1, and of the matrix metalloproteinase genes Mmp-12 and Mmp-9, were U0126 sensitive--whereas regulation of the inflammatory gene macrophage Csf-1 was U0126 insensitive. U 0126 152-157 colony stimulating factor 1 Homo sapiens 224-229 18973838-7 2009 A high oxygen tension markedly prolonged the duration of osteoclast precursor formation in the presence of supporting cells, and also markedly and persistently increased the production of macrophage colony stimulating factor (M-CSF) by supporting cells. Oxygen 7-13 colony stimulating factor 1 Homo sapiens 188-224 18973838-7 2009 A high oxygen tension markedly prolonged the duration of osteoclast precursor formation in the presence of supporting cells, and also markedly and persistently increased the production of macrophage colony stimulating factor (M-CSF) by supporting cells. Oxygen 7-13 colony stimulating factor 1 Homo sapiens 226-231 18973838-8 2009 Furthermore, we found an increase of cells expressing M-CSF and cells positive for tartrate-resistant acid phosphatase (TRAP) in hypervascular destructive bone lesions of RA patients where ROS were also abundant. Reactive Oxygen Species 189-192 colony stimulating factor 1 Homo sapiens 54-59 20877672-10 2009 Sunitinib inhibits the vascular endothelial growth factor receptor (VEGFR), the platelet-derived growth factor receptor (PDGFR), c-kit and the colony-stimulating factor 1 (CSF-1) receptor. Sunitinib 0-9 colony stimulating factor 1 Homo sapiens 143-170 18814279-2 2009 Recently, it has been reported that imatinib also targets the macrophage colony-stimulating factor (M-CSF) receptor c-Fms. Imatinib Mesylate 36-44 colony stimulating factor 1 Homo sapiens 62-98 18814279-2 2009 Recently, it has been reported that imatinib also targets the macrophage colony-stimulating factor (M-CSF) receptor c-Fms. Imatinib Mesylate 36-44 colony stimulating factor 1 Homo sapiens 100-105 18814279-7 2009 Coimmunoprecipitation assays showed that imatinib inhibited the M-CSF-induced phosphorylation of c-Fms in osteoclast precursor cells as well as the PDGF-induced PDGFR phosphorylation in MDA-MB-231 human breast cancer cells. Imatinib Mesylate 41-49 colony stimulating factor 1 Homo sapiens 64-69 20204061-4 2009 Therefore, we examined the effect of IL-1beta and/or celecoxib on the expression of macrophage colony-stimulating factor (M-CSF), receptor activator of NF-kappaB ligand (RANKL), and osteoprotegerin (OPG) in human chondrocytes, and the indirect effect of IL-1beta on osteoclast-like cell formation using RAW264.7 cells. Celecoxib 53-62 colony stimulating factor 1 Homo sapiens 84-120 20204061-4 2009 Therefore, we examined the effect of IL-1beta and/or celecoxib on the expression of macrophage colony-stimulating factor (M-CSF), receptor activator of NF-kappaB ligand (RANKL), and osteoprotegerin (OPG) in human chondrocytes, and the indirect effect of IL-1beta on osteoclast-like cell formation using RAW264.7 cells. Celecoxib 53-62 colony stimulating factor 1 Homo sapiens 122-127 18282599-5 2008 Imatinib mesylate, a tyrosine kinase inhibitor that can target the M-CSF receptor, also prevented the effect of CM. Imatinib Mesylate 0-17 colony stimulating factor 1 Homo sapiens 67-72 18691974-2 2008 We show that binding of M-CSF to its receptor c-Fms generates a signaling complex comprising phosphorylated DAP12, an adaptor containing an immunoreceptor tyrosine-based activation motif (ITAM) and the nonreceptor tyrosine kinase Syk. Tyrosine 155-163 colony stimulating factor 1 Homo sapiens 24-29 18691974-5 2008 Retroviral transduction of null precursors with wild-type or mutant DAP12 or Syk reveals that the SH2 domain of Syk and the ITAM tyrosine residues and transmembrane domain of DAP12 mediate M-CSF signaling. Tyrosine 129-137 colony stimulating factor 1 Homo sapiens 189-194 18708368-2 2008 Recently, we described GAPDH binding the AU-rich terminal 144 nt of the colony-stimulating factor-1 (CSF-1) 3" untranslated region (UTR), which we showed to be an mRNA decay element in ovarian cancer cells. Gold 41-43 colony stimulating factor 1 Homo sapiens 72-99 18708368-2 2008 Recently, we described GAPDH binding the AU-rich terminal 144 nt of the colony-stimulating factor-1 (CSF-1) 3" untranslated region (UTR), which we showed to be an mRNA decay element in ovarian cancer cells. Gold 41-43 colony stimulating factor 1 Homo sapiens 101-106 18708368-6 2008 RNA footprinting analysis of the 144 nt CSF-1 sequence revealed that GAPDH associates with a large AU-rich-containing region. Gold 99-101 colony stimulating factor 1 Homo sapiens 40-45 18279525-5 2008 In this study, we investigate the relevance of ICA in gaining new insights into well characterized regulatory mechanisms of M-CSF dependent macrophage differentiation. ica 47-50 colony stimulating factor 1 Homo sapiens 124-129 18516765-1 2008 Axitinib is an oral inhibitor of the VEGF, PDGF and colony stimulating factor-1 receptor tyrosine kinases and is currently in development by Pfizer Inc for the potential treatment of various solid tumors. Axitinib 0-8 colony stimulating factor 1 Homo sapiens 52-79 18453574-7 2008 GC dexamethasone was essential for increased surface expression of functional TGF-betaRII because its effect was observed also in combination with IL-13, M-CSF, and GM-CSF. Dexamethasone 3-16 colony stimulating factor 1 Homo sapiens 154-159 18661071-3 2008 alpha-MEM which contains RANKL and M-CSF was used as the culture medium. alpha minimal essential medium 0-9 colony stimulating factor 1 Homo sapiens 35-40 18378004-0 2008 The selective M-CSF receptor tyrosine kinase inhibitor Ki20227 suppresses experimental autoimmune encephalomyelitis. N-(4-((6,7-dimethoxy-4-quinolyl)oxy)-2-methoxyphenyl)-N'-(1-(1,3-thiazole-2-yl)ethyl)urea 55-62 colony stimulating factor 1 Homo sapiens 14-19 18378004-3 2008 We previously reported that Ki20227 (N-{4-[(6,7-dimethoxy-4-quinolyl)oxy]-2-methoxyphenyl}-N"-[1-(1,3-thiazole-2-yl)ethyl]urea) is a highly selective M-CSF receptor (c-fms) tyrosine kinase inhibitor. N-(4-((6,7-dimethoxy-4-quinolyl)oxy)-2-methoxyphenyl)-N'-(1-(1,3-thiazole-2-yl)ethyl)urea 28-35 colony stimulating factor 1 Homo sapiens 150-155 18378004-3 2008 We previously reported that Ki20227 (N-{4-[(6,7-dimethoxy-4-quinolyl)oxy]-2-methoxyphenyl}-N"-[1-(1,3-thiazole-2-yl)ethyl]urea) is a highly selective M-CSF receptor (c-fms) tyrosine kinase inhibitor. N-(4-((6,7-dimethoxy-4-quinolyl)oxy)-2-methoxyphenyl)-N'-(1-(1,3-thiazole-2-yl)ethyl)urea 37-126 colony stimulating factor 1 Homo sapiens 150-155 17981685-6 2008 At high concentrations, progesterone is a potent inducer of Th2-type cytokines as well as of LIF and M-CSF production by T cells. Progesterone 24-36 colony stimulating factor 1 Homo sapiens 101-106 17664049-8 2008 The ratio of CSF2/CSF1 sTNFR1 levels of patients with dexamethasone was significantly lower than that without dexamethasone (p = 0.0063). Dexamethasone 54-67 colony stimulating factor 1 Homo sapiens 18-22 18083161-7 2008 Under M-CSF- and RANKL-deprived condition, berberine increased the active form of caspase-3 in osteoclasts. Berberine 43-52 colony stimulating factor 1 Homo sapiens 6-12 17855501-11 2007 These studies demonstrated that the PI-3K inhibitors, wortmannin and LY294002, antagonize the ability of CSF-1 to inhibit DC differentiation and to promote caspase activation. Wortmannin 54-64 colony stimulating factor 1 Homo sapiens 105-110 17855501-11 2007 These studies demonstrated that the PI-3K inhibitors, wortmannin and LY294002, antagonize the ability of CSF-1 to inhibit DC differentiation and to promote caspase activation. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 69-77 colony stimulating factor 1 Homo sapiens 105-110 17390341-11 2007 This action of M-CSF was suppressed by the phosphatidylinositol 3-kinase (PI3-kinase) inhibitor wortmannin, suggesting that M-CSF increases Vitaxin"s inhibitory effect by inside-out activation of alphavbeta3. Wortmannin 96-106 colony stimulating factor 1 Homo sapiens 15-20 17922812-7 2007 Only the NF-kappaB blocker dimethylfumarate and the dn IKK2, but not januskinase inhibitor-1 (JNK-I), were able to block the TNF-alpha-induced increase in M-CSF production in these cells, suggesting that the induction of M-CSF through TNF-alpha is mainly dependent on the activation of the NF-kappaB pathway. Dimethyl Fumarate 27-43 colony stimulating factor 1 Homo sapiens 155-160 17971207-4 2007 Dkk1 and -2 increased the expression of the osteoclast differentiation factors, receptor activator of NF-kappaB ligand (RANKL) and macrophage-colony stimulating factor (M-CSF), upon stimulation with Wnt3a/1,25-dihydroxyvitamine D3 and Wnt3a/BMP2, respectively. 1,25-dihydroxyvitamine d3 205-230 colony stimulating factor 1 Homo sapiens 131-167 17390341-11 2007 This action of M-CSF was suppressed by the phosphatidylinositol 3-kinase (PI3-kinase) inhibitor wortmannin, suggesting that M-CSF increases Vitaxin"s inhibitory effect by inside-out activation of alphavbeta3. Wortmannin 96-106 colony stimulating factor 1 Homo sapiens 124-129 17393431-4 2007 The ATP binding motifs of nuclear actin are essential for its function in regulating CSF1 gene transcription, and upon actin overexpression, there is an increase in the ATPase activity of nuclear proteins. Adenosine Triphosphate 4-7 colony stimulating factor 1 Homo sapiens 85-89 17907802-6 2007 The anti-cancer agent Imatinib inhibited M-CSF receptor activation and restored the apoptotic sensitivity of HIV-1-infected macrophages, suggesting a novel strategy to curtail viral persistence in the macrophage reservoir. Imatinib Mesylate 22-30 colony stimulating factor 1 Homo sapiens 41-46 17785789-5 2007 We have then focused on novel ATPgammaS and PGE2 target genes in MoDCs including CSF-1, MCP-4/CCL13 chemokine, vascular endothelial growth factor-A, and neuropilin-1. adenosine 5'-O-(3-thiotriphosphate) 30-39 colony stimulating factor 1 Homo sapiens 81-86 17785789-5 2007 We have then focused on novel ATPgammaS and PGE2 target genes in MoDCs including CSF-1, MCP-4/CCL13 chemokine, vascular endothelial growth factor-A, and neuropilin-1. Dinoprostone 44-48 colony stimulating factor 1 Homo sapiens 81-86 17510321-6 2007 AZD6244 down-regulates the expression/secretion of osteoclast (OC)-activating factors from MM cells and inhibits in vitro differentiation of MM patient PBMCs to OCs induced by ligand for receptor activator of NF-kappaB (RANKL) and macrophage-colony stimulating factor (M-CSF). AZD 6244 0-7 colony stimulating factor 1 Homo sapiens 231-267 17681043-5 2007 At high concentrations progesterone is a potent inducer of Th2-type cytokines as well as of LIF and M-CSF production by T cells. Progesterone 23-35 colony stimulating factor 1 Homo sapiens 100-105 17510321-6 2007 AZD6244 down-regulates the expression/secretion of osteoclast (OC)-activating factors from MM cells and inhibits in vitro differentiation of MM patient PBMCs to OCs induced by ligand for receptor activator of NF-kappaB (RANKL) and macrophage-colony stimulating factor (M-CSF). AZD 6244 0-7 colony stimulating factor 1 Homo sapiens 269-274 17659436-14 2007 CONCLUSIONS: Persistently increased urinary levels of RANTES and M-CSF after initial remission are predictors of renal flare in patients with SLE DPGN. dpgn 146-150 colony stimulating factor 1 Homo sapiens 65-70 17443671-4 2007 However, in the presence of a phorbol ester, TPA, TF-1-fms cells definitely switched their responsiveness to M-CSF from proliferation to differentiation, as evidenced by a more drastic morphological change and the appearance of cells with a higher level of phagocytic activity. Phorbol Esters 30-43 colony stimulating factor 1 Homo sapiens 109-114 17443671-4 2007 However, in the presence of a phorbol ester, TPA, TF-1-fms cells definitely switched their responsiveness to M-CSF from proliferation to differentiation, as evidenced by a more drastic morphological change and the appearance of cells with a higher level of phagocytic activity. Tetradecanoylphorbol Acetate 45-48 colony stimulating factor 1 Homo sapiens 109-114 17443671-5 2007 In TF-1-fms cells expressing HIV-1 Nef protein in a conditionally active-manner, both M-CSF-mediated proliferation and M-CSF/TPA-mediated differentiation were inhibited by the activation of Nef. Tetradecanoylphorbol Acetate 125-128 colony stimulating factor 1 Homo sapiens 119-124 17443671-7 2007 Under the proliferation-inducing conditions (TPA-free), parental or Nef-inactive cells showed modest ERK activation following M-CSF stimulation, whereas Nef-active cells showed an earlier and transient ERK activation, despite a decrease in their proliferation rate. Tetradecanoylphorbol Acetate 45-48 colony stimulating factor 1 Homo sapiens 126-131 17666255-6 2007 Macrolide antibiotics reduced RANKL mRNA and M-CSF expression by nasal polyp fibroblasts in a dose-dependent manner, and inhibited osteoclastogenesis from PBMCs. macrolide antibiotics 0-21 colony stimulating factor 1 Homo sapiens 45-50 17420255-0 2007 c-Fms tyrosine 559 is a major mediator of M-CSF-induced proliferation of primary macrophages. Tyrosine 6-14 colony stimulating factor 1 Homo sapiens 42-47 17420256-0 2007 M-CSF regulates the cytoskeleton via recruitment of a multimeric signaling complex to c-Fms Tyr-559/697/721. Tyrosine 92-95 colony stimulating factor 1 Homo sapiens 0-5 17342254-6 2007 Simultaneous addition of 10(-4) M indomethacin eliminated the effects of nicotine and LPS on ALPase activity, PGE(2) production, and M-CSF expression. Indomethacin 34-46 colony stimulating factor 1 Homo sapiens 133-138 17501767-9 2007 RESULTS: Amniotic fluid M-CSF concentrations were 6525 pg/mL (median) in the SGA group and 4790 pg/mL in the AGA group; the concentrations were significantly higher in the SGA group than in the AGA group. aga 109-112 colony stimulating factor 1 Homo sapiens 24-29 17342254-6 2007 Simultaneous addition of 10(-4) M indomethacin eliminated the effects of nicotine and LPS on ALPase activity, PGE(2) production, and M-CSF expression. Nicotine 73-81 colony stimulating factor 1 Homo sapiens 133-138 17342254-8 2007 These results suggest that LPS enhances the production of nicotine-induced PGE(2) by an increase in COX-2 expression in osteoblasts, that nicotine-LPS-induced PGE2 interacts with the osteoblast Ep4 receptor primarily in autocrine or paracrine mode, and that the nicotine-LPS-induced PGE(2) then decreases ALPase activity and increases M-CSF expression. Nicotine 58-66 colony stimulating factor 1 Homo sapiens 335-340 17342254-8 2007 These results suggest that LPS enhances the production of nicotine-induced PGE(2) by an increase in COX-2 expression in osteoblasts, that nicotine-LPS-induced PGE2 interacts with the osteoblast Ep4 receptor primarily in autocrine or paracrine mode, and that the nicotine-LPS-induced PGE(2) then decreases ALPase activity and increases M-CSF expression. Nicotine 138-146 colony stimulating factor 1 Homo sapiens 335-340 17342254-8 2007 These results suggest that LPS enhances the production of nicotine-induced PGE(2) by an increase in COX-2 expression in osteoblasts, that nicotine-LPS-induced PGE2 interacts with the osteoblast Ep4 receptor primarily in autocrine or paracrine mode, and that the nicotine-LPS-induced PGE(2) then decreases ALPase activity and increases M-CSF expression. Dinoprostone 159-163 colony stimulating factor 1 Homo sapiens 335-340 17342254-8 2007 These results suggest that LPS enhances the production of nicotine-induced PGE(2) by an increase in COX-2 expression in osteoblasts, that nicotine-LPS-induced PGE2 interacts with the osteoblast Ep4 receptor primarily in autocrine or paracrine mode, and that the nicotine-LPS-induced PGE(2) then decreases ALPase activity and increases M-CSF expression. Nicotine 138-146 colony stimulating factor 1 Homo sapiens 335-340 17342254-8 2007 These results suggest that LPS enhances the production of nicotine-induced PGE(2) by an increase in COX-2 expression in osteoblasts, that nicotine-LPS-induced PGE2 interacts with the osteoblast Ep4 receptor primarily in autocrine or paracrine mode, and that the nicotine-LPS-induced PGE(2) then decreases ALPase activity and increases M-CSF expression. Prostaglandins E 159-162 colony stimulating factor 1 Homo sapiens 335-340 17327610-3 2007 Sunitinib inhibits other tyrosine kinases including, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malignancies including small-cell lung cancer, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma. Sunitinib 0-9 colony stimulating factor 1 Homo sapiens 64-91 17327610-3 2007 Sunitinib inhibits other tyrosine kinases including, KIT, FLT3, colony-stimulating factor 1 (CSF-1), and RET, which are involved in a number of malignancies including small-cell lung cancer, GI stromal tumors (GISTs), breast cancer, acute myelogenous leukemia, multiple endocrine neoplasia types 2A and 2B, and familial medullary thyroid carcinoma. Sunitinib 0-9 colony stimulating factor 1 Homo sapiens 93-98 16931806-1 2007 M-CSF induces PI 3-kinase activation, resulting in reactive oxygen species (ROS) production. Reactive Oxygen Species 51-74 colony stimulating factor 1 Homo sapiens 0-5 17068143-4 2007 In contrast, exposing these cells to CSF-1 in the presence of CO(2)/HCO(3)(-) causes a rapid and sustained cellular alkalinization. co(2) 62-67 colony stimulating factor 1 Homo sapiens 37-42 17068143-4 2007 In contrast, exposing these cells to CSF-1 in the presence of CO(2)/HCO(3)(-) causes a rapid and sustained cellular alkalinization. Bicarbonates 68-75 colony stimulating factor 1 Homo sapiens 37-42 17068143-5 2007 The CSF-1-induced rise in pH(i) is not blocked by 4,4"-diisothiocyanatostilbene-2,2"-disulfonic acid, an inhibitor of HCO(3)(-) transporters but is abolished by removing extracellular sodium. Sodium 184-190 colony stimulating factor 1 Homo sapiens 4-9 17068143-8 2007 Moreover, CSF-1 promotes osteoclast survival in the presence of CO(2)/HCO(3)(-) buffer but not in its absence. co(2) 64-69 colony stimulating factor 1 Homo sapiens 10-15 17068143-8 2007 Moreover, CSF-1 promotes osteoclast survival in the presence of CO(2)/HCO(3)(-) buffer but not in its absence. Bicarbonates 70-79 colony stimulating factor 1 Homo sapiens 10-15 17062603-8 2007 One of these pinocytosis-stimulatory factors is M-CSF, which is induced by a process involving cholesterol trafficking to the endoplasmic reticulum and signaling through PI-3K and ERK MAPK pathways. Cholesterol 95-106 colony stimulating factor 1 Homo sapiens 48-53 16931806-1 2007 M-CSF induces PI 3-kinase activation, resulting in reactive oxygen species (ROS) production. Reactive Oxygen Species 76-79 colony stimulating factor 1 Homo sapiens 0-5 16931806-2 2007 Previously, we reported that ROS mediate macrophage colony-stimulating factor (M-CSF)-induced extracellular regulated kinase (Erk) activation and monocyte survival. Reactive Oxygen Species 29-32 colony stimulating factor 1 Homo sapiens 79-84 16931806-3 2007 In this work, we hypothesized that M-CSF-stimulated ROS products modulated Akt1 and p38 activation. Reactive Oxygen Species 52-55 colony stimulating factor 1 Homo sapiens 35-40 16931806-8 2007 Moreover, the p38 MAPK inhibitor, SB203580, inhibited p38 activity and M-CSF-induced monocyte survival. SB 203580 34-42 colony stimulating factor 1 Homo sapiens 71-76 16931806-9 2007 These findings demonstrate that ROS generated from the NADPH oxidase complex contribute to monocyte/macrophage survival induced by M-CSF via regulation of Akt and p38 MAPK. Reactive Oxygen Species 32-35 colony stimulating factor 1 Homo sapiens 131-136 16514418-4 2006 CSF-1-induced proliferation and survival are sensitive to glycolytic inhibitors, 2-deoxyglucose and 3-bromopyruvate. Deoxyglucose 81-95 colony stimulating factor 1 Homo sapiens 0-5 17214584-8 2006 At the same time, PGE2 suppresses osteoclastogenesis by inhibiting M-CSF expression of fibroblast-like synoviocytes as well as both IL-17 and IL-17-induced TNF-alpha expression of macrophages. Dinoprostone 18-22 colony stimulating factor 1 Homo sapiens 67-72 17934310-9 2007 In particular, progesterone is a potent inducer of production of Th2-type cytokines, LIF and M-CSF. Progesterone 15-27 colony stimulating factor 1 Homo sapiens 93-98 17151781-2 2006 Recently, we showed that nicotine affected mineralized nodule formation, and that nicotine and lipopolysaccharide stimulated the formation of osteoclast-like cells by increasing production of macrophage colony-stimulating factor (M-CSF) and prostaglandin E2 (PGE2) by human osteoblastic Saos-2 cells. Nicotine 82-90 colony stimulating factor 1 Homo sapiens 192-228 17151781-2 2006 Recently, we showed that nicotine affected mineralized nodule formation, and that nicotine and lipopolysaccharide stimulated the formation of osteoclast-like cells by increasing production of macrophage colony-stimulating factor (M-CSF) and prostaglandin E2 (PGE2) by human osteoblastic Saos-2 cells. Nicotine 82-90 colony stimulating factor 1 Homo sapiens 230-235 17151781-2 2006 Recently, we showed that nicotine affected mineralized nodule formation, and that nicotine and lipopolysaccharide stimulated the formation of osteoclast-like cells by increasing production of macrophage colony-stimulating factor (M-CSF) and prostaglandin E2 (PGE2) by human osteoblastic Saos-2 cells. Dinoprostone 259-263 colony stimulating factor 1 Homo sapiens 192-228 16514418-4 2006 CSF-1-induced proliferation and survival are sensitive to glycolytic inhibitors, 2-deoxyglucose and 3-bromopyruvate. bromopyruvate 100-115 colony stimulating factor 1 Homo sapiens 0-5 16568213-5 2006 DFPP theoretically removes monocyte-activating cytokines, such as monocyte colony-stimulating factor (M-CSF) from the circulation, and therefore may prove to be an effective treatment for corticosteroid resistant, rapidly developing cases of AOSD. dfpp 0-4 colony stimulating factor 1 Homo sapiens 66-100 16909430-2 2006 Sanglifehrin A inhibits M-CSF-dependent macrophage proliferation by arresting the G1 phase of the cell cycle but does not affect cell viability. sanglifehrin A 0-14 colony stimulating factor 1 Homo sapiens 24-29 16909430-5 2006 In the early steps of M-CSF signaling, SfA inhibits the phosphorylation of Raf-1 and the external regulated kinases (ERK)1/2 and mitogen-activated protein kinase phosphatase-1, which are required for proliferation. sanglifehrin A 39-42 colony stimulating factor 1 Homo sapiens 22-27 16568213-5 2006 DFPP theoretically removes monocyte-activating cytokines, such as monocyte colony-stimulating factor (M-CSF) from the circulation, and therefore may prove to be an effective treatment for corticosteroid resistant, rapidly developing cases of AOSD. dfpp 0-4 colony stimulating factor 1 Homo sapiens 102-107 16606620-0 2006 Constitutive receptor-independent low density lipoprotein uptake and cholesterol accumulation by macrophages differentiated from human monocytes with macrophage-colony-stimulating factor (M-CSF). Cholesterol 69-80 colony stimulating factor 1 Homo sapiens 188-193 16606620-7 2006 Differentiation of macrophages from human monocytes in fetal bovine serum with macrophage-colony-stimulating factor (M-CSF) produced a macrophage phenotype demonstrating constitutive fluid-phase uptake of native LDL leading to macrophage cholesterol accumulation. Cholesterol 238-249 colony stimulating factor 1 Homo sapiens 79-115 16606620-7 2006 Differentiation of macrophages from human monocytes in fetal bovine serum with macrophage-colony-stimulating factor (M-CSF) produced a macrophage phenotype demonstrating constitutive fluid-phase uptake of native LDL leading to macrophage cholesterol accumulation. Cholesterol 238-249 colony stimulating factor 1 Homo sapiens 117-122 16734568-8 2006 The effect on M-CSF expression could be partially blocked by pyrrolidine-dithiocarbamate ammonium salt and LY294002 but not by NS398. pyrrolidine-dithiocarbamate ammonium salt 61-102 colony stimulating factor 1 Homo sapiens 14-19 16734568-8 2006 The effect on M-CSF expression could be partially blocked by pyrrolidine-dithiocarbamate ammonium salt and LY294002 but not by NS398. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 107-115 colony stimulating factor 1 Homo sapiens 14-19 16538029-2 2006 In the present study, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), a glucosylceramide synthase inhibitor, completely inhibited osteoclastogenesis induced by macrophage-colony stimulating factor (M-CSF) and receptor activator of NF-kappaB ligand (RANKL). RV 538 22-78 colony stimulating factor 1 Homo sapiens 179-215 16845445-3 2006 BMMs were stimulated with testosterone in the presence of macrophage colony stimulating factor (M-CSF) or without. Testosterone 26-38 colony stimulating factor 1 Homo sapiens 58-94 16845445-3 2006 BMMs were stimulated with testosterone in the presence of macrophage colony stimulating factor (M-CSF) or without. Testosterone 26-38 colony stimulating factor 1 Homo sapiens 96-101 16266722-0 2006 Nicotine and lipopolysaccharide stimulate the formation of osteoclast-like cells by increasing macrophage colony-stimulating factor and prostaglandin E2 production by osteoblasts. Nicotine 0-8 colony stimulating factor 1 Homo sapiens 95-131 16266722-2 2006 The present study was undertaken to determine the effect of nicotine and LPS on the expression of macrophage colony-stimulating factor (M-CSF), osteoprotegerin (OPG), and prostaglandin E2 (PGE2) in osteoblasts, and the indirect effect of nicotine and LPS on the formation of osteoclast-like cells. Nicotine 60-68 colony stimulating factor 1 Homo sapiens 98-134 16266722-2 2006 The present study was undertaken to determine the effect of nicotine and LPS on the expression of macrophage colony-stimulating factor (M-CSF), osteoprotegerin (OPG), and prostaglandin E2 (PGE2) in osteoblasts, and the indirect effect of nicotine and LPS on the formation of osteoclast-like cells. Nicotine 60-68 colony stimulating factor 1 Homo sapiens 136-141 16266722-7 2006 M-CSF and PGE2 expression increased markedly in cells cultured with nicotine and LPS compared with those cultured with nicotine alone. Nicotine 68-76 colony stimulating factor 1 Homo sapiens 0-5 16266722-7 2006 M-CSF and PGE2 expression increased markedly in cells cultured with nicotine and LPS compared with those cultured with nicotine alone. Nicotine 119-127 colony stimulating factor 1 Homo sapiens 0-5 16266722-9 2006 The conditioned medium containing M-CSF and PGE2 produced by nicotine and LPS-treated Saos-2 cells with soluble RANKL increased the TRAP staining of osteoclast precursors compared with that produced by nicotine treatment alone. Nicotine 61-69 colony stimulating factor 1 Homo sapiens 34-39 16266722-9 2006 The conditioned medium containing M-CSF and PGE2 produced by nicotine and LPS-treated Saos-2 cells with soluble RANKL increased the TRAP staining of osteoclast precursors compared with that produced by nicotine treatment alone. Nicotine 202-210 colony stimulating factor 1 Homo sapiens 34-39 16266722-10 2006 These results suggest that nicotine and LPS stimulate the formation of osteoclast-like cells via an increase in M-CSF and PGE2 production and that the stimulation is greater than with nicotine treatment alone. Nicotine 27-35 colony stimulating factor 1 Homo sapiens 112-117 16538029-2 2006 In the present study, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), a glucosylceramide synthase inhibitor, completely inhibited osteoclastogenesis induced by macrophage-colony stimulating factor (M-CSF) and receptor activator of NF-kappaB ligand (RANKL). RV 538 22-78 colony stimulating factor 1 Homo sapiens 217-222 16538029-2 2006 In the present study, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), a glucosylceramide synthase inhibitor, completely inhibited osteoclastogenesis induced by macrophage-colony stimulating factor (M-CSF) and receptor activator of NF-kappaB ligand (RANKL). RV 538 80-86 colony stimulating factor 1 Homo sapiens 179-215 16538029-2 2006 In the present study, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), a glucosylceramide synthase inhibitor, completely inhibited osteoclastogenesis induced by macrophage-colony stimulating factor (M-CSF) and receptor activator of NF-kappaB ligand (RANKL). RV 538 80-86 colony stimulating factor 1 Homo sapiens 217-222 16780390-7 2006 Serum levels of M-CSF were significantly decreased only in the simvastatin group (from 403 +/- 71 to 303 +/- 116 pg/mL; p = 0.009). Simvastatin 63-74 colony stimulating factor 1 Homo sapiens 16-21 16780390-9 2006 Simvastatin decreased serum M-CSF levels independently of changes in total cholesterol or low-density lipoprotein-cholesterol. Simvastatin 0-11 colony stimulating factor 1 Homo sapiens 28-33 16780390-10 2006 CONCLUSIONS: The results of this study indicate that simvastatin decreases serum levels of M-CSF while losartan increases plasma levels of TGF-beta, suggesting that the two drugs may have different anti-atherosclerotic properties. Simvastatin 53-64 colony stimulating factor 1 Homo sapiens 91-96 16859503-7 2006 Adhered monocytes, after 3-day preincubation with IL-10 and M-CSF, could produce more IL-1beta and IL-6 in response to TNF-alpha in the presence of dibutyryl cAMP, as compared with the cells preincubated with or without IL-10 or M-CSF alone. Cyclic AMP 158-162 colony stimulating factor 1 Homo sapiens 60-65 16289055-5 2005 Additionally, special inhibitor of Syk Piceatannol suppressed the increase of CSF-1 mRNA caused by the engagement of PSGL-1. 3,3',4,5'-tetrahydroxystilbene 39-50 colony stimulating factor 1 Homo sapiens 78-83 16404151-1 2005 We show that sulforaphane inhibits osteoclastogenesis in the presence of macrophage colony-stimulating factor (M-CSF) and receptor for activation of nuclear factor-kB ligand (RANKL) in osteoclast (OC) precursors. sulforaphane 13-25 colony stimulating factor 1 Homo sapiens 73-109 16404151-1 2005 We show that sulforaphane inhibits osteoclastogenesis in the presence of macrophage colony-stimulating factor (M-CSF) and receptor for activation of nuclear factor-kB ligand (RANKL) in osteoclast (OC) precursors. sulforaphane 13-25 colony stimulating factor 1 Homo sapiens 111-116 16164417-4 2005 We addressed the question whether M-CSF regulates FAK tyrosine phosphorylation in macrophages, and found that M-CSF induces FAK phosphorylation at all known tyrosine residues. Tyrosine 54-62 colony stimulating factor 1 Homo sapiens 34-39 16164417-4 2005 We addressed the question whether M-CSF regulates FAK tyrosine phosphorylation in macrophages, and found that M-CSF induces FAK phosphorylation at all known tyrosine residues. Tyrosine 54-62 colony stimulating factor 1 Homo sapiens 110-115 16164417-4 2005 We addressed the question whether M-CSF regulates FAK tyrosine phosphorylation in macrophages, and found that M-CSF induces FAK phosphorylation at all known tyrosine residues. Tyrosine 157-165 colony stimulating factor 1 Homo sapiens 110-115 15894167-3 2005 In this study, we showed that SKAP55-related (SKAP55R) adaptor protein is expressed in myeloid cells and macrophages and is rapidly and transiently tyrosine-phosphorylated in response to M-CSF. Tyrosine 148-156 colony stimulating factor 1 Homo sapiens 187-192 15993849-3 2005 Exposure of A549 to ethanol (0.1-1%) dose-dependently inhibited (by 15-49%) the release of G-CSF and IL-8, but not of M-CSF, triggered by IL1beta or TNFalpha. Ethanol 20-27 colony stimulating factor 1 Homo sapiens 118-123 15894167-4 2005 M-CSF induced SKAP55R association with other tyrosine-phosphorylated proteins and with actin. Tyrosine 45-53 colony stimulating factor 1 Homo sapiens 0-5 15885469-6 2005 RESULTS: In the presence of M-CSF, large numbers of TRAP(+) and VNR(+) multinucleated cells capable of lacunar resorption, were noted in co-cultures of monocytes and RANKL-expressing AFbs. afbs 183-187 colony stimulating factor 1 Homo sapiens 28-33 15867372-2 2005 It has been suggested that CSF-1 3" untranslated region containing AU-rich elements (ARE) could regulate CSF-1 posttranscriptional expression and be responsible for its aberrant abundance in such cancer cells. Gold 67-69 colony stimulating factor 1 Homo sapiens 27-32 15867372-2 2005 It has been suggested that CSF-1 3" untranslated region containing AU-rich elements (ARE) could regulate CSF-1 posttranscriptional expression and be responsible for its aberrant abundance in such cancer cells. Gold 67-69 colony stimulating factor 1 Homo sapiens 105-110 15947117-7 2005 Treatment of HDS cells with gefitinib produced a significant reduction in the levels of secreted macrophage colony-stimulating factor (M-CSF) and cell-associated receptor activator of NF-kappaB ligand (RANKL) in both cell lines, as assessed by using specific ELISA and Western blotting techniques. Gefitinib 28-37 colony stimulating factor 1 Homo sapiens 97-133 15947117-7 2005 Treatment of HDS cells with gefitinib produced a significant reduction in the levels of secreted macrophage colony-stimulating factor (M-CSF) and cell-associated receptor activator of NF-kappaB ligand (RANKL) in both cell lines, as assessed by using specific ELISA and Western blotting techniques. Gefitinib 28-37 colony stimulating factor 1 Homo sapiens 135-140 15894964-10 2005 M-CSF remained related to 11-dehydro-TXB 2 excretion during both treatment phases (P < .01) suggesting that cytokine-mediated thromboxane A 2 production was not altered by aspirin. 11-dehydro-thromboxane B2 26-42 colony stimulating factor 1 Homo sapiens 0-5 15626739-8 2005 Because of aberrant molecular association, the tyrosine-phosphorylation/activation of the receptor in response to M-CSF was markedly diminished in Nef-active cells. Tyrosine 47-55 colony stimulating factor 1 Homo sapiens 114-119 15870290-2 2005 Here, we show that bone marrow macrophages of SHIP(-/-) animals have elevated levels of phosphatidylinositol 3,4,5-trisphosphate [PI (3,4,5)P(3)] and displayed higher and more prolonged chemotactic responses to macrophage colony-stimulating factor (M-CSF) and elevated levels of F-actin relative to wild-type macrophages. Phosphorus 49-50 colony stimulating factor 1 Homo sapiens 211-247 15870290-2 2005 Here, we show that bone marrow macrophages of SHIP(-/-) animals have elevated levels of phosphatidylinositol 3,4,5-trisphosphate [PI (3,4,5)P(3)] and displayed higher and more prolonged chemotactic responses to macrophage colony-stimulating factor (M-CSF) and elevated levels of F-actin relative to wild-type macrophages. Phosphorus 49-50 colony stimulating factor 1 Homo sapiens 249-254 15870290-6 2005 We conclude that Vav acts as a PI 3-kinase-dependent activator for Rac activation in macrophages stimulated with M-CSF and that SHIP regulates macrophage M-CSF-triggered chemotaxis by hydrolysis of PI (3,4,5)P(3). pi (3,4,5)p 198-209 colony stimulating factor 1 Homo sapiens 154-159 15637141-0 2005 Macrophage colony-stimulating factor receptor c-fms is a novel target of imatinib. Imatinib Mesylate 73-81 colony stimulating factor 1 Homo sapiens 0-36 15626739-9 2005 Consequently, Nef activation caused the inhibition of M-CSF-mediated proliferation of TF-1-fms cells and macrophage differentiation of the cells induced by M-CSF and 12-O-tetradecanoylphorbol 13-acetate. Tetradecanoylphorbol Acetate 166-202 colony stimulating factor 1 Homo sapiens 54-59 15637141-5 2005 Here, we demonstrate for the first time that imatinib targets the macrophage colony-stimulating factor (M-CSF) receptor c-fms. Imatinib Mesylate 45-53 colony stimulating factor 1 Homo sapiens 66-102 15637141-5 2005 Here, we demonstrate for the first time that imatinib targets the macrophage colony-stimulating factor (M-CSF) receptor c-fms. Imatinib Mesylate 45-53 colony stimulating factor 1 Homo sapiens 104-109 15637141-7 2005 Imatinib was also found to inhibit M-CSF-induced proliferation of a cytokine-dependent cell line, further supporting the hypothesis that imatinib affects the growth and development of monocyte and/or macrophages through inhibition of c-fms signaling. Imatinib Mesylate 0-8 colony stimulating factor 1 Homo sapiens 35-40 15637141-7 2005 Imatinib was also found to inhibit M-CSF-induced proliferation of a cytokine-dependent cell line, further supporting the hypothesis that imatinib affects the growth and development of monocyte and/or macrophages through inhibition of c-fms signaling. Imatinib Mesylate 137-145 colony stimulating factor 1 Homo sapiens 35-40 15557176-4 2004 We report that 1) SHIP2 was tyrosine-phosphorylated in M-CSF-stimulated human alveolar macrophages, human THP-1 cells, murine macrophages, and the murine macrophage cell line RAW264; 2) SHIP2 associated with the M-CSF receptor after M-CSF stimulation; and 3) SHIP2 associated with the actin-binding protein filamin and localization to the cell membrane, requiring the proline-rich domain, but not on the Src homology 2 domain of SHIP2. Tyrosine 28-36 colony stimulating factor 1 Homo sapiens 55-60 15678256-6 2005 In addition, ALA supplementation resulted in a significant decrease in the serum concentration of serum amyloid A (SAA) (p=0.014), C-reactive protein (CRP) (p=0.013), macrophage colony-stimulating factor (MCSF) (p<0.001), and interleukin (IL)-6 (p=0.028). alpha-Linolenic Acid 13-16 colony stimulating factor 1 Homo sapiens 167-203 15678256-6 2005 In addition, ALA supplementation resulted in a significant decrease in the serum concentration of serum amyloid A (SAA) (p=0.014), C-reactive protein (CRP) (p=0.013), macrophage colony-stimulating factor (MCSF) (p<0.001), and interleukin (IL)-6 (p=0.028). alpha-Linolenic Acid 13-16 colony stimulating factor 1 Homo sapiens 205-209 15710175-3 2005 While arsenite was found to induce cell death in a culture system containing macrophage colony stimulating factor (M-CSF), macrophages induced by granulocyte-macrophage CSF (GM-CSF) survived the treatment, but were morphologically, phenotypically, and functionally altered. arsenite 6-14 colony stimulating factor 1 Homo sapiens 115-120 15661041-6 2005 Imatinib also reduced the ability of M-CSF and GM-CSF stimulated CM to phagocytose zymosan particles, with uptake of non-opsonized zymosan by M-CSF stimulated CM (M-CM) being most affected. Imatinib Mesylate 0-8 colony stimulating factor 1 Homo sapiens 37-42 15661041-6 2005 Imatinib also reduced the ability of M-CSF and GM-CSF stimulated CM to phagocytose zymosan particles, with uptake of non-opsonized zymosan by M-CSF stimulated CM (M-CM) being most affected. Imatinib Mesylate 0-8 colony stimulating factor 1 Homo sapiens 48-53 15661041-6 2005 Imatinib also reduced the ability of M-CSF and GM-CSF stimulated CM to phagocytose zymosan particles, with uptake of non-opsonized zymosan by M-CSF stimulated CM (M-CM) being most affected. Zymosan 83-90 colony stimulating factor 1 Homo sapiens 37-42 15661041-6 2005 Imatinib also reduced the ability of M-CSF and GM-CSF stimulated CM to phagocytose zymosan particles, with uptake of non-opsonized zymosan by M-CSF stimulated CM (M-CM) being most affected. Zymosan 83-90 colony stimulating factor 1 Homo sapiens 48-53 15557176-4 2004 We report that 1) SHIP2 was tyrosine-phosphorylated in M-CSF-stimulated human alveolar macrophages, human THP-1 cells, murine macrophages, and the murine macrophage cell line RAW264; 2) SHIP2 associated with the M-CSF receptor after M-CSF stimulation; and 3) SHIP2 associated with the actin-binding protein filamin and localization to the cell membrane, requiring the proline-rich domain, but not on the Src homology 2 domain of SHIP2. Proline 368-375 colony stimulating factor 1 Homo sapiens 55-60 15485493-9 2004 As MCSF is endogenously expressed within the brain, and both its level and that of the MCSF receptor are dramatically increased in the AD brain, the neurotoxicity resulting from ROS release by fA beta/MCSF coactivated microglia may be a more appropriate model for assessing fA beta-induced microglial-mediated neuropathology in AD. Reactive Oxygen Species 178-181 colony stimulating factor 1 Homo sapiens 3-7 15494511-5 2004 Two variants of the alternative reading frame of M-CSF peptide substituted at P2 or P2 and P9 with Ala display weak or no T cell activation. Alanine 99-102 colony stimulating factor 1 Homo sapiens 49-54 15803435-6 2004 MCSF secretion into culture medium was measured using an enzyme immunoassay following 24 hours of treatment with Ang II alone or in combination with losartan or PD 123319. Losartan 149-157 colony stimulating factor 1 Homo sapiens 0-4 15803435-7 2004 Phorbol-myristate-acetate, known to stimulate release of AA and MCSF, was used as a positive control in both experiments. Tetradecanoylphorbol Acetate 0-25 colony stimulating factor 1 Homo sapiens 64-68 15485493-8 2004 Furthermore, inhibiting the generation of reactive oxygen species (ROS) using the specific NADPH oxidase inhibitor apocynin reversed fA beta/MCSF-induced neurotoxicity while L-NIO had little effect. Reactive Oxygen Species 42-65 colony stimulating factor 1 Homo sapiens 141-145 15485493-9 2004 As MCSF is endogenously expressed within the brain, and both its level and that of the MCSF receptor are dramatically increased in the AD brain, the neurotoxicity resulting from ROS release by fA beta/MCSF coactivated microglia may be a more appropriate model for assessing fA beta-induced microglial-mediated neuropathology in AD. Reactive Oxygen Species 178-181 colony stimulating factor 1 Homo sapiens 87-91 15485493-8 2004 Furthermore, inhibiting the generation of reactive oxygen species (ROS) using the specific NADPH oxidase inhibitor apocynin reversed fA beta/MCSF-induced neurotoxicity while L-NIO had little effect. Reactive Oxygen Species 67-70 colony stimulating factor 1 Homo sapiens 141-145 15485493-9 2004 As MCSF is endogenously expressed within the brain, and both its level and that of the MCSF receptor are dramatically increased in the AD brain, the neurotoxicity resulting from ROS release by fA beta/MCSF coactivated microglia may be a more appropriate model for assessing fA beta-induced microglial-mediated neuropathology in AD. Reactive Oxygen Species 178-181 colony stimulating factor 1 Homo sapiens 87-91 15388891-3 2004 Therefore, we hypothesized that MMP may also be involved in the membrane-bound M-CSF-mediated juxtacrine mechanism. juxtacrine 94-104 colony stimulating factor 1 Homo sapiens 79-84 15020512-8 2004 11-dehydro-TxB2 excretion with and without aspirin was related to MCSF concentrations (p < 0.01), and the percentage reduction of MCSF by aspirin was related to the reduction of 11-dehydro-TxB2 (p < 0.05) and the reduction of the ischaemic burden compared with placebo (p < 0.05). Aspirin 43-50 colony stimulating factor 1 Homo sapiens 66-70 15474071-0 2004 Synergistic effect of interleukin (IL)-1alpha and ceramide analogue on the production of IL-6, IL-8, and macrophage colony-stimulating factor by endometrial stromal cells. Ceramides 50-58 colony stimulating factor 1 Homo sapiens 105-141 15474071-2 2004 DESIGN: The effects of IL-1alpha, IL-1 receptor antagonist (IL-1RA), C2-ceramide, and C6-ceramide on the production of IL-6, IL-8, and M-CSF by ESC. N-acetylsphingosine 69-80 colony stimulating factor 1 Homo sapiens 135-140 15474071-2 2004 DESIGN: The effects of IL-1alpha, IL-1 receptor antagonist (IL-1RA), C2-ceramide, and C6-ceramide on the production of IL-6, IL-8, and M-CSF by ESC. N-caproylsphingosine 86-97 colony stimulating factor 1 Homo sapiens 135-140 15215307-3 2004 To find out whether these autophosphorylation sites can be used to identify downstream signaling proteins, synthetic peptides based on an autophosphorylation site in the colony-stimulating factor-1 (CSF-1) receptor were linked to agarose beads and incubated with lysates from macrophages. Peptides 117-125 colony stimulating factor 1 Homo sapiens 170-197 15215307-3 2004 To find out whether these autophosphorylation sites can be used to identify downstream signaling proteins, synthetic peptides based on an autophosphorylation site in the colony-stimulating factor-1 (CSF-1) receptor were linked to agarose beads and incubated with lysates from macrophages. Sepharose 230-237 colony stimulating factor 1 Homo sapiens 170-197 15268899-3 2004 In this report, we now show that non-antibiotic analogues of doxycycline (CMT-3) and minocycline (CMT-8) are potent inhibitors of osteoclastogenesis in vitro from human peripheral blood mononuclear cells (PBMC) stimulated with macrophage colony stimulating factor (MCSF) and receptor activator of NF-kappaB ligand (RANKL), through an action that is independent of osteoblast-osteoclast interactions. Minocycline 85-96 colony stimulating factor 1 Homo sapiens 227-263 15268899-3 2004 In this report, we now show that non-antibiotic analogues of doxycycline (CMT-3) and minocycline (CMT-8) are potent inhibitors of osteoclastogenesis in vitro from human peripheral blood mononuclear cells (PBMC) stimulated with macrophage colony stimulating factor (MCSF) and receptor activator of NF-kappaB ligand (RANKL), through an action that is independent of osteoblast-osteoclast interactions. Minocycline 85-96 colony stimulating factor 1 Homo sapiens 265-269 15268899-3 2004 In this report, we now show that non-antibiotic analogues of doxycycline (CMT-3) and minocycline (CMT-8) are potent inhibitors of osteoclastogenesis in vitro from human peripheral blood mononuclear cells (PBMC) stimulated with macrophage colony stimulating factor (MCSF) and receptor activator of NF-kappaB ligand (RANKL), through an action that is independent of osteoblast-osteoclast interactions. cmt 98-101 colony stimulating factor 1 Homo sapiens 227-263 15268899-3 2004 In this report, we now show that non-antibiotic analogues of doxycycline (CMT-3) and minocycline (CMT-8) are potent inhibitors of osteoclastogenesis in vitro from human peripheral blood mononuclear cells (PBMC) stimulated with macrophage colony stimulating factor (MCSF) and receptor activator of NF-kappaB ligand (RANKL), through an action that is independent of osteoblast-osteoclast interactions. cmt 98-101 colony stimulating factor 1 Homo sapiens 265-269 15289345-0 2004 Colony-stimulating factor-1 blockade by antisense oligonucleotides and small interfering RNAs suppresses growth of human mammary tumor xenografts in mice. Oligonucleotides 50-66 colony stimulating factor 1 Homo sapiens 0-27 15474071-9 2004 Production of both IL-8 and M-CSF was statistically significantly increased by IL-1alpha plus C6-ceramide as compared with IL-1alpha alone; however, IL-6 production was not increased. N-caproylsphingosine 94-105 colony stimulating factor 1 Homo sapiens 28-33 15474071-10 2004 CONCLUSION(S): The results suggest that IL-1alpha stimulates the production of IL-8 and M-CSF by a mechanism that involves the sphingomyelin-ceramide system. Sphingomyelins 127-140 colony stimulating factor 1 Homo sapiens 88-93 15474071-10 2004 CONCLUSION(S): The results suggest that IL-1alpha stimulates the production of IL-8 and M-CSF by a mechanism that involves the sphingomyelin-ceramide system. Ceramides 141-149 colony stimulating factor 1 Homo sapiens 88-93 15474071-11 2004 Ceramide may be important in increasing the production of IL-8 and M-CSF in the human endometrium. Ceramides 0-8 colony stimulating factor 1 Homo sapiens 67-72 15268899-3 2004 In this report, we now show that non-antibiotic analogues of doxycycline (CMT-3) and minocycline (CMT-8) are potent inhibitors of osteoclastogenesis in vitro from human peripheral blood mononuclear cells (PBMC) stimulated with macrophage colony stimulating factor (MCSF) and receptor activator of NF-kappaB ligand (RANKL), through an action that is independent of osteoblast-osteoclast interactions. Doxycycline 61-72 colony stimulating factor 1 Homo sapiens 227-263 15268899-3 2004 In this report, we now show that non-antibiotic analogues of doxycycline (CMT-3) and minocycline (CMT-8) are potent inhibitors of osteoclastogenesis in vitro from human peripheral blood mononuclear cells (PBMC) stimulated with macrophage colony stimulating factor (MCSF) and receptor activator of NF-kappaB ligand (RANKL), through an action that is independent of osteoblast-osteoclast interactions. Doxycycline 61-72 colony stimulating factor 1 Homo sapiens 265-269 15268899-3 2004 In this report, we now show that non-antibiotic analogues of doxycycline (CMT-3) and minocycline (CMT-8) are potent inhibitors of osteoclastogenesis in vitro from human peripheral blood mononuclear cells (PBMC) stimulated with macrophage colony stimulating factor (MCSF) and receptor activator of NF-kappaB ligand (RANKL), through an action that is independent of osteoblast-osteoclast interactions. cmt 74-77 colony stimulating factor 1 Homo sapiens 227-263 15268899-3 2004 In this report, we now show that non-antibiotic analogues of doxycycline (CMT-3) and minocycline (CMT-8) are potent inhibitors of osteoclastogenesis in vitro from human peripheral blood mononuclear cells (PBMC) stimulated with macrophage colony stimulating factor (MCSF) and receptor activator of NF-kappaB ligand (RANKL), through an action that is independent of osteoblast-osteoclast interactions. cmt 74-77 colony stimulating factor 1 Homo sapiens 265-269 15129424-11 2004 RESULTS: Curcumin inhibited the ligand-stimulated autophosphorylation of EGF-R and CSF1-R that were crucially involved in the development of osteomimetic properties of C4-2B cells. Curcumin 9-17 colony stimulating factor 1 Homo sapiens 83-87 14969583-2 2004 After adding CSF-1 to M1 myeloid cells expressing CSF-1R (CSF-1 receptor), tyrosine phosphorylation of many cellular proteins occurs, which might be linked to subsequent macrophage differentiation. Tyrosine 75-83 colony stimulating factor 1 Homo sapiens 13-18 15020512-8 2004 11-dehydro-TxB2 excretion with and without aspirin was related to MCSF concentrations (p < 0.01), and the percentage reduction of MCSF by aspirin was related to the reduction of 11-dehydro-TxB2 (p < 0.05) and the reduction of the ischaemic burden compared with placebo (p < 0.05). Aspirin 141-148 colony stimulating factor 1 Homo sapiens 133-137 15003795-5 2004 PMMA and TNF-alpha both stimulated M-CSF and sRANKL production whereas PMMA decreased and TNF-alpha augmented OPG release by Ob. Polymethyl Methacrylate 0-4 colony stimulating factor 1 Homo sapiens 35-40 12446614-0 2002 Tyrosines 559 and 807 in the cytoplasmic tail of the macrophage colony-stimulating factor receptor play distinct roles in osteoclast differentiation and function. Tyrosine 0-9 colony stimulating factor 1 Homo sapiens 53-89 14687666-2 2004 In this report, we characterize how monocytes and macrophages differentiated from monocytes with M-CSF and GM-CSF regulate their cGMP levels by controlling which phosphodiesterases (PDEs) and guanylyl cyclases (GCs) are expressed. Cyclic GMP 129-133 colony stimulating factor 1 Homo sapiens 97-102 15012615-9 2004 Significant negative correlations between plasma levels of both OPG and M-CSF with estradiol concentrations were observed in women (r=-0.39, P<0.01; r=-0.25, P<0.001 respectively). Estradiol 83-92 colony stimulating factor 1 Homo sapiens 72-77 14523050-13 2004 M-CSF deprivation resulted in activation of acid sphingomyelinase (A-SMase), increased ceramide levels, and a decrease in intracellular Cer-1-P. Exogenously added Cer-1-P inhibited A-SMase in intact BMDMs at concentrations that also prevented apoptosis. Ceramides 87-95 colony stimulating factor 1 Homo sapiens 0-5 12967481-0 2003 Mirimostim (macrophage colony-stimulating factor; M-CSF) improves chemotherapy-induced impaired natural killer cell activity, Th1/Th2 balance, and granulocyte function. mirimostim 0-10 colony stimulating factor 1 Homo sapiens 50-55 12967481-1 2003 The purpose of this study was to clarify the effects of mirimostim (macrophage colony-stimulating factor; M-CSF) on immunological functions after chemotherapy. mirimostim 56-66 colony stimulating factor 1 Homo sapiens 106-111 12684699-3 2003 Recently we found that macrophage colony-stimulating factor (M-CSF) inhibits 8-Br-cAMP-induced decidualization, differentiation to prolactin (PRL)-secreting cells, by suppressing viable decidualizing cells. 8-Bromo Cyclic Adenosine Monophosphate 77-86 colony stimulating factor 1 Homo sapiens 23-59 12684699-3 2003 Recently we found that macrophage colony-stimulating factor (M-CSF) inhibits 8-Br-cAMP-induced decidualization, differentiation to prolactin (PRL)-secreting cells, by suppressing viable decidualizing cells. 8-Bromo Cyclic Adenosine Monophosphate 77-86 colony stimulating factor 1 Homo sapiens 61-66 12684699-6 2003 A high concentration of M-CSF strongly suppressed the viable cell numbers and PRL secretion of stromal cells co-stimulated with 8-Br-cAMP and M-CSF, although G-CSF release from the co-stimulated stromal cells was not affected by M-CSF. 8-Bromo Cyclic Adenosine Monophosphate 128-137 colony stimulating factor 1 Homo sapiens 24-29 12684699-8 2003 These results indicate that M-CSF enhances G-CSF secretion from 8-Br-cAMP-unstimulated human endometrial stromal cells but not from 8-Br-cAMP-stimulated stromal cells, thus suggesting that there exists a functional subpopulation of G-CSF-secreting stromal cells that are different from the predecidualized ESCs that differentiate into PRL-secreting ESCs under stimuli with 8-Br-cAMP. 8-Bromo Cyclic Adenosine Monophosphate 64-73 colony stimulating factor 1 Homo sapiens 28-33 12684699-8 2003 These results indicate that M-CSF enhances G-CSF secretion from 8-Br-cAMP-unstimulated human endometrial stromal cells but not from 8-Br-cAMP-stimulated stromal cells, thus suggesting that there exists a functional subpopulation of G-CSF-secreting stromal cells that are different from the predecidualized ESCs that differentiate into PRL-secreting ESCs under stimuli with 8-Br-cAMP. 8-br 64-68 colony stimulating factor 1 Homo sapiens 28-33 12684699-8 2003 These results indicate that M-CSF enhances G-CSF secretion from 8-Br-cAMP-unstimulated human endometrial stromal cells but not from 8-Br-cAMP-stimulated stromal cells, thus suggesting that there exists a functional subpopulation of G-CSF-secreting stromal cells that are different from the predecidualized ESCs that differentiate into PRL-secreting ESCs under stimuli with 8-Br-cAMP. Cyclic AMP 69-73 colony stimulating factor 1 Homo sapiens 28-33 12594260-3 2003 Treatment by BP markedly inhibited the formation of adherent macrophagic cells deriving from monocytes upon the action of either GM-CSF or M-CSF. Benzo(a)pyrene 13-15 colony stimulating factor 1 Homo sapiens 130-135 12529666-4 2003 Furthermore, gel-shift analysis of APL cells showed elevated levels of PU.1 binding activity to the M-CSF receptor promoter, particularly after ATRA stimulation. Tretinoin 144-148 colony stimulating factor 1 Homo sapiens 100-105 12529666-6 2003 A variable proportion of ATRA-induced APL cells exhibited monocyte-like morphology and immunophenotype: the proportion of monocytic cells was consistently increased by combined treatment with ATRA and diverse hematopoietic growth factors cocktails, which always comprised M-CSF. Tretinoin 25-29 colony stimulating factor 1 Homo sapiens 272-277 12529666-6 2003 A variable proportion of ATRA-induced APL cells exhibited monocyte-like morphology and immunophenotype: the proportion of monocytic cells was consistently increased by combined treatment with ATRA and diverse hematopoietic growth factors cocktails, which always comprised M-CSF. Tretinoin 192-196 colony stimulating factor 1 Homo sapiens 272-277 15679045-10 2004 Exposure to LY294002 significantly decreased both CSF-1 and Dex-induced adhesiveness to the level of control cells. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 12-20 colony stimulating factor 1 Homo sapiens 50-55 14673177-0 2004 Phorbol 12-myristate 13-acetate-induced release of the colony-stimulating factor 1 receptor cytoplasmic domain into the cytosol involves two separate cleavage events. Tetradecanoylphorbol Acetate 0-31 colony stimulating factor 1 Homo sapiens 55-82 14579277-4 2003 Only very high doses of cyclosporin A and FK506 inhibited macrophage proliferation induced by growth factors, such as M-CSF, granulocyte-macrophage (GM)-CSF or IL-3. Cyclosporine 24-37 colony stimulating factor 1 Homo sapiens 118-123 14579277-4 2003 Only very high doses of cyclosporin A and FK506 inhibited macrophage proliferation induced by growth factors, such as M-CSF, granulocyte-macrophage (GM)-CSF or IL-3. Tacrolimus 42-47 colony stimulating factor 1 Homo sapiens 118-123 12882960-4 2003 In the human monocytic cell line, THP-1, SHIP-1 became tyrosine-phosphorylated following M-CSF activation in a Src family kinase-dependent manner. Tyrosine 55-63 colony stimulating factor 1 Homo sapiens 89-94 14499874-8 2003 CONCLUSIONS: MM and M-CSF-induced VSMC killing requires MM binding to VSMC mediated by Mac-1 and ICAM-1, and Fas-FasL interaction. vsmc 34-38 colony stimulating factor 1 Homo sapiens 20-25 12970769-6 2003 Imatinib blocked monocyte/macrophage development in cultures stimulated with and without M-CSF, suggesting that inhibition of the M-CSF receptor, c-fms, by imatinib was unlikely to be responsible. Imatinib Mesylate 0-8 colony stimulating factor 1 Homo sapiens 89-94 14680610-0 2003 [Effect of estradiol and progesterone on production of macrophage colony-stimulating factor by human granulosa cells in vitro]. Estradiol 11-20 colony stimulating factor 1 Homo sapiens 55-91 14680610-0 2003 [Effect of estradiol and progesterone on production of macrophage colony-stimulating factor by human granulosa cells in vitro]. Progesterone 25-37 colony stimulating factor 1 Homo sapiens 55-91 14680610-1 2003 OBJECTIVE: To investigate the effect of estradiol (E(2)) and progesterone (P) on macrophage colony-stimulating factor (M-CSF) production by human luteinized granulosa cells in vitro. Estradiol 40-49 colony stimulating factor 1 Homo sapiens 81-117 14680610-1 2003 OBJECTIVE: To investigate the effect of estradiol (E(2)) and progesterone (P) on macrophage colony-stimulating factor (M-CSF) production by human luteinized granulosa cells in vitro. Estradiol 40-49 colony stimulating factor 1 Homo sapiens 119-124 14680610-1 2003 OBJECTIVE: To investigate the effect of estradiol (E(2)) and progesterone (P) on macrophage colony-stimulating factor (M-CSF) production by human luteinized granulosa cells in vitro. Progesterone 61-73 colony stimulating factor 1 Homo sapiens 81-117 14680610-1 2003 OBJECTIVE: To investigate the effect of estradiol (E(2)) and progesterone (P) on macrophage colony-stimulating factor (M-CSF) production by human luteinized granulosa cells in vitro. Progesterone 61-73 colony stimulating factor 1 Homo sapiens 119-124 14680610-6 2003 RESULTS: The basic concentration of M-CSF in cultivated granulosa cells without E(2) stimulation was low (47 +/- 15 ng/L). Estradiol 80-84 colony stimulating factor 1 Homo sapiens 36-41 14680610-10 2003 CONCLUSIONS: Estradiol can stimulate M-CSF production by luteinized granulosa cells in vitro in a dose-dependent mode, on the other hand P cannot induce M-CSF production by luteinized granulosa cells. Estradiol 13-22 colony stimulating factor 1 Homo sapiens 37-42 12748184-0 2003 Hyaluronan-mediated CD44 interaction with RhoGEF and Rho kinase promotes Grb2-associated binder-1 phosphorylation and phosphatidylinositol 3-kinase signaling leading to cytokine (macrophage-colony stimulating factor) production and breast tumor progression. Hyaluronic Acid 0-10 colony stimulating factor 1 Homo sapiens 179-215 12748184-6 2003 Our results also demonstrate that HA/CD44-mediated oncogenic events (e.g. AKT activation, M-CSF production and breast tumor cell-specific phenotypes) can be effectively blocked by a PI 3-kinase inhibitor (LY294002). 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 205-213 colony stimulating factor 1 Homo sapiens 90-95 12750385-11 2003 M-CSF deprivation resulted in activation of acid sphingomyelinase and an increase in ceramide levels. Ceramides 85-93 colony stimulating factor 1 Homo sapiens 0-5 12750385-12 2003 Desipramine (a sphingomyelinase inhibitor) prevented the increase in ceramide and inhibited apoptosis after M-CSF deprivation. Desipramine 0-11 colony stimulating factor 1 Homo sapiens 108-113 12750385-13 2003 Ox-LDL completely blocked the increase in acid sphingomyelinase activity as well as the increase in ceramide after M-CSF deprivation. Ceramides 100-108 colony stimulating factor 1 Homo sapiens 115-120 14506958-7 2003 The number of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells (MNCs) and the percentage area of lacunar resorption induced by RANKL and M-CSF were decreased when menatetrenone or geranylgeraniol was added to the cultures. menatetrenone 187-200 colony stimulating factor 1 Homo sapiens 161-166 12535753-8 2003 HDL cholesterol correlated inversely with IL-6, M-CSF, E-selectin, and HOMA IR. Cholesterol 4-15 colony stimulating factor 1 Homo sapiens 48-53 12554805-3 2003 M-CSF induced rapid catalytic activation of PKC-delta and membrane translocation of the tyrosine phosphorylated form of PKC-delta. Tyrosine 88-96 colony stimulating factor 1 Homo sapiens 0-5 12554805-4 2003 Mutation of tyrosine 807 in the M-CSF receptor (Fms) abrogates cell differentiation but not a proliferative response to M-CSF, and FmsY807F failed to activate PKC-delta. Tyrosine 12-20 colony stimulating factor 1 Homo sapiens 32-37 12393560-8 2002 In addition, z-VAD-fmk amplifies the differentiation-associated production of radical oxygen species in both phorbol ester-differentiated U937 cells and M-CSF-treated monocytes, shifting the differentiation process to nonapoptotic cell death. benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone 13-22 colony stimulating factor 1 Homo sapiens 153-158 12393560-8 2002 In addition, z-VAD-fmk amplifies the differentiation-associated production of radical oxygen species in both phorbol ester-differentiated U937 cells and M-CSF-treated monocytes, shifting the differentiation process to nonapoptotic cell death. radical 78-85 colony stimulating factor 1 Homo sapiens 153-158 12393560-8 2002 In addition, z-VAD-fmk amplifies the differentiation-associated production of radical oxygen species in both phorbol ester-differentiated U937 cells and M-CSF-treated monocytes, shifting the differentiation process to nonapoptotic cell death. oxygen species 86-100 colony stimulating factor 1 Homo sapiens 153-158 12446614-8 2002 Thus, we have identified specific tyrosine residues in the cytoplasmic tail of c-Fms that are critical for transmitting M-CSF-initiated signals individually required for OC formation or function, respectively. Tyrosine 34-42 colony stimulating factor 1 Homo sapiens 120-125 12372416-0 2002 Vitamin D(3) and analogues modulate the expression of CSF-1 and its receptor in human dendritic cells. Vitamin D 0-9 colony stimulating factor 1 Homo sapiens 54-59 12444151-1 2002 We previously reported that activation of the phosphatidylinositol (PI) 3-kinase pathway was important in M-CSF-induced monocyte survival. Phosphatidylinositols 46-66 colony stimulating factor 1 Homo sapiens 106-111 12444151-3 2002 We found that, in addition to the MAP/Erk kinase inhibitor PD098059, the PI 3-kinase inhibitors LY294002 and wortmannin both suppressed Erk activation in M-CSF-treated monocytes, suggesting that 3-phosphorylated products of PI 3-kinase played a role in Erk activation. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 59-67 colony stimulating factor 1 Homo sapiens 154-159 12444151-3 2002 We found that, in addition to the MAP/Erk kinase inhibitor PD098059, the PI 3-kinase inhibitors LY294002 and wortmannin both suppressed Erk activation in M-CSF-treated monocytes, suggesting that 3-phosphorylated products of PI 3-kinase played a role in Erk activation. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 96-104 colony stimulating factor 1 Homo sapiens 154-159 12444151-3 2002 We found that, in addition to the MAP/Erk kinase inhibitor PD098059, the PI 3-kinase inhibitors LY294002 and wortmannin both suppressed Erk activation in M-CSF-treated monocytes, suggesting that 3-phosphorylated products of PI 3-kinase played a role in Erk activation. Wortmannin 109-119 colony stimulating factor 1 Homo sapiens 154-159 12444151-4 2002 Investigating the biochemical pathways regulated by PI 3-kinase to activate Erk, we found that, in response to M-CSF, normal human monocytes induced reactive oxygen species (ROS), which were suppressed by the PI 3-kinase inhibitor wortmannin but not by the solvent control DMSO or the MAP/Erk kinase inhibitor PD098059. Reactive Oxygen Species 149-172 colony stimulating factor 1 Homo sapiens 111-116 12444151-4 2002 Investigating the biochemical pathways regulated by PI 3-kinase to activate Erk, we found that, in response to M-CSF, normal human monocytes induced reactive oxygen species (ROS), which were suppressed by the PI 3-kinase inhibitor wortmannin but not by the solvent control DMSO or the MAP/Erk kinase inhibitor PD098059. Reactive Oxygen Species 174-177 colony stimulating factor 1 Homo sapiens 111-116 12444151-4 2002 Investigating the biochemical pathways regulated by PI 3-kinase to activate Erk, we found that, in response to M-CSF, normal human monocytes induced reactive oxygen species (ROS), which were suppressed by the PI 3-kinase inhibitor wortmannin but not by the solvent control DMSO or the MAP/Erk kinase inhibitor PD098059. Wortmannin 231-241 colony stimulating factor 1 Homo sapiens 111-116 12444151-4 2002 Investigating the biochemical pathways regulated by PI 3-kinase to activate Erk, we found that, in response to M-CSF, normal human monocytes induced reactive oxygen species (ROS), which were suppressed by the PI 3-kinase inhibitor wortmannin but not by the solvent control DMSO or the MAP/Erk kinase inhibitor PD098059. Dimethyl Sulfoxide 273-277 colony stimulating factor 1 Homo sapiens 111-116 12444151-4 2002 Investigating the biochemical pathways regulated by PI 3-kinase to activate Erk, we found that, in response to M-CSF, normal human monocytes induced reactive oxygen species (ROS), which were suppressed by the PI 3-kinase inhibitor wortmannin but not by the solvent control DMSO or the MAP/Erk kinase inhibitor PD098059. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 310-318 colony stimulating factor 1 Homo sapiens 111-116 12444151-7 2002 To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes. Reactive Oxygen Species 21-24 colony stimulating factor 1 Homo sapiens 36-41 12444151-7 2002 To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes. Reactive Oxygen Species 21-24 colony stimulating factor 1 Homo sapiens 164-169 12444151-7 2002 To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes. Acetylcysteine 89-105 colony stimulating factor 1 Homo sapiens 36-41 12444151-7 2002 To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes. Acetylcysteine 89-105 colony stimulating factor 1 Homo sapiens 164-169 12444151-7 2002 To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes. diphenyleneiodonium 110-129 colony stimulating factor 1 Homo sapiens 36-41 12444151-7 2002 To determine whether ROS induced by M-CSF played a role in Erk activation, we found that N-acetylcysteine and diphenyleneiodonium both suppressed Erk activation in M-CSF-treated monocytes. diphenyleneiodonium 110-129 colony stimulating factor 1 Homo sapiens 164-169 12444151-9 2002 These data suggest that, in M-CSF-stimulated human monocytes, PI 3-kinase products and ROS production play a role in Erk activation and monocyte survival. Reactive Oxygen Species 87-90 colony stimulating factor 1 Homo sapiens 28-33 12207034-4 2002 Conversely, transfected CSF-1(L241-S353), attached C-terminally on the DCN prepropeptide, contained almost exclusively d-glucuronate. Glucuronic Acid 119-132 colony stimulating factor 1 Homo sapiens 24-29 12207034-5 2002 Transfected intact chimeric DCN(M1-Q153)-CSF-1(L241-S353), with two glycosaminoglycan chains, also contained almost exclusively d-glucuronate in chains at both sites, as did chimeras in which alanine was substituted for serine at either of the glycosaminoglycan attachment sites. Glycosaminoglycans 68-85 colony stimulating factor 1 Homo sapiens 41-46 12207034-5 2002 Transfected intact chimeric DCN(M1-Q153)-CSF-1(L241-S353), with two glycosaminoglycan chains, also contained almost exclusively d-glucuronate in chains at both sites, as did chimeras in which alanine was substituted for serine at either of the glycosaminoglycan attachment sites. Glucuronic Acid 128-141 colony stimulating factor 1 Homo sapiens 41-46 12207034-7 2002 C-terminal truncation constructs were prepared from the full-length chimera with an alanine substitution at the CSF-1 glycosaminoglycan attachment site. Alanine 84-91 colony stimulating factor 1 Homo sapiens 112-117 12207034-7 2002 C-terminal truncation constructs were prepared from the full-length chimera with an alanine substitution at the CSF-1 glycosaminoglycan attachment site. Glycosaminoglycans 118-135 colony stimulating factor 1 Homo sapiens 112-117 12372416-7 2002 The results showed that 1,25(OH)(2)D(3) and tacalcitol significantly up-regulated CSF-1 mRNA-expression and protein secretion in a dose-dependent manner. 1 alpha,24-dihydroxyvitamin D3 44-54 colony stimulating factor 1 Homo sapiens 82-87 12372416-12 2002 These data point towards a distinct and specific regulation of CSF-1 and its receptor by 1,25(OH)(2)D(3) and its analogue tacalcitol in human monocytes which parallels the inhibition of differentiation into dendritic cells without altering survival. 1 alpha,24-dihydroxyvitamin D3 122-132 colony stimulating factor 1 Homo sapiens 63-68 12126567-11 2002 M-CSF enhances estradiol and progesterone production by LGC and FSH has an additional or synergetic effect with M-CSF. Estradiol 15-24 colony stimulating factor 1 Homo sapiens 0-5 12110011-8 2002 In situ hybridization was performed using digoxigenin labeled M-CSF specific probe. Digoxigenin 42-53 colony stimulating factor 1 Homo sapiens 62-67 12110011-13 2002 CONCLUSIONS: Our findings suggest that the increase in M-CSF-stimulated local production of nitric oxide may be a major mediator in the development of reflux nephropathy. Nitric Oxide 92-104 colony stimulating factor 1 Homo sapiens 55-60 12126567-1 2002 OBJECTIVE: To investigate the effects of macrophage colony-stimulating factor (M-CSF) on estradiol and progesterone production by human luteinized granulosa cells in vitro and to detect M-CSF receptor in human granulosa cells. Estradiol 89-98 colony stimulating factor 1 Homo sapiens 41-77 12126567-1 2002 OBJECTIVE: To investigate the effects of macrophage colony-stimulating factor (M-CSF) on estradiol and progesterone production by human luteinized granulosa cells in vitro and to detect M-CSF receptor in human granulosa cells. Estradiol 89-98 colony stimulating factor 1 Homo sapiens 79-84 12126567-11 2002 M-CSF enhances estradiol and progesterone production by LGC and FSH has an additional or synergetic effect with M-CSF. Progesterone 29-41 colony stimulating factor 1 Homo sapiens 0-5 12126567-1 2002 OBJECTIVE: To investigate the effects of macrophage colony-stimulating factor (M-CSF) on estradiol and progesterone production by human luteinized granulosa cells in vitro and to detect M-CSF receptor in human granulosa cells. Progesterone 103-115 colony stimulating factor 1 Homo sapiens 41-77 12126567-1 2002 OBJECTIVE: To investigate the effects of macrophage colony-stimulating factor (M-CSF) on estradiol and progesterone production by human luteinized granulosa cells in vitro and to detect M-CSF receptor in human granulosa cells. Progesterone 103-115 colony stimulating factor 1 Homo sapiens 79-84 12038073-13 2002 Significant increase of M-CSF levels in the AMYL group could lead to greater activation of monocyte-macrophage system and could serve as factor supporting amyloid deposition process. amyl 44-48 colony stimulating factor 1 Homo sapiens 24-29 12126567-9 2002 Thus M-CSF caused a significant dose dependent increase of estradiol and progesterone production (P < 0.05), and M-CSF+ FSH further stimulated higher production of E(2) and P by LGC than M-CSF or FSH alone (P < 0.05). Estradiol 59-68 colony stimulating factor 1 Homo sapiens 5-10 12126567-9 2002 Thus M-CSF caused a significant dose dependent increase of estradiol and progesterone production (P < 0.05), and M-CSF+ FSH further stimulated higher production of E(2) and P by LGC than M-CSF or FSH alone (P < 0.05). Progesterone 73-85 colony stimulating factor 1 Homo sapiens 5-10 12079557-7 2002 Addition of AZT or ritonavir before or after establishment of productive HIV infection dramatically reduces virus replication and M-CSF production by human MDMs. Zidovudine 12-15 colony stimulating factor 1 Homo sapiens 130-135 12079557-7 2002 Addition of AZT or ritonavir before or after establishment of productive HIV infection dramatically reduces virus replication and M-CSF production by human MDMs. Ritonavir 19-28 colony stimulating factor 1 Homo sapiens 130-135 12050183-4 2002 We have found that EPA induces cell death of the monocyte via apoptosis, even in the presence of M-CSF or GM-CSF, and inhibits differentiation from the monocyte to macrophage by inducing H2O2 production. Eicosapentaenoic Acid 19-22 colony stimulating factor 1 Homo sapiens 97-102 12010778-4 2002 NS-398 (1 microM), a cyclo-oxygenase-2 (COX-2) inhibitor, inhibited IL-6 and VEGF production (35+/-4% and 26+/-2%, respectively) but enhanced M-CSF production (38+/-4%) by IL-1beta (1 ng ml(-1)) in synovial fibroblasts isolated from patients with osteoarthritis (OA) and rheumatoid arthritis (RA). N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide 0-6 colony stimulating factor 1 Homo sapiens 142-147 12010778-7 2002 8-Bromo cyclic AMP and dibutyryl cyclic AMP, cyclic AMP analogues, mimicked the effects of PGE(2) on IL-6, M-CSF, and VEGF production by OA fibroblasts. 8-Bromo Cyclic Adenosine Monophosphate 0-18 colony stimulating factor 1 Homo sapiens 107-112 12010778-7 2002 8-Bromo cyclic AMP and dibutyryl cyclic AMP, cyclic AMP analogues, mimicked the effects of PGE(2) on IL-6, M-CSF, and VEGF production by OA fibroblasts. Bucladesine 23-43 colony stimulating factor 1 Homo sapiens 107-112 12010778-7 2002 8-Bromo cyclic AMP and dibutyryl cyclic AMP, cyclic AMP analogues, mimicked the effects of PGE(2) on IL-6, M-CSF, and VEGF production by OA fibroblasts. Cyclic AMP 8-18 colony stimulating factor 1 Homo sapiens 107-112 12010778-7 2002 8-Bromo cyclic AMP and dibutyryl cyclic AMP, cyclic AMP analogues, mimicked the effects of PGE(2) on IL-6, M-CSF, and VEGF production by OA fibroblasts. Prostaglandins E 91-94 colony stimulating factor 1 Homo sapiens 107-112 12010778-14 2002 These results suggest that endogenous PGE(2) regulates the production of IL-6, M-CSF, and VEGF by IL-1beta-stimulated human synovial fibroblasts through the activation of EP(2) and EP(4) receptors with increase in cyclic AMP. Prostaglandins E 38-41 colony stimulating factor 1 Homo sapiens 79-84 11959396-2 2002 In monotypic microglial cultures, M-CSF strongly augments amyloid beta (Abeta) induced microglial production of proinflammatory cytokines and nitric oxide. Nitric Oxide 142-154 colony stimulating factor 1 Homo sapiens 34-39 11956031-9 2002 Median CSF-1 levels were dramatically higher in patients with newly diagnosed tumours of the head & neck (604 pg/ml), in men with prostate cancer metastatic to bone (627 pg/ml) and women with advanced metastatic breast cancer (867 pg/ml) than those seen in patients with newly diagnosed breast tumours (334 pg/ml). Adenosine Monophosphate 99-102 colony stimulating factor 1 Homo sapiens 7-12 11850825-0 2002 C-Cbl binds the CSF-1 receptor at tyrosine 973, a novel phosphorylation site in the receptor"s carboxy-terminus. Tyrosine 34-42 colony stimulating factor 1 Homo sapiens 16-21 11850825-2 2002 Binding of CSF-1 to its receptor results in activation of the kinase domain and autophosphorylation on a number of tyrosine residues. Tyrosine 115-123 colony stimulating factor 1 Homo sapiens 11-16 11818450-0 2002 Cyclosporin A inhibition of macrophage colony-stimulating factor (M-CSF) production by activated human T lymphocytes. Cyclosporine 0-13 colony stimulating factor 1 Homo sapiens 28-64 11818450-0 2002 Cyclosporin A inhibition of macrophage colony-stimulating factor (M-CSF) production by activated human T lymphocytes. Cyclosporine 0-13 colony stimulating factor 1 Homo sapiens 66-71 11828794-12 2002 The relationship with the acetylcholine induction dose clarified that plasma M-CSF levels were highest in patients with active VSA in the acetylcholine low-dose group (825 +/- 177 pg/ml, p < 0.001). Acetylcholine 26-39 colony stimulating factor 1 Homo sapiens 77-82 11789672-8 2002 When M-CSF was added to cultured PBM, the level of IL-8 in the supernatant increased with the concentration of M-CSF. pbm 33-36 colony stimulating factor 1 Homo sapiens 5-10 11789672-8 2002 When M-CSF was added to cultured PBM, the level of IL-8 in the supernatant increased with the concentration of M-CSF. pbm 33-36 colony stimulating factor 1 Homo sapiens 111-116 11828794-12 2002 The relationship with the acetylcholine induction dose clarified that plasma M-CSF levels were highest in patients with active VSA in the acetylcholine low-dose group (825 +/- 177 pg/ml, p < 0.001). Acetylcholine 138-151 colony stimulating factor 1 Homo sapiens 77-82 11684285-8 2001 Monoclonal antibody (McAb) against M-CSF and anti-sense oligodeoxynucleotides (ASON) blocking M-CSF expression inhibited the proliferation of HL-60 cells. Oligodeoxyribonucleotides 56-77 colony stimulating factor 1 Homo sapiens 94-99 11704643-7 2001 HT-29 cells secreted bioactive levels of GM-CSF, G-CSF and M-CSF when stimulated with IL-1ss and TNF-alpha, and diclofenac (10(-7)-10(-4) M), indomethacin (10(-7)-10(-4) M) and sodium salicylate (10(-5)-10(-2) M) induced concentration-dependent increases in GM-CSF secretion. Indomethacin 142-154 colony stimulating factor 1 Homo sapiens 42-47 11704643-7 2001 HT-29 cells secreted bioactive levels of GM-CSF, G-CSF and M-CSF when stimulated with IL-1ss and TNF-alpha, and diclofenac (10(-7)-10(-4) M), indomethacin (10(-7)-10(-4) M) and sodium salicylate (10(-5)-10(-2) M) induced concentration-dependent increases in GM-CSF secretion. Sodium Salicylate 177-194 colony stimulating factor 1 Homo sapiens 42-47 11556524-6 2001 CONCLUSIONS: These data support the elevation of HDC expression during human monocytic differentiation and the possibility that monocyte-derived histamine is partially involved in regulation of M-CSF induced in vitro human monocyte/macrophage phagocytic differentiation. Histamine 145-154 colony stimulating factor 1 Homo sapiens 194-199 11714163-1 2001 CSF1PO is one of the thirteen core loci used for the CODIS database, and alleles reported for this short tandem repeat (STR) locus contain from 6 to 15 repeats of the tetranucleotide AGAT. tetranucleotide 167-182 colony stimulating factor 1 Homo sapiens 0-4 11714451-7 2001 Moreover, in these M-CSF-treated patients, the percentage of superoxide anion production by granulocytes was maintained at the level before chemotherapy. Superoxides 61-77 colony stimulating factor 1 Homo sapiens 19-24 11606030-8 2001 Moreover, the saponin fraction induced apoptotic cell death of macrophages only when they were stimulated by M-CSF; it did not affect the viability of macrophages cultured without M-CSF or with granulocyte/macrophage-CSF. Saponins 14-21 colony stimulating factor 1 Homo sapiens 109-114 11513742-0 2001 Colony-stimulating factor-1 (CSF-1) receptor-mediated macrophage differentiation in myeloid cells: a role for tyrosine 559-dependent protein phosphatase 2A (PP2A) activity. Tyrosine 110-118 colony stimulating factor 1 Homo sapiens 0-27 11513742-0 2001 Colony-stimulating factor-1 (CSF-1) receptor-mediated macrophage differentiation in myeloid cells: a role for tyrosine 559-dependent protein phosphatase 2A (PP2A) activity. Tyrosine 110-118 colony stimulating factor 1 Homo sapiens 29-34 11513742-4 2001 We report that the extent of CSF-1-mediated tyrosine phosphorylation of protein phosphatase 2A (PP2A), and the associated loss of its activity were reduced in M1 cells transfected with the CSF-1R with a tyrosine-to-phenylalanine mutation at position 559 (M1/559 cells), compared with the corresponding responses in CSF-1-treated M1/WT cells. Tyrosine 44-52 colony stimulating factor 1 Homo sapiens 29-34 11513742-4 2001 We report that the extent of CSF-1-mediated tyrosine phosphorylation of protein phosphatase 2A (PP2A), and the associated loss of its activity were reduced in M1 cells transfected with the CSF-1R with a tyrosine-to-phenylalanine mutation at position 559 (M1/559 cells), compared with the corresponding responses in CSF-1-treated M1/WT cells. Tyrosine 44-52 colony stimulating factor 1 Homo sapiens 189-194 11513742-5 2001 This evidence for an involvement of a reduction in PP2A activity in the differentiation process was supported by the restoration of the defect in the CSF-1-mediated differentiation of M1/559 cells by the addition of the PP2A inhibitor, okadaic acid. Okadaic Acid 236-248 colony stimulating factor 1 Homo sapiens 150-155 11368781-11 2001 Wholly, these studies indicate that elevated cAMP antagonizes IL-1-induced M-CSF transcription by up-regulating IkappaBalpha gene induction and its consequent attenuation of NF-kappaB activation. Cyclic AMP 45-49 colony stimulating factor 1 Homo sapiens 75-80 11368781-1 2001 We have recently reported that interleukin-1alpha (IL-1alpha) can induce human macrophage colony-stimulating factor (M-CSF) expression through nuclear factor kappaB (NF-kappaB) activation, and treatment of human pancreatic MIA PaCa-2 cancer cells with forskolin or cAMP attenuated the NF-kappaB activation as well as M-CSF expression. Colforsin 252-261 colony stimulating factor 1 Homo sapiens 117-122 11212113-0 2001 Securiosides A and B, novel acylated triterpene bisdesmosides with selective cytotoxic activity against M-CSF-stimulated macrophages. securiosides a and b 0-20 colony stimulating factor 1 Homo sapiens 104-109 11368781-1 2001 We have recently reported that interleukin-1alpha (IL-1alpha) can induce human macrophage colony-stimulating factor (M-CSF) expression through nuclear factor kappaB (NF-kappaB) activation, and treatment of human pancreatic MIA PaCa-2 cancer cells with forskolin or cAMP attenuated the NF-kappaB activation as well as M-CSF expression. Cyclic AMP 265-269 colony stimulating factor 1 Homo sapiens 117-122 11357885-0 2001 Dexamethasone increases the expression of membrane macrophage colony stimulating factor from retrovirally transduced tumor cells expressing macrophage colony stimulating factor. Dexamethasone 0-13 colony stimulating factor 1 Homo sapiens 51-87 11357885-0 2001 Dexamethasone increases the expression of membrane macrophage colony stimulating factor from retrovirally transduced tumor cells expressing macrophage colony stimulating factor. Dexamethasone 0-13 colony stimulating factor 1 Homo sapiens 140-176 11357885-3 2001 M-CSF-transfected tumor cells expressed additional mM-CSF in response to 18-72 h incubations with 3-15 microg/ml dexamethasone, while non-transfected parental cells were unaffected by this treatment. Dexamethasone 113-126 colony stimulating factor 1 Homo sapiens 0-5 11357885-7 2001 All trans-retinal and 1,25-dihydroxy vitamin D3 compounds that have been reported to induce M-CSF expression failed to increase mM-CSF. Calcitriol 22-47 colony stimulating factor 1 Homo sapiens 92-97 11238916-11 2001 The results suggest that paxillin is dephosphorylated by PTP phi in dorsal ruffles, using Pyk2 as a bridging molecule, resulting in a reduced pool of tyrosine-phosphorylated paxillin available for incorporation into focal complexes, thereby mediating CSF-1 regulation of macrophage morphology, adhesion, and motility. Tyrosine 150-158 colony stimulating factor 1 Homo sapiens 251-256 11212113-2 2001 Securiosides A and B showed potent selective cytotoxic activity against M-CSF-stimulated macrophages and were suggested to have potential as new agents for the treatment of inflammatory diseases such as RA and atherosclerosis. securiosides a and b 0-20 colony stimulating factor 1 Homo sapiens 72-77 11211941-7 2001 The production of M-CSF was markedly increased over the basal level after treatment with forskolin (10 microM) for 24 (P < 0.02) and 48 hr (P < 0.01); however, the production of MCP-1 was unchanged. Colforsin 89-98 colony stimulating factor 1 Homo sapiens 18-23 11211941-8 2001 CONCLUSIONS: Our data suggest that M-CSF and MCP-1 may play an important role in human preovulatory processes and that M-CSF, in particular, may be regulated by cyclic adenosine monophosphate. Cyclic AMP 161-191 colony stimulating factor 1 Homo sapiens 119-124 11372744-0 2001 Tyrosine phosphorylation of proteins in primary human myeloid leukemic cells stimulated by macrophage colony-stimulating factor: analysis by disease type and comparison with normal human hematopoietic cells. Tyrosine 0-8 colony stimulating factor 1 Homo sapiens 91-127 11223707-3 2001 M-CSF alone affected neither the viable cell numbers nor PRL release of nonstimulated stromal cells, while high concentrations of M-CSF strongly suppressed the viable cell numbers and PRL secretion of stromal cells costimulated with 8-Br-cAMP and M-CSF. 8-Bromo Cyclic Adenosine Monophosphate 233-242 colony stimulating factor 1 Homo sapiens 130-135 11223707-3 2001 M-CSF alone affected neither the viable cell numbers nor PRL release of nonstimulated stromal cells, while high concentrations of M-CSF strongly suppressed the viable cell numbers and PRL secretion of stromal cells costimulated with 8-Br-cAMP and M-CSF. 8-Bromo Cyclic Adenosine Monophosphate 233-242 colony stimulating factor 1 Homo sapiens 130-135 11372744-1 2001 We investigated tyrosine phosphorylation of proteins in primary human leukemic cells stimulated by macrophage colony-stimulating factor (M-CSF) in 60 patients with acute myeloid leukemia (AML) and 5 patients with chronic myelomonocytic leukemia and compared the findings for leukemic cells with those of normal human monocytes and bone marrow immature hematopoietic cells. Tyrosine 16-24 colony stimulating factor 1 Homo sapiens 99-135 11372744-1 2001 We investigated tyrosine phosphorylation of proteins in primary human leukemic cells stimulated by macrophage colony-stimulating factor (M-CSF) in 60 patients with acute myeloid leukemia (AML) and 5 patients with chronic myelomonocytic leukemia and compared the findings for leukemic cells with those of normal human monocytes and bone marrow immature hematopoietic cells. Tyrosine 16-24 colony stimulating factor 1 Homo sapiens 137-142 11372744-2 2001 M-CSF induced tyrosine phosphorylation of p140-200, p110, p60, p44, and p42 frequently, and that of p95 and p55 less frequently, in primary myeloid leukemic cells, whereas M-CSF-induced phosphorylation of proteins was not detected in the normal human hematopoietic cells tested. Tyrosine 14-22 colony stimulating factor 1 Homo sapiens 0-5 11372744-4 2001 M-CSF-induced tyrosine phosphorylation was observed frequently (89%) in AML of French-American-British class M4 and infrequently in all other subtypes of AML, including M5. Tyrosine 14-22 colony stimulating factor 1 Homo sapiens 0-5 11372744-8 2001 We also identified tyrosine phosphorylation of Vav, Shc, and extracellular signal-regulated kinase by M-CSF in some cases. Tyrosine 19-27 colony stimulating factor 1 Homo sapiens 102-107 11372744-9 2001 These findings clarified an M-CSF-specific pattern of protein tyrosine phosphorylation and the responsiveness to M-CSF of primary human myeloid cells. Tyrosine 62-70 colony stimulating factor 1 Homo sapiens 28-33 11090705-2 2000 Administration of M-CSF increased the number of splenic NK1.1(+) cells (vs. saline: P<0.01). Sodium Chloride 76-82 colony stimulating factor 1 Homo sapiens 18-23 11192516-6 2000 In order to elucidate the cause of hypolipidemia in AA, we assayed serum macrophage colony stimulating factor (M-CSF), which is well known to have apparent cholesterol-lowering activity, by using an enzyme-linked immunosorbent assay in seven patients with hypocholesterolemia and compared the results with those obtained in patients with iron-deficiency anemia (IDA). Cholesterol 156-167 colony stimulating factor 1 Homo sapiens 73-109 11192516-6 2000 In order to elucidate the cause of hypolipidemia in AA, we assayed serum macrophage colony stimulating factor (M-CSF), which is well known to have apparent cholesterol-lowering activity, by using an enzyme-linked immunosorbent assay in seven patients with hypocholesterolemia and compared the results with those obtained in patients with iron-deficiency anemia (IDA). Cholesterol 156-167 colony stimulating factor 1 Homo sapiens 111-116 11192516-10 2000 The serum M-CSF level was significantly higher in patients with TC levels lower than 150 mg/dL compared with controls. Technetium 64-66 colony stimulating factor 1 Homo sapiens 10-15 10830300-4 2000 Here we demonstrate, using the inhibitors wortmannin and LY294002, that activation of phosphatidylinositol 3-kinase (PI3-K) is required for CSF-1-induced spreading in osteoclasts. Wortmannin 42-52 colony stimulating factor 1 Homo sapiens 140-145 11000582-3 2000 The maximum response was obtained with 10 ng/ml (3857 U/ml) of M-CSF by counting the viable cell number using the trypan blue exclusion assay. Trypan Blue 114-125 colony stimulating factor 1 Homo sapiens 63-68 11000582-4 2000 [(3)H]-thymidine incorporation by these cells was also suppressed following a 96-h incubation with M-CSF. Thymidine 7-16 colony stimulating factor 1 Homo sapiens 99-104 11034310-2 2000 Here we have first shown that M-CSFR is the major Mona partner in M-CSF signaling, the interaction being mediated through tyrosine 697 of the receptor. Tyrosine 122-130 colony stimulating factor 1 Homo sapiens 30-35 10926834-0 2000 cAMP attenuates interleukin-1-stimulated macrophage colony-stimulating factor (M-CSF) expression. Cyclic AMP 0-4 colony stimulating factor 1 Homo sapiens 41-77 10926834-0 2000 cAMP attenuates interleukin-1-stimulated macrophage colony-stimulating factor (M-CSF) expression. Cyclic AMP 0-4 colony stimulating factor 1 Homo sapiens 79-84 10926834-4 2000 Treatment of the cells with forskolin or dibutyryl-cAMP attenuated the expression of M-CSF induced by IL-1alpha or LPS, but not by PMA. Colforsin 28-37 colony stimulating factor 1 Homo sapiens 85-90 10926834-4 2000 Treatment of the cells with forskolin or dibutyryl-cAMP attenuated the expression of M-CSF induced by IL-1alpha or LPS, but not by PMA. Bucladesine 41-55 colony stimulating factor 1 Homo sapiens 85-90 10926834-9 2000 M-CSF promoter-driven luciferase reporter-gene assays revealed that cAMP elevation attenuated the IL-1-induced transcription activation of the M-CSF promoter, but it had no effect on PMA-induced transcription. Cyclic AMP 68-72 colony stimulating factor 1 Homo sapiens 0-5 10926834-9 2000 M-CSF promoter-driven luciferase reporter-gene assays revealed that cAMP elevation attenuated the IL-1-induced transcription activation of the M-CSF promoter, but it had no effect on PMA-induced transcription. Cyclic AMP 68-72 colony stimulating factor 1 Homo sapiens 143-148 10926834-10 2000 Our findings suggest that cAMP regulates M-CSF gene expression at the transcriptional level and that its inhibitory effect involves NF-kappaB signalling pathway. Cyclic AMP 26-30 colony stimulating factor 1 Homo sapiens 41-46 10852823-5 2000 TGF(beta)-preincubation enhanced OCL formation at least partly by preventing the development of resistance to OCL-induction that otherwise occurs when precursors are incubated in M-CSF. ocl 110-113 colony stimulating factor 1 Homo sapiens 179-184 10931170-7 2000 G-CSF and M-CSF gradually decreased after DFPPs was started. dfpps 42-47 colony stimulating factor 1 Homo sapiens 10-15 10830300-4 2000 Here we demonstrate, using the inhibitors wortmannin and LY294002, that activation of phosphatidylinositol 3-kinase (PI3-K) is required for CSF-1-induced spreading in osteoclasts. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 57-65 colony stimulating factor 1 Homo sapiens 140-145 10770207-16 2000 In conclusion, our results suggest that both gonadotropins (FSH and hCG) and cytokines (TGFbeta1 and M-CSF) may be involved in the support of luteal function via suppression of apoptosis, and that TNFalpha and PGF2alpha may contribute to ovarian dysfunction and/or luteal regression via its induction in human luteinized granulosa cells. Dinoprost 210-219 colony stimulating factor 1 Homo sapiens 101-106 10799521-5 2000 CD34(+) HSCs, but not hMSCs, express PPAR-gamma, and 15-deoxy-Delta(12, 14)-prostaglandin-J2 (15d-PG-J2), a PPAR-gamma agonist, completely blocked the effects of sOPGL and M-CSF on Ocl formation and activity. 9-deoxy-delta-9-prostaglandin D2 74-92 colony stimulating factor 1 Homo sapiens 172-177 10602717-2 2000 In C. albicans-infected mice which had been immunosuppressed with cyclophosphamide, treatment with hM-CSF at a daily dose of 8 x 10(5) units/kg of body weight or greater slightly but significantly prolonged survival. Cyclophosphamide 66-82 colony stimulating factor 1 Homo sapiens 99-105 10666565-3 2000 Although the rate of fatty acid synthesis in a macrophage cell line was dramatically stimulated in response to the growth factor, CSF-1, it was not regulated by the cell cycle. Fatty Acids 21-31 colony stimulating factor 1 Homo sapiens 130-135 10648820-1 2000 Tyrosine phosphorylation of Cbl and its association with signal-transducing molecules in response to macrophage colony-stimulating factor (M-CSF) were analyzed by using cell lines which express the wild-type and a mutant M-CSF receptor, Fms. Tyrosine 0-8 colony stimulating factor 1 Homo sapiens 101-137 10648820-1 2000 Tyrosine phosphorylation of Cbl and its association with signal-transducing molecules in response to macrophage colony-stimulating factor (M-CSF) were analyzed by using cell lines which express the wild-type and a mutant M-CSF receptor, Fms. Tyrosine 0-8 colony stimulating factor 1 Homo sapiens 139-144 10648820-4 2000 These results suggest that phosphorylation of tyrosine 723 is particularly important for the recruitment of Cbl to the M-CSF receptor, but is not required for the phosphorylation and binding of Cbl to signal-transducing molecules such as p85. Tyrosine 46-54 colony stimulating factor 1 Homo sapiens 119-124 10602717-4 2000 The activities of peritoneal macrophages and neutrophils from mice administered hM-CSF plus AMPH-B in combination for inhibition of hyphal growth of C. albicans cells and intracellular phagocytosis and killing of the cells were greater than those of comparable phagocytic cells from control mice to which hM-CSF plus AMPH-B was not administered. Amphotericin B 92-98 colony stimulating factor 1 Homo sapiens 305-311 10602717-5 2000 These results suggest that intravenous administration of hM-CSF augments the efficacy of AMPH-B by enhancing the antifungal activities of macrophages and neutrophils. Amphotericin B 89-95 colony stimulating factor 1 Homo sapiens 57-63 10652202-4 2000 Activin A was most effective when precursors were exposed to RANKL and activin A simultaneously: resistance to OCL-induction that occurs when precursors are pre-incubated in M-CSF was reduced. ocl 111-114 colony stimulating factor 1 Homo sapiens 174-179 10602717-3 2000 Furthermore, the therapeutic efficacy of amphotericin B (AMPH-B) in infected mice was enhanced by its combined use with hM-CSF, while that of fluconazole (FLCZ) was not. Amphotericin B 41-55 colony stimulating factor 1 Homo sapiens 120-126 10602717-3 2000 Furthermore, the therapeutic efficacy of amphotericin B (AMPH-B) in infected mice was enhanced by its combined use with hM-CSF, while that of fluconazole (FLCZ) was not. Amphotericin B 57-63 colony stimulating factor 1 Homo sapiens 120-126 10602507-3 1999 Unexpectedly, CSF-1 substantially inhibited estradiol (E2) and insulin-dependent proliferation of MCF-7 transfectants (MCF-7fms) and prevented cyclin E/cdk2 and cyclin A/cdk2 activation, consistent with a G1 arrest. Estradiol 44-53 colony stimulating factor 1 Homo sapiens 14-19 10585470-3 1999 CSF-1-induced protein tyrosine phosphorylation levels were similar in wild-type and me/me BMM, except for the constitutive hyperphosphorylation of a 62-kDa phosphoprotein (pp62) in me/me macrophages. Tyrosine 22-30 colony stimulating factor 1 Homo sapiens 0-5 10585470-4 1999 pp62 was identified as the RASGAP-associated p62(DOK) and was shown to be the major CSF-1R-associated tyrosine-phosphorylated protein in CSF-1-treated BMM. Tyrosine 102-110 colony stimulating factor 1 Homo sapiens 84-89 10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 41-54 colony stimulating factor 1 Homo sapiens 181-186 10590316-2 1999 In our previous studies, M-CSF regresses atherosclerotic lesions preformed in aorta of high cholesterol-fed rabbit. Cholesterol 92-103 colony stimulating factor 1 Homo sapiens 25-30 10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 41-54 colony stimulating factor 1 Homo sapiens 187-192 10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 56-58 colony stimulating factor 1 Homo sapiens 181-186 10395955-0 1999 Prostaglandin E2 regulates macrophage colony stimulating factor secretion by human bone marrow stromal cells. Dinoprostone 0-16 colony stimulating factor 1 Homo sapiens 27-63 10554038-2 1999 Here, we have investigated the effect of retinoic acid (RA), an important regulator of normal differentiation of mammary epithelial tissues, on the expression of the c-fms gene and CSF-1/CSF-1 receptor-induced invasion and anchorage-independent growth in breast carcinoma cells. Tretinoin 56-58 colony stimulating factor 1 Homo sapiens 187-192 10554038-7 1999 Our results also showed that atRA, by itself and in the presence of CSF-1, can increase the ability of breast carcinoma cells to invade in vitro. Tretinoin 29-33 colony stimulating factor 1 Homo sapiens 68-73 10554038-8 1999 Furthermore, we demonstrated that atRA is able to abolish the CSF-1-induced increase in anchorage-independent growth of breast carcinoma cells without affecting the anchorage-dependent growth. Tretinoin 34-38 colony stimulating factor 1 Homo sapiens 62-67 10554525-1 1999 Monocytes differentiate from myeloid precursors towards the macrophage state of differentiation under the influence of 1,25-dihydroxy vitamins D3 (1,25 [OH]2 vitamin D3) and other factors and this is further propagated by colony stimulating factors (MCSF and GMCSF). 2 vitamin d3 156-168 colony stimulating factor 1 Homo sapiens 250-254 10473597-3 1999 M-CSF treatment induced M-CSF receptor tyrosine phosphorylation and recruitment of the p85 subunit of phosphatidylinositol 3-kinase (PI3K) to these receptors. Tyrosine 39-47 colony stimulating factor 1 Homo sapiens 24-29 10473597-7 1999 In normal human monocytes, M-CSF increased the levels of tyrosine-phosphorylated proteins and induced Akt activation in a PI3K-dependent manner. Tyrosine 57-65 colony stimulating factor 1 Homo sapiens 27-32 10473597-8 1999 The PI3K inhibitor LY294002 blocked M-CSF-mediated monocyte survival, an effect that was partially restored by caspase-9 inhibitors. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 19-27 colony stimulating factor 1 Homo sapiens 36-41 10458713-9 1999 MCSF, IL-6, and CRP were all reduced after 6 weeks of aspirin treatment (P<0.05). Aspirin 54-61 colony stimulating factor 1 Homo sapiens 0-4 10473597-3 1999 M-CSF treatment induced M-CSF receptor tyrosine phosphorylation and recruitment of the p85 subunit of phosphatidylinositol 3-kinase (PI3K) to these receptors. Tyrosine 39-47 colony stimulating factor 1 Homo sapiens 0-5 10614708-7 1999 Ligands of scavenger receptors, which are receptors for oxidized LDL, such as dextran sulphate, polyinosinic acid, heparin and acetylated LDL also significantly induced M-CSF production from human monocytes, although this was at levels below 2 ng/ml. Dextran Sulfate 78-94 colony stimulating factor 1 Homo sapiens 169-174 10614708-7 1999 Ligands of scavenger receptors, which are receptors for oxidized LDL, such as dextran sulphate, polyinosinic acid, heparin and acetylated LDL also significantly induced M-CSF production from human monocytes, although this was at levels below 2 ng/ml. Poly I 96-113 colony stimulating factor 1 Homo sapiens 169-174 10614708-7 1999 Ligands of scavenger receptors, which are receptors for oxidized LDL, such as dextran sulphate, polyinosinic acid, heparin and acetylated LDL also significantly induced M-CSF production from human monocytes, although this was at levels below 2 ng/ml. Heparin 115-122 colony stimulating factor 1 Homo sapiens 169-174 10395955-7 1999 cAMP elevating agents (forskolin and cholera toxin) mimic the PGE2-induced inhibition of M-CSF production. Cyclic AMP 0-4 colony stimulating factor 1 Homo sapiens 89-94 10395955-7 1999 cAMP elevating agents (forskolin and cholera toxin) mimic the PGE2-induced inhibition of M-CSF production. Colforsin 23-32 colony stimulating factor 1 Homo sapiens 89-94 10395955-7 1999 cAMP elevating agents (forskolin and cholera toxin) mimic the PGE2-induced inhibition of M-CSF production. Dinoprostone 62-66 colony stimulating factor 1 Homo sapiens 89-94 10395955-3 1999 The lipid mediator prostaglandin E2 (PGE2) markedly reduces in a time- and dose-dependent manner the constitutive and TNF-alpha-induced M-CSF synthesis by bone marrow stromal cells. Dinoprostone 19-35 colony stimulating factor 1 Homo sapiens 136-141 10395955-8 1999 In conclusion, PGE2 is a potent regulator of M-CSF production by human bone marrow stromal cells, its effects being mediated via cAMP and PGE receptor EP2/EP4 subtypes. Dinoprostone 15-19 colony stimulating factor 1 Homo sapiens 45-50 10395955-3 1999 The lipid mediator prostaglandin E2 (PGE2) markedly reduces in a time- and dose-dependent manner the constitutive and TNF-alpha-induced M-CSF synthesis by bone marrow stromal cells. Dinoprostone 37-41 colony stimulating factor 1 Homo sapiens 136-141 10395955-5 1999 EP2/EP4 selective agonists (11-deoxy PGE1 and 1-OH PGE1) and EP2 agonist (19-OH PGE2) inhibit M-CSF synthesis by bone marrow stromal cells while an EP1/EP3 agonist (sulprostone) has no effect. 11-deoxy 28-36 colony stimulating factor 1 Homo sapiens 94-99 10395955-5 1999 EP2/EP4 selective agonists (11-deoxy PGE1 and 1-OH PGE1) and EP2 agonist (19-OH PGE2) inhibit M-CSF synthesis by bone marrow stromal cells while an EP1/EP3 agonist (sulprostone) has no effect. Alprostadil 37-41 colony stimulating factor 1 Homo sapiens 94-99 10395955-5 1999 EP2/EP4 selective agonists (11-deoxy PGE1 and 1-OH PGE1) and EP2 agonist (19-OH PGE2) inhibit M-CSF synthesis by bone marrow stromal cells while an EP1/EP3 agonist (sulprostone) has no effect. 1-oh pge1 46-55 colony stimulating factor 1 Homo sapiens 94-99 10395955-5 1999 EP2/EP4 selective agonists (11-deoxy PGE1 and 1-OH PGE1) and EP2 agonist (19-OH PGE2) inhibit M-CSF synthesis by bone marrow stromal cells while an EP1/EP3 agonist (sulprostone) has no effect. 19-oh pge2 74-84 colony stimulating factor 1 Homo sapiens 94-99 15374073-5 1999 Among the general laboratory tests, there was only a significant correlation between M-CSF and serum creatinine; however, no significant correlation was found between M-CSF and other tests including blood cell counts. Creatinine 101-111 colony stimulating factor 1 Homo sapiens 85-90 10445847-1 1999 The downregulation of tyrosine kinase receptors attenuates signalling and is thought to be dependent upon intrinsic receptor kinase activity, largely because down-regulation is inhibited by a kinase-inactivating mutation of an invariant lysine residue of the receptors for EGF, insulin, M-CSF and PDGF. Lysine 237-243 colony stimulating factor 1 Homo sapiens 287-292 10567946-11 1999 1 alpha, 25 dihydroxy vitamin D3 (D3) stimulated M-CSF secretion into the culture medium of both HPLF and HPLF-Y, but the stretching inhibited M-CSF secretion and completely blocked the enhancement by D3. Calcitriol 0-32 colony stimulating factor 1 Homo sapiens 49-54 10567946-11 1999 1 alpha, 25 dihydroxy vitamin D3 (D3) stimulated M-CSF secretion into the culture medium of both HPLF and HPLF-Y, but the stretching inhibited M-CSF secretion and completely blocked the enhancement by D3. Calcitriol 0-32 colony stimulating factor 1 Homo sapiens 143-148 10340379-1 1999 Expression of a receptor for human macrophage-colony stimulating factor (M-CSF or CSF-1), containing a point mutation which changes an aspartate to a valine at position 802 of the activating loop of the kinase domain, potently transforms the haemopoietic cell line FDC-P1 yet prevents Rat-2 fibroblast transformation. fdc-p1 265-271 colony stimulating factor 1 Homo sapiens 73-78 10329719-3 1999 ERK activity was approximately 2-fold higher in cycling BMM compared with growth-arrested BMM; in addition, CSF-1-stimulated BMM DNA synthesis was partially inhibited by PD98059, a specific inhibitor of MEK activation, suggesting a role for a mitogen-activated protein-ERK kinase (MEK)/ERK pathway in the control of DNA synthesis but surprisingly not in the control of cyclin D1 mRNA or c-myc mRNA expression. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 170-177 colony stimulating factor 1 Homo sapiens 108-113 10330148-4 1999 A small pool of CSF-1R formed a multimeric complex with phosphatidylinositol-3 kinase (PI-3 kinase), SHP-1, Grb2, Shc, c-Src, Cbl, and a significant number of tyrosine-phosphorylated proteins in CSF-1-stimulated cells. Tyrosine 159-167 colony stimulating factor 1 Homo sapiens 16-21 10329719-6 1999 Relatively high concentrations of the p38 inhibitor, SKB202190, suppressed CSF-1-stimulated BMM DNA synthesis. skb202190 53-62 colony stimulating factor 1 Homo sapiens 75-80 10340379-1 1999 Expression of a receptor for human macrophage-colony stimulating factor (M-CSF or CSF-1), containing a point mutation which changes an aspartate to a valine at position 802 of the activating loop of the kinase domain, potently transforms the haemopoietic cell line FDC-P1 yet prevents Rat-2 fibroblast transformation. fdc-p1 265-271 colony stimulating factor 1 Homo sapiens 82-87 10356364-4 1999 The Src tyrosine kinases c-Src, c-Yes, c-Fyn, and c-Hck were tyrosine phosphorylated in the M1/WT cells in response to CSF-1 and bound to the WT CSF-1R through their SH2 domains. Tyrosine 8-16 colony stimulating factor 1 Homo sapiens 119-124 10199558-5 1999 Increases in MCSF mRNA are also seen after stimulation with dexamethasone. Dexamethasone 60-73 colony stimulating factor 1 Homo sapiens 13-17 9931547-1 1999 Possible explanation for opposite responses of EVT and TCL-1 cells to endogenous CSF-1 EVT 47-50 colony stimulating factor 1 Homo sapiens 81-86 10382942-4 1999 The addition of IL-6 or both IL-6 and MGF to M-CSF containing cultures resulted in significant higher numbers of colony-forming unit-macrophage (CFU-M) as tested in clonogenic and 3H-thymidine assays. Tritium 180-182 colony stimulating factor 1 Homo sapiens 45-50 10382942-4 1999 The addition of IL-6 or both IL-6 and MGF to M-CSF containing cultures resulted in significant higher numbers of colony-forming unit-macrophage (CFU-M) as tested in clonogenic and 3H-thymidine assays. Thymidine 183-192 colony stimulating factor 1 Homo sapiens 45-50 10023015-8 1999 Especially in kidney cell lines, the levels of granulocyte-macrophage-CSF (GM-CSF), M-CSF and IL-6 were further strongly increased by the TPA and IL-1 pretreatment. Tetradecanoylphorbol Acetate 138-141 colony stimulating factor 1 Homo sapiens 76-81 10022505-8 1999 Enforced ectopic expression of Mad1 in the cells results in inhibition of [3H]thymidine incorporation and proliferation in response to CSF-1. Tritium 75-77 colony stimulating factor 1 Homo sapiens 135-140 9795343-6 1998 Results revealed that normal invasive EVT cells in culture express both CSF-1 and c-fms mRNA and protein. EVT 38-41 colony stimulating factor 1 Homo sapiens 72-77 10025673-0 1999 CSF-1 stimulated multiubiquitination of the CSF-1 receptor and of Cbl follows their tyrosine phosphorylation and association with other signaling proteins. Tyrosine 84-92 colony stimulating factor 1 Homo sapiens 0-5 10025673-1 1999 Addition of colony stimulating factor-1 (CSF-1) to macrophages stimulates the rapid, transient tyrosine phosphorylation, membrane association and multiubiquitination of Cbl (Wang et al. Tyrosine 95-103 colony stimulating factor 1 Homo sapiens 12-39 10025673-1 1999 Addition of colony stimulating factor-1 (CSF-1) to macrophages stimulates the rapid, transient tyrosine phosphorylation, membrane association and multiubiquitination of Cbl (Wang et al. Tyrosine 95-103 colony stimulating factor 1 Homo sapiens 41-46 9922157-11 1998 Finally, a comparison of cleavage site selection in the presence and absence of tunicamycin treatment showed that N-glycosylation of certain mutant forms of CSF-1(256) sterically interfered with protease accessibility, which in turn had an effect on the selection of the site used for cleavage. Tunicamycin 80-91 colony stimulating factor 1 Homo sapiens 157-162 9922157-11 1998 Finally, a comparison of cleavage site selection in the presence and absence of tunicamycin treatment showed that N-glycosylation of certain mutant forms of CSF-1(256) sterically interfered with protease accessibility, which in turn had an effect on the selection of the site used for cleavage. Nitrogen 114-115 colony stimulating factor 1 Homo sapiens 157-162 9616179-5 1998 Because macrophage colony-stimulating factor (M-CSF) is a well-known survival factor for MO, we measured the M-CSF content of MO culture supernatants using enzyme-linked immunosorbent assay and found that RA suppressed the constitutive secretion of M-CSF. Tretinoin 205-207 colony stimulating factor 1 Homo sapiens 109-114 9710206-5 1998 M-CSF production by DC was driven by GM-CSF and inhibited by the specific phosphatidylinositol 3-kinase inhibitor wortmannin. Wortmannin 114-124 colony stimulating factor 1 Homo sapiens 0-5 9642280-1 1998 Stimulation of macrophages with colony-stimulating factor-1 (CSF-1) results in the protein tyrosine phosphorylation of the CSF-1 receptor (CSF-1R) and many other, primarily cytosolic, proteins. Tyrosine 91-99 colony stimulating factor 1 Homo sapiens 32-59 9642280-1 1998 Stimulation of macrophages with colony-stimulating factor-1 (CSF-1) results in the protein tyrosine phosphorylation of the CSF-1 receptor (CSF-1R) and many other, primarily cytosolic, proteins. Tyrosine 91-99 colony stimulating factor 1 Homo sapiens 61-66 9642280-2 1998 Stimulation by CSF-1 at 4 degreesC was used to facilitate the purification and identification of the proteins of the cytosolic anti-phosphotyrosine (PY)-reactive fraction (alphaPY-RF) involved in downstream signaling pathways. Phosphotyrosine 132-147 colony stimulating factor 1 Homo sapiens 15-20 9642280-2 1998 Stimulation by CSF-1 at 4 degreesC was used to facilitate the purification and identification of the proteins of the cytosolic anti-phosphotyrosine (PY)-reactive fraction (alphaPY-RF) involved in downstream signaling pathways. py 149-151 colony stimulating factor 1 Homo sapiens 15-20 9642280-8 1998 These studies indicate that CSF-1-induced protein tyrosine phosphorylation is associated with the reorganization of complexes of cytoskeletal, signaling, and other proteins that mediate CSF-1-regulated motility and growth. Tyrosine 50-58 colony stimulating factor 1 Homo sapiens 28-33 9642280-8 1998 These studies indicate that CSF-1-induced protein tyrosine phosphorylation is associated with the reorganization of complexes of cytoskeletal, signaling, and other proteins that mediate CSF-1-regulated motility and growth. Tyrosine 50-58 colony stimulating factor 1 Homo sapiens 186-191 9645689-3 1998 Addition of indomethacin to macrophage colony-stimulating factor (M-CSF)-treated cultures nearly abolished osteoclast parameters, indicating that prostaglandins are virtually essential for human osteoclast formation. Indomethacin 12-24 colony stimulating factor 1 Homo sapiens 28-64 9645689-3 1998 Addition of indomethacin to macrophage colony-stimulating factor (M-CSF)-treated cultures nearly abolished osteoclast parameters, indicating that prostaglandins are virtually essential for human osteoclast formation. Indomethacin 12-24 colony stimulating factor 1 Homo sapiens 66-71 9645689-3 1998 Addition of indomethacin to macrophage colony-stimulating factor (M-CSF)-treated cultures nearly abolished osteoclast parameters, indicating that prostaglandins are virtually essential for human osteoclast formation. Prostaglandins 146-160 colony stimulating factor 1 Homo sapiens 28-64 9645689-3 1998 Addition of indomethacin to macrophage colony-stimulating factor (M-CSF)-treated cultures nearly abolished osteoclast parameters, indicating that prostaglandins are virtually essential for human osteoclast formation. Prostaglandins 146-160 colony stimulating factor 1 Homo sapiens 66-71 9645689-5 1998 The effects of M-CSF and PGE2 are independent, as demonstrated by unaltered PGE2 concentrations in culture supernatants in spite of the dose-responsive increase in osteoclast parameters in response to M-CSF. Dinoprostone 25-29 colony stimulating factor 1 Homo sapiens 201-206 9632647-3 1998 Both core protein bands were recognized by an antibody to PG-100, an antibody that recognizes the proteoglycan form of macrophage colony-stimulating factor (PG-100/PG-MCSF). pg-100 58-64 colony stimulating factor 1 Homo sapiens 167-171 9632647-5 1998 In this system, PG-100/PG-MCSF was resolved further into two forms. pg 16-18 colony stimulating factor 1 Homo sapiens 26-30 9632647-9 1998 The glycosaminoglycan chains of PG-100/PG-MCSF, but not the core proteins, were responsible for binding to native LDL. Glycosaminoglycans 4-21 colony stimulating factor 1 Homo sapiens 42-46 9632647-10 1998 Mildly oxidized LDL and methyl-LDL, which have an electrophoretic charge similar to that of native LDL, also bound PG-100/PG-MCSF. pg-100 115-121 colony stimulating factor 1 Homo sapiens 125-129 9616179-5 1998 Because macrophage colony-stimulating factor (M-CSF) is a well-known survival factor for MO, we measured the M-CSF content of MO culture supernatants using enzyme-linked immunosorbent assay and found that RA suppressed the constitutive secretion of M-CSF. Tretinoin 205-207 colony stimulating factor 1 Homo sapiens 109-114 9710599-1 1998 An antibody that specifically recognized phosphothreonine 72 in ets-2 was used to determine the phosphorylation status of endogenous ets-2 in response to colony-stimulating factor 1 (CSF-1)/c-fms signaling. Phosphothreonine 41-57 colony stimulating factor 1 Homo sapiens 183-188 9710599-7 1998 Immune depletion experiments and the use of the MAP kinase kinase inhibitor PD98059 indicate that these two MAP kinases are the major ets-2 kinases activated in response to CSF-1/c-fms signaling. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 76-83 colony stimulating factor 1 Homo sapiens 173-178 9616179-5 1998 Because macrophage colony-stimulating factor (M-CSF) is a well-known survival factor for MO, we measured the M-CSF content of MO culture supernatants using enzyme-linked immunosorbent assay and found that RA suppressed the constitutive secretion of M-CSF. Tretinoin 205-207 colony stimulating factor 1 Homo sapiens 8-44 9616179-5 1998 Because macrophage colony-stimulating factor (M-CSF) is a well-known survival factor for MO, we measured the M-CSF content of MO culture supernatants using enzyme-linked immunosorbent assay and found that RA suppressed the constitutive secretion of M-CSF. Tretinoin 205-207 colony stimulating factor 1 Homo sapiens 46-51 9616179-6 1998 Northern analysis showed that the M-CSF mRNA expression was only slightly reduced by RA treatment, suggesting regulation on the posttranscriptional level. Tretinoin 85-87 colony stimulating factor 1 Homo sapiens 34-39 9616179-8 1998 Because M-CSF is not only a survival-promoting but also a differentiation-promoting factor for myeloid cells, we analyzed the effect of RA on MO to MAC maturation. Tretinoin 136-138 colony stimulating factor 1 Homo sapiens 8-13 9616179-10 1998 The addition of exogenous M-CSF to RA-containing MO cultures fails to overcome the RA-induced inhibition of MO differentiation. Tretinoin 35-37 colony stimulating factor 1 Homo sapiens 26-31 9616179-12 1998 We conclude that RA acts via two different mechanisms on monocyte survival and differentiation: posttranscriptionally by controlling M-CSF secretion, which decreases MO survival, and transcriptionally regulating the expression of differentiation-associated genes. Tretinoin 17-19 colony stimulating factor 1 Homo sapiens 133-138 9616179-13 1998 The regulation of M-CSF production may contribute to the antileukemic effect of RA in vivo by reducing autocrine M-CSF production by leukemic cells. Tretinoin 80-82 colony stimulating factor 1 Homo sapiens 18-23 9616179-13 1998 The regulation of M-CSF production may contribute to the antileukemic effect of RA in vivo by reducing autocrine M-CSF production by leukemic cells. Tretinoin 80-82 colony stimulating factor 1 Homo sapiens 113-118 9636846-5 1998 M-CSF enhances cytotoxicity, superoxide production, phagocytosis, chemotaxis, and secondary cytokine production in monocytes and macrophages. Superoxides 29-39 colony stimulating factor 1 Homo sapiens 0-5 9600092-5 1998 Treatment of human PBMCs with sODF together with M-CSF induced OCLs, which expressed tartrate-resistant acid phosphatase and vitronectin receptors, produced cAMP in response to calcitonin, and formed resorption pits on dentine slices. Cyclic AMP 157-161 colony stimulating factor 1 Homo sapiens 49-54 9573036-0 1998 The related adhesion focal tyrosine kinase (RAFTK) is tyrosine phosphorylated and participates in colony-stimulating factor-1/macrophage colony-stimulating factor signaling in monocyte-macrophages. Tyrosine 27-35 colony stimulating factor 1 Homo sapiens 98-125 9573036-4 1998 Colony-stimulating factor-1 (CSF-1)/macrophage colony-stimulating factor (M-CSF) stimulation of THP1 cells increased the tyrosine phosphorylation of RAFTK; similar increases in phosphorylation were also detected after lipopolysaccharide stimulation. Tyrosine 121-129 colony stimulating factor 1 Homo sapiens 0-27 9573036-4 1998 Colony-stimulating factor-1 (CSF-1)/macrophage colony-stimulating factor (M-CSF) stimulation of THP1 cells increased the tyrosine phosphorylation of RAFTK; similar increases in phosphorylation were also detected after lipopolysaccharide stimulation. Tyrosine 121-129 colony stimulating factor 1 Homo sapiens 29-34 9573036-4 1998 Colony-stimulating factor-1 (CSF-1)/macrophage colony-stimulating factor (M-CSF) stimulation of THP1 cells increased the tyrosine phosphorylation of RAFTK; similar increases in phosphorylation were also detected after lipopolysaccharide stimulation. Tyrosine 121-129 colony stimulating factor 1 Homo sapiens 74-79 9464244-4 1998 Pretreatment with phorbol ester, IL-1 beta, or IFN-gamma increased the level of G-CSF, GM-CSF, and M-CSF in KU-19-19 CM. Phorbol Esters 18-31 colony stimulating factor 1 Homo sapiens 88-93 9525925-6 1998 However, ATP or PAF together with colony stimulating factor-1 (CSF-1) synergistically stimulated arachidonic acid release. Arachidonic Acid 97-113 colony stimulating factor 1 Homo sapiens 63-68 9525925-8 1998 Arachidonic acid release was more rapid in response to CSF-1 plus ATP or PAF than zymosan and correlated with the time course of the cPLA2 gel shift. Arachidonic Acid 0-16 colony stimulating factor 1 Homo sapiens 55-60 9491785-8 1998 Finally, addition of M-CSF to the cultures reversed the 17beta-E2-induced inhibitory effect. 17beta-e2 56-65 colony stimulating factor 1 Homo sapiens 21-26 9491785-9 1998 These observations suggest that regulation of the synthesis of membrane-bound M-CSF plays a role in 17beta-E2-induced inhibition of bone resorption. 17beta-e2 100-109 colony stimulating factor 1 Homo sapiens 78-83 9507032-4 1998 CSF-1 treatment protected cells expressing the CSF1R/IR from staurosporine-induced apoptosis. Staurosporine 61-74 colony stimulating factor 1 Homo sapiens 0-5 9507032-9 1998 CSF-1 stimulated glucose uptake, mitogen-activated protein kinases, and IRS-1-associated phosphatidylinositol 3" kinase in cells expressing the CSF1R/IR but not in cells expressing the CSF1R/IRDelta960. Glucose 17-24 colony stimulating factor 1 Homo sapiens 0-5 9507032-10 1998 Surprisingly, the CSF1R/IRDelta960 was as effective as the CSF1R/IR in mediating CSF-1 protection of cells from staurosporine-induced apoptosis. Staurosporine 112-125 colony stimulating factor 1 Homo sapiens 81-86 9631577-6 1998 Proteoglycan type M-CSF, which contains chondroitin sulfate chains, was found in 1992. Chondroitin Sulfates 40-59 colony stimulating factor 1 Homo sapiens 18-23 9257850-7 1997 We analyzed the phosphorylation on tyrosine residue(s) of the M-CSF receptor in response to these M-CSFs that trigger mitogenic responses. Tyrosine 35-43 colony stimulating factor 1 Homo sapiens 62-67 9973638-5 1998 Gel fractions extracted from SDS-PAGE had macrophage colony-stimulating factor (M-CSF)-specific amino acid sequences. Sodium Dodecyl Sulfate 29-32 colony stimulating factor 1 Homo sapiens 42-78 9973638-5 1998 Gel fractions extracted from SDS-PAGE had macrophage colony-stimulating factor (M-CSF)-specific amino acid sequences. Sodium Dodecyl Sulfate 29-32 colony stimulating factor 1 Homo sapiens 80-85 9973638-7 1998 Anti-M-CSF but not anti-IL-6 antibody abrogated CSA in KPB-M15-CM. Cyclosporine 48-51 colony stimulating factor 1 Homo sapiens 5-10 9395179-5 1997 They responded to morphine exposure in vitro with a cell rounding and becoming immobile for only 20 min whereas normal cells would remain round and immobile for up to 1-2 h. An examination of the plasma from the HM patient revealed that monocyte colony stimulating factor (MCSF) levels were elevated (6.4 and 5.78 compared to a control range of 1-1.75 ng/ml). Morphine 18-26 colony stimulating factor 1 Homo sapiens 237-271 9278333-5 1997 Furthermore, the TGF-beta1-induced M-CSF mRNA expression was inhibited by catalase, but not by superoxide dismutase, suggesting that H2O2 rather than superoxide anion (O2.-) is the primary mediator of the effects of TGF-beta1. Superoxides 150-166 colony stimulating factor 1 Homo sapiens 35-40 9278333-5 1997 Furthermore, the TGF-beta1-induced M-CSF mRNA expression was inhibited by catalase, but not by superoxide dismutase, suggesting that H2O2 rather than superoxide anion (O2.-) is the primary mediator of the effects of TGF-beta1. Superoxides 135-137 colony stimulating factor 1 Homo sapiens 35-40 9278333-6 1997 Transient transfection studies using deletional M-CSF promoter constructs demonstrated that TGF-beta1 produced a 13-fold induction in M-CSF promoter activity that was repressed by >85% with GSNO and catalase, in part through inhibitory effects on kappaB cis-acting elements. S-Nitrosoglutathione 193-197 colony stimulating factor 1 Homo sapiens 134-139 9278333-8 1997 In a concentration-dependent manner, treatment with exogenous H2O2 produced 14- and 4.6-fold increases in M-CSF promoter activity and mRNA expression, respectively. Hydrogen Peroxide 62-66 colony stimulating factor 1 Homo sapiens 106-111 9278333-9 1997 These results indicate that the generation of H2O2 and activation of NF-kappaB by TGF-beta1 are required for the induction of M-CSF gene transcription. Hydrogen Peroxide 46-50 colony stimulating factor 1 Homo sapiens 126-131 9395179-5 1997 They responded to morphine exposure in vitro with a cell rounding and becoming immobile for only 20 min whereas normal cells would remain round and immobile for up to 1-2 h. An examination of the plasma from the HM patient revealed that monocyte colony stimulating factor (MCSF) levels were elevated (6.4 and 5.78 compared to a control range of 1-1.75 ng/ml). Morphine 18-26 colony stimulating factor 1 Homo sapiens 273-277 9366562-0 1997 Colony-stimulating factor-1 induces cytoskeletal reorganization and c-src-dependent tyrosine phosphorylation of selected cellular proteins in rodent osteoclasts. Tyrosine 84-92 colony stimulating factor 1 Homo sapiens 0-27 9366562-5 1997 CSF-1 increases membrane phosphotyrosine staining in osteoclasts and induces the phosphorylation of several cellular proteins in cultured, osteoclast-like cells, including c-fms, c-src, and an 85-kD Grb2-binding protein. Phosphotyrosine 25-40 colony stimulating factor 1 Homo sapiens 0-5 9278333-2 1997 Here we show that TGF-beta1 induces the expression of macrophage-CSF (M-CSF) in vascular endothelial cells via a signaling pathway(s) involving hydrogen peroxide (H2O2). Hydrogen Peroxide 144-161 colony stimulating factor 1 Homo sapiens 54-68 9278333-2 1997 Here we show that TGF-beta1 induces the expression of macrophage-CSF (M-CSF) in vascular endothelial cells via a signaling pathway(s) involving hydrogen peroxide (H2O2). Hydrogen Peroxide 144-161 colony stimulating factor 1 Homo sapiens 70-75 9278333-2 1997 Here we show that TGF-beta1 induces the expression of macrophage-CSF (M-CSF) in vascular endothelial cells via a signaling pathway(s) involving hydrogen peroxide (H2O2). Hydrogen Peroxide 163-167 colony stimulating factor 1 Homo sapiens 54-68 9278333-2 1997 Here we show that TGF-beta1 induces the expression of macrophage-CSF (M-CSF) in vascular endothelial cells via a signaling pathway(s) involving hydrogen peroxide (H2O2). Hydrogen Peroxide 163-167 colony stimulating factor 1 Homo sapiens 70-75 9278333-4 1997 This increase in M-CSF expression was attenuated by a nitric oxide donor, S-nitrosoglutathione (GSNO), and by a nonspecific oxidase inhibitor, diphenylene iodonium. Nitric Oxide 54-66 colony stimulating factor 1 Homo sapiens 17-22 9278333-4 1997 This increase in M-CSF expression was attenuated by a nitric oxide donor, S-nitrosoglutathione (GSNO), and by a nonspecific oxidase inhibitor, diphenylene iodonium. S-Nitrosoglutathione 74-94 colony stimulating factor 1 Homo sapiens 17-22 9278333-4 1997 This increase in M-CSF expression was attenuated by a nitric oxide donor, S-nitrosoglutathione (GSNO), and by a nonspecific oxidase inhibitor, diphenylene iodonium. S-Nitrosoglutathione 96-100 colony stimulating factor 1 Homo sapiens 17-22 9278333-4 1997 This increase in M-CSF expression was attenuated by a nitric oxide donor, S-nitrosoglutathione (GSNO), and by a nonspecific oxidase inhibitor, diphenylene iodonium. diphenyleneiodonium 143-163 colony stimulating factor 1 Homo sapiens 17-22 9278333-5 1997 Furthermore, the TGF-beta1-induced M-CSF mRNA expression was inhibited by catalase, but not by superoxide dismutase, suggesting that H2O2 rather than superoxide anion (O2.-) is the primary mediator of the effects of TGF-beta1. Hydrogen Peroxide 133-137 colony stimulating factor 1 Homo sapiens 35-40 9266003-7 1997 RESULTS: Serum M-CSF levels were significantly lower in the non-pregnant RSA patients (460.0 +/- 185.6 U/ml; mean +/- SD) than in the control group (726.5 +/- 134.0 U/ml) and also were lower at the 8th, but not the 4th or 6th gestational week in those patients of both the bed-rest and IDI therapy groups whose outcome was pregnancy failure. rabbit sperm membrane autoantigen 73-76 colony stimulating factor 1 Homo sapiens 15-20 9150350-11 1997 However, LPS enhanced the TPA-induced M-CSF production. Tetradecanoylphorbol Acetate 26-29 colony stimulating factor 1 Homo sapiens 38-43 9115260-2 1997 The addition of CSF-1 to cells transfected with the CSF1R/IR chimera cDNA stimulated the tyrosine phosphorylation of a protein that was immunoprecipitated by an antibody directed against the carboxyl terminus of the insulin receptor. Tyrosine 89-97 colony stimulating factor 1 Homo sapiens 16-21 9115260-4 1997 CSF-1 stimulated the tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and Shc in cells expressing the CSF1R/IR chimera. Tyrosine 21-29 colony stimulating factor 1 Homo sapiens 0-5 9150350-10 1997 Vice versa, secretion of macrophage CSF (M-CSF) could be induced by TPA, but not by LPS. Tetradecanoylphorbol Acetate 68-71 colony stimulating factor 1 Homo sapiens 41-46 9110154-3 1997 By using a specific and sensitive ELISA, we found that the spontaneous production of M-CSF by human marrow stromal cells is enhanced after stimulation with lipopolysaccharide (LPS), phorbol myristic acetate (PMA) and most interestingly by the lipidic mediator of inflammation platelet-activating factor (PAF). phorbol myristic acetate 182-206 colony stimulating factor 1 Homo sapiens 85-90 9110154-3 1997 By using a specific and sensitive ELISA, we found that the spontaneous production of M-CSF by human marrow stromal cells is enhanced after stimulation with lipopolysaccharide (LPS), phorbol myristic acetate (PMA) and most interestingly by the lipidic mediator of inflammation platelet-activating factor (PAF). Tetradecanoylphorbol Acetate 208-211 colony stimulating factor 1 Homo sapiens 85-90 9012632-0 1997 Effects of CSF-1 on cholesterol accumulation and efflux by macrophages. Cholesterol 20-31 colony stimulating factor 1 Homo sapiens 11-16 9059942-0 1997 The effects of prednisolone and interferons on serum macrophage colony stimulating factor concentrations in chronic hepatitis B. BACKGROUNDS/AIMS: Serum concentrations of macrophage-colony stimulating factor (M-CSF) are increased in parallel with hepatic inflammation. Prednisolone 15-27 colony stimulating factor 1 Homo sapiens 171-207 9059942-3 1997 RESULTS: Serum concentrations of M-CSF significantly decreased during prednisolone administration, but significantly increased following prednisolone withdrawal, similar to the increase during acute exacerbation. Prednisolone 70-82 colony stimulating factor 1 Homo sapiens 33-38 9059942-3 1997 RESULTS: Serum concentrations of M-CSF significantly decreased during prednisolone administration, but significantly increased following prednisolone withdrawal, similar to the increase during acute exacerbation. Prednisolone 137-149 colony stimulating factor 1 Homo sapiens 33-38 9352744-6 1997 Furthermore, treatment of stromal cells with vesnarinone repressed the production of G, GM, M-CSF, suggesting that the agent may cause a hematopoietic disorder, agranulocytosis, through the impairment of stromal cell function. vesnarinone 45-56 colony stimulating factor 1 Homo sapiens 92-97 9071993-5 1997 The hCSF-GM was found to be a more potent stimulator of pp125FAK induction than 1,25 (OH)2 D3; interestingly, the presence of both hCSF-GM and 1,25 (OH)2 D3 showed co-operative effect. hcsf-gm 4-11 colony stimulating factor 1 Homo sapiens 131-144 9012632-8 1997 Similarly, CSF-1 also increased the accumulation of cholesterol and its esters nonspecifically. Cholesterol 52-63 colony stimulating factor 1 Homo sapiens 11-16 9012632-8 1997 Similarly, CSF-1 also increased the accumulation of cholesterol and its esters nonspecifically. Esters 72-78 colony stimulating factor 1 Homo sapiens 11-16 9012632-9 1997 CSF-1 did have a marked and specific effect on the composition of cholesterol esters, decreasing the proportion of polyunsaturated esters relative to monounsaturated and saturated esters. Cholesterol Esters 66-84 colony stimulating factor 1 Homo sapiens 0-5 9012632-9 1997 CSF-1 did have a marked and specific effect on the composition of cholesterol esters, decreasing the proportion of polyunsaturated esters relative to monounsaturated and saturated esters. polyunsaturated esters 115-137 colony stimulating factor 1 Homo sapiens 0-5 9012632-9 1997 CSF-1 did have a marked and specific effect on the composition of cholesterol esters, decreasing the proportion of polyunsaturated esters relative to monounsaturated and saturated esters. Esters 78-84 colony stimulating factor 1 Homo sapiens 0-5 9012632-11 1997 Thus, the enhanced macrophage catabolism of modified LDLs by CSF-1 is part of a nonspecific action on the cells but could contribute to a reduction in circulating cholesterol, observed in some situations of CSF-1 presentation in humans. Cholesterol 163-174 colony stimulating factor 1 Homo sapiens 61-66 9012632-11 1997 Thus, the enhanced macrophage catabolism of modified LDLs by CSF-1 is part of a nonspecific action on the cells but could contribute to a reduction in circulating cholesterol, observed in some situations of CSF-1 presentation in humans. Cholesterol 163-174 colony stimulating factor 1 Homo sapiens 207-212 8981358-11 1997 Conversely, cyclin D1-rescued cells were inhibited from forming CSF-1-dependent colonies in agar when challenged with either a dominant-negative c-myc mutant or mad, a transcription factor which competes with myc for max, its requisite heterodimeric partner. Agar 92-96 colony stimulating factor 1 Homo sapiens 64-69 9815538-6 1997 In vitro, CsA significantly enhanced the efficacy of PCL against lung (Lu-CSF-1 and 3LL) and oropharyngeal (CSCC-20) cancer cell lines. Cyclosporine 10-13 colony stimulating factor 1 Homo sapiens 74-87 9815538-6 1997 In vitro, CsA significantly enhanced the efficacy of PCL against lung (Lu-CSF-1 and 3LL) and oropharyngeal (CSCC-20) cancer cell lines. Paclitaxel 53-56 colony stimulating factor 1 Homo sapiens 74-87 9015756-6 1997 The expression of c-src, c-fms, and macrophage colony stimulating factor (M-CSF) was induced by TPA treatment; however, TPA-induced M-CSF gene transcription was attenuated by the subsequent addition of 1,25-(OH)2D3. Tetradecanoylphorbol Acetate 96-99 colony stimulating factor 1 Homo sapiens 36-72 9015756-6 1997 The expression of c-src, c-fms, and macrophage colony stimulating factor (M-CSF) was induced by TPA treatment; however, TPA-induced M-CSF gene transcription was attenuated by the subsequent addition of 1,25-(OH)2D3. Tetradecanoylphorbol Acetate 96-99 colony stimulating factor 1 Homo sapiens 74-79 9015756-6 1997 The expression of c-src, c-fms, and macrophage colony stimulating factor (M-CSF) was induced by TPA treatment; however, TPA-induced M-CSF gene transcription was attenuated by the subsequent addition of 1,25-(OH)2D3. Tetradecanoylphorbol Acetate 120-123 colony stimulating factor 1 Homo sapiens 36-72 9015756-6 1997 The expression of c-src, c-fms, and macrophage colony stimulating factor (M-CSF) was induced by TPA treatment; however, TPA-induced M-CSF gene transcription was attenuated by the subsequent addition of 1,25-(OH)2D3. Tetradecanoylphorbol Acetate 120-123 colony stimulating factor 1 Homo sapiens 74-79 9015756-6 1997 The expression of c-src, c-fms, and macrophage colony stimulating factor (M-CSF) was induced by TPA treatment; however, TPA-induced M-CSF gene transcription was attenuated by the subsequent addition of 1,25-(OH)2D3. Tetradecanoylphorbol Acetate 120-123 colony stimulating factor 1 Homo sapiens 132-137 9015756-7 1997 Furthermore, both dexamethasone and IFN-gamma impaired the attenuation of M-CSF expression, suggesting that the transient expression of M-CSF may be important for the formation of osteoclast-like cells. Dexamethasone 18-31 colony stimulating factor 1 Homo sapiens 74-79 9015756-7 1997 Furthermore, both dexamethasone and IFN-gamma impaired the attenuation of M-CSF expression, suggesting that the transient expression of M-CSF may be important for the formation of osteoclast-like cells. Dexamethasone 18-31 colony stimulating factor 1 Homo sapiens 136-141 8981366-5 1997 Tumor cell expression of CSF-1R is under the control of several steroid hormones (glucocorticoids and progestins) and the binding of several bHLH transcription factors, while tumor cell expression of CSF-1 appears to be regulated by other hormones, some of which are involved in normal lactogenic differentiation. Steroids 64-80 colony stimulating factor 1 Homo sapiens 25-30 8981369-8 1997 Treatment of rabbits with recombinant human M-CSF (rhM-CSF) increased M-CSF staining, which correlated with reduced cholesterol content of these foam cells. Cholesterol 116-127 colony stimulating factor 1 Homo sapiens 44-49 8981369-8 1997 Treatment of rabbits with recombinant human M-CSF (rhM-CSF) increased M-CSF staining, which correlated with reduced cholesterol content of these foam cells. Cholesterol 116-127 colony stimulating factor 1 Homo sapiens 53-58 8920951-2 1996 The seven cysteine residues in CSF-1(256) form three intrachain disulfide bonds (Cys7-Cys90, Cys48-Cys139, and Cys 102-Cys146), and one interchain disulfide bond (Cys31-Cys31). Cysteine 10-18 colony stimulating factor 1 Homo sapiens 31-36 9000134-6 1996 Replacement of Y807 with phenylalanine led to a complete block of activation of all STAT proteins in response to CSF-1, however, this phosphotyrosine does not appear to represent a STAT binding site of the receptor as a phosphopeptide spanning Y809 of the human CSF-1 receptor could not compete any STAT/DNA complex formation in electrophoretic mobility shift assays. Phenylalanine 25-38 colony stimulating factor 1 Homo sapiens 113-118 8931561-3 1996 Peptide mapping of the reaction products by mass spectrometry showed that, with low DEP:M-CSF ratios (< 50:1), there was selective modification of histidine residues, whereas at higher ratios (> 50:1), Tyr and Lys residues were also modified. Histidine 150-159 colony stimulating factor 1 Homo sapiens 88-93 8931561-3 1996 Peptide mapping of the reaction products by mass spectrometry showed that, with low DEP:M-CSF ratios (< 50:1), there was selective modification of histidine residues, whereas at higher ratios (> 50:1), Tyr and Lys residues were also modified. Tyrosine 208-211 colony stimulating factor 1 Homo sapiens 88-93 8931561-3 1996 Peptide mapping of the reaction products by mass spectrometry showed that, with low DEP:M-CSF ratios (< 50:1), there was selective modification of histidine residues, whereas at higher ratios (> 50:1), Tyr and Lys residues were also modified. Lysine 216-219 colony stimulating factor 1 Homo sapiens 88-93 8920951-2 1996 The seven cysteine residues in CSF-1(256) form three intrachain disulfide bonds (Cys7-Cys90, Cys48-Cys139, and Cys 102-Cys146), and one interchain disulfide bond (Cys31-Cys31). Disulfides 64-73 colony stimulating factor 1 Homo sapiens 31-36 8920951-2 1996 The seven cysteine residues in CSF-1(256) form three intrachain disulfide bonds (Cys7-Cys90, Cys48-Cys139, and Cys 102-Cys146), and one interchain disulfide bond (Cys31-Cys31). CYS7 81-85 colony stimulating factor 1 Homo sapiens 31-36 8920951-2 1996 The seven cysteine residues in CSF-1(256) form three intrachain disulfide bonds (Cys7-Cys90, Cys48-Cys139, and Cys 102-Cys146), and one interchain disulfide bond (Cys31-Cys31). Cysteine 81-84 colony stimulating factor 1 Homo sapiens 31-36 8920951-2 1996 The seven cysteine residues in CSF-1(256) form three intrachain disulfide bonds (Cys7-Cys90, Cys48-Cys139, and Cys 102-Cys146), and one interchain disulfide bond (Cys31-Cys31). Disulfides 147-156 colony stimulating factor 1 Homo sapiens 31-36 8920951-4 1996 We showed that each of the seven cysteines of CSF-1(256) is essential for its biological activity. Cysteine 33-42 colony stimulating factor 1 Homo sapiens 46-51 8920951-6 1996 In contrast, substitution of Cys7 or Cys90 affected CSF-1 dimer formation to a lesser degree but did not significantly affect cell surface expression of CSF-1. CYS7 29-33 colony stimulating factor 1 Homo sapiens 52-57 8920951-7 1996 Furthermore, disruption of the interchain disulfide bond led to efficient cell surface expression of monomeric CSF-1. Disulfides 42-51 colony stimulating factor 1 Homo sapiens 111-116 8920951-9 1996 The electrophoretic mobilities of the cleaved dimeric ectodomains of these mutant CSF-1 proteins on SDS-PAGE exhibited distinctly different patterns as compared with the wild type. Sodium Dodecyl Sulfate 100-103 colony stimulating factor 1 Homo sapiens 82-87 8960658-0 1996 [Successful treatment of acute non-lymphoblastic leukemia from myelodysplastic syndrome by combination of human macrophage colony-stimulating factor (M-CSF) and low dose cytosine arabinoside: M-CSF-induced proliferation and tyrosine phosphorylation in leukemic blasts]. Cytarabine 170-190 colony stimulating factor 1 Homo sapiens 192-197 8914012-13 1996 The production of macrophage colony-stimulating factor (M-CSF) was stimulated in the presence of 1,25(OH)2D3 (50 nM), TNF-alpha (2 ng/ml) or both in MG-63 cells. Calcitriol 97-108 colony stimulating factor 1 Homo sapiens 18-54 8914012-13 1996 The production of macrophage colony-stimulating factor (M-CSF) was stimulated in the presence of 1,25(OH)2D3 (50 nM), TNF-alpha (2 ng/ml) or both in MG-63 cells. Calcitriol 97-108 colony stimulating factor 1 Homo sapiens 56-61 8960658-0 1996 [Successful treatment of acute non-lymphoblastic leukemia from myelodysplastic syndrome by combination of human macrophage colony-stimulating factor (M-CSF) and low dose cytosine arabinoside: M-CSF-induced proliferation and tyrosine phosphorylation in leukemic blasts]. Tyrosine 224-232 colony stimulating factor 1 Homo sapiens 192-197 8839845-3 1996 M-CSF was found to induce substantial bone resorption and osteoclast formation in a dose-responsive and time-dependent manner above that induced by 1,25 dihydroxyvitamin D3 (1,25 vitamin D3) in cultures of human bone marrow (BM) stromal cells sedimented onto devitalized bone. Calcitriol 148-172 colony stimulating factor 1 Homo sapiens 0-5 8960658-3 1996 Stimulation of the blasts by macrophage colony-stimulating factor (M-CSF) resulted in tyrosine phosphorylation of several cellular proteins. Tyrosine 86-94 colony stimulating factor 1 Homo sapiens 29-65 8960658-3 1996 Stimulation of the blasts by macrophage colony-stimulating factor (M-CSF) resulted in tyrosine phosphorylation of several cellular proteins. Tyrosine 86-94 colony stimulating factor 1 Homo sapiens 67-72 8960658-5 1996 Based upon these findings, combined therapy with M-CSF and low dose cytosine arabinoside (ara-C) was successful. Cytarabine 90-95 colony stimulating factor 1 Homo sapiens 49-54 8960658-7 1996 These results suggest that M-CSF could enhance the cytotoxic effect of ara-C on leukemic blasts via its intracellular signaling pathway linked to proliferation. Cytarabine 71-76 colony stimulating factor 1 Homo sapiens 27-32 8839845-8 1996 We also found that 1,25 vitamin D3 increased, to a minor but significant degree, both bone resorption and the concentration of M-CSF in the culture supernatants above that in vehicle-treated cultures, indicating that M-CSF is present in our BM cultures, but that there is insufficient to induce substantial osteoclast formation. 1,25 vitamin d3 19-34 colony stimulating factor 1 Homo sapiens 127-132 8839845-8 1996 We also found that 1,25 vitamin D3 increased, to a minor but significant degree, both bone resorption and the concentration of M-CSF in the culture supernatants above that in vehicle-treated cultures, indicating that M-CSF is present in our BM cultures, but that there is insufficient to induce substantial osteoclast formation. 1,25 vitamin d3 19-34 colony stimulating factor 1 Homo sapiens 217-222 8839845-3 1996 M-CSF was found to induce substantial bone resorption and osteoclast formation in a dose-responsive and time-dependent manner above that induced by 1,25 dihydroxyvitamin D3 (1,25 vitamin D3) in cultures of human bone marrow (BM) stromal cells sedimented onto devitalized bone. Cholecalciferol 162-172 colony stimulating factor 1 Homo sapiens 0-5 8781564-8 1996 However, coincubation of mesangial cells with TNF-alpha and either dbcAMP, forskolin, or pertussis toxin inhibited TNF-alpha-induced M-CSF gene expression. Bucladesine 67-73 colony stimulating factor 1 Homo sapiens 133-138 8781564-8 1996 However, coincubation of mesangial cells with TNF-alpha and either dbcAMP, forskolin, or pertussis toxin inhibited TNF-alpha-induced M-CSF gene expression. Colforsin 75-84 colony stimulating factor 1 Homo sapiens 133-138 8840537-6 1996 The serum macrophage/monocyte-colony stimulating factor (M-CSF) levels in DEX stimulation were lower than in either G-CSF stimulation or no stimulation. Dexamethasone 74-77 colony stimulating factor 1 Homo sapiens 10-55 8840537-6 1996 The serum macrophage/monocyte-colony stimulating factor (M-CSF) levels in DEX stimulation were lower than in either G-CSF stimulation or no stimulation. Dexamethasone 74-77 colony stimulating factor 1 Homo sapiens 57-62 8760301-3 1996 We report that 8-bromo-cAMP (8Br-cAMP) and lipopolysaccharide (LPS) potently reduced CSF-1-stimulated cyclin D1 protein, and cyclin-dependent kinase (cdk) 4 mRNA and protein levels, while the inhibitory effects of the Na+/ H+ antiport inhibitor 5-(N",N"-dimethyl) amiloride (DMA) and interferon gamma (IFN gamma ) were only weak. 8-Bromo Cyclic Adenosine Monophosphate 15-27 colony stimulating factor 1 Homo sapiens 85-90 8760301-3 1996 We report that 8-bromo-cAMP (8Br-cAMP) and lipopolysaccharide (LPS) potently reduced CSF-1-stimulated cyclin D1 protein, and cyclin-dependent kinase (cdk) 4 mRNA and protein levels, while the inhibitory effects of the Na+/ H+ antiport inhibitor 5-(N",N"-dimethyl) amiloride (DMA) and interferon gamma (IFN gamma ) were only weak. 5-dimethylamiloride 245-273 colony stimulating factor 1 Homo sapiens 85-90 8882959-5 1996 In support of these results, all three ATL cell lines established from these patients secreted M-CSF in vitro after stimulation with phorbol myristate acetate (PMA) or concanavalin A (Con A). Tetradecanoylphorbol Acetate 133-158 colony stimulating factor 1 Homo sapiens 95-100 8882959-5 1996 In support of these results, all three ATL cell lines established from these patients secreted M-CSF in vitro after stimulation with phorbol myristate acetate (PMA) or concanavalin A (Con A). Tetradecanoylphorbol Acetate 160-163 colony stimulating factor 1 Homo sapiens 95-100 8760301-3 1996 We report that 8-bromo-cAMP (8Br-cAMP) and lipopolysaccharide (LPS) potently reduced CSF-1-stimulated cyclin D1 protein, and cyclin-dependent kinase (cdk) 4 mRNA and protein levels, while the inhibitory effects of the Na+/ H+ antiport inhibitor 5-(N",N"-dimethyl) amiloride (DMA) and interferon gamma (IFN gamma ) were only weak. 5-dimethylamiloride 275-278 colony stimulating factor 1 Homo sapiens 85-90 8760301-5 1996 Furthermore, 8Br-cAMP and to a lesser extent IFN gamma, also reduced CSF-1-stimulated levels of E2F DNA binding activity in a macrophage cell line, BAC1.2F5. 8-Bromo Cyclic Adenosine Monophosphate 13-21 colony stimulating factor 1 Homo sapiens 69-74 8760301-3 1996 We report that 8-bromo-cAMP (8Br-cAMP) and lipopolysaccharide (LPS) potently reduced CSF-1-stimulated cyclin D1 protein, and cyclin-dependent kinase (cdk) 4 mRNA and protein levels, while the inhibitory effects of the Na+/ H+ antiport inhibitor 5-(N",N"-dimethyl) amiloride (DMA) and interferon gamma (IFN gamma ) were only weak. 8-Bromo Cyclic Adenosine Monophosphate 29-37 colony stimulating factor 1 Homo sapiens 85-90 7499838-10 1995 The glycosaminoglycan chain of the growth factor was not only shown to inhibit CSF-1 activity but also to increase the stability of the core protein when the CSF-1-producing osteosarcoma cells were maintained in a collagen lattice. Glycosaminoglycans 4-21 colony stimulating factor 1 Homo sapiens 79-84 8631923-10 1996 Taken together, these data demonstrate that in M-CSF-treated macrophages adherent to vitronectin, paxillin localizes to focal contacts in the absence of FAK expression and is predominantly phosphorylated on serine residue(s) in a PKC-dependent manner. Serine 207-213 colony stimulating factor 1 Homo sapiens 47-52 8591991-3 1996 Glutaraldehyde-fixed cell layers supported proliferation of the macrophage cell line BAC1.2F5, suggesting the presence of membrane- or/and matrix-associated CSF-1. Glutaral 0-14 colony stimulating factor 1 Homo sapiens 157-162 8591991-6 1996 After labeling the cellular proteins with [35S] met/cys or [35S] SO4(2-), CSF-1 was immunoprecipitated and analyzed by SDS-PAGE. Sodium Dodecyl Sulfate 119-122 colony stimulating factor 1 Homo sapiens 74-79 8591991-12 1996 CSF-1 released with trypsin from the membrane fraction yielded on SDS-PAGE a band with MW of 60 and 30 kd under nonreducing and reducing conditions, respectively. Sodium Dodecyl Sulfate 66-69 colony stimulating factor 1 Homo sapiens 0-5 8615820-1 1996 (1) Treatment of resident peritoneal macrophages for 8 h with macrophage colony-stimulating factor (M-CSF) increased release of superoxide anion (O2-) stimulated by phorbol 12-myristate 13-acetate. Superoxides 128-144 colony stimulating factor 1 Homo sapiens 62-98 8615820-1 1996 (1) Treatment of resident peritoneal macrophages for 8 h with macrophage colony-stimulating factor (M-CSF) increased release of superoxide anion (O2-) stimulated by phorbol 12-myristate 13-acetate. Superoxides 128-144 colony stimulating factor 1 Homo sapiens 100-105 8615820-1 1996 (1) Treatment of resident peritoneal macrophages for 8 h with macrophage colony-stimulating factor (M-CSF) increased release of superoxide anion (O2-) stimulated by phorbol 12-myristate 13-acetate. Superoxides 146-148 colony stimulating factor 1 Homo sapiens 62-98 8615820-1 1996 (1) Treatment of resident peritoneal macrophages for 8 h with macrophage colony-stimulating factor (M-CSF) increased release of superoxide anion (O2-) stimulated by phorbol 12-myristate 13-acetate. Superoxides 146-148 colony stimulating factor 1 Homo sapiens 100-105 8615820-1 1996 (1) Treatment of resident peritoneal macrophages for 8 h with macrophage colony-stimulating factor (M-CSF) increased release of superoxide anion (O2-) stimulated by phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 165-196 colony stimulating factor 1 Homo sapiens 62-98 8615820-1 1996 (1) Treatment of resident peritoneal macrophages for 8 h with macrophage colony-stimulating factor (M-CSF) increased release of superoxide anion (O2-) stimulated by phorbol 12-myristate 13-acetate. Tetradecanoylphorbol Acetate 165-196 colony stimulating factor 1 Homo sapiens 100-105 8615820-2 1996 Gel electrophoresis of pulse-labelled proteins with L-[35S]methionine showed that a number of proteins were induced during activation by M-CSF. L-Methionine-35S 52-69 colony stimulating factor 1 Homo sapiens 137-142 8615820-3 1996 Immunoblot analysis with antibody against heat shock protein (HSP) 90, HSP70, or HSP60 demonstrated that M-CSF induced these stress-inducible HSPs; the timing of induction and level of each HSP correlated with the increase in O2- production. Superoxides 226-228 colony stimulating factor 1 Homo sapiens 105-110 8615820-5 1996 M-CSF also stimulated the synthesis of a heat shock cognate protein (HSC70); however, the induction occurred at 1 h, when O2- production was not yet augmented, but at which time L-[35S]methionine incorporation into cell proteins was already enhanced. Superoxides 122-124 colony stimulating factor 1 Homo sapiens 0-5 8615820-5 1996 M-CSF also stimulated the synthesis of a heat shock cognate protein (HSC70); however, the induction occurred at 1 h, when O2- production was not yet augmented, but at which time L-[35S]methionine incorporation into cell proteins was already enhanced. Methionine 185-195 colony stimulating factor 1 Homo sapiens 0-5 8615820-6 1996 (2) Gel mobility shift assay with oligonucleotide coding for the heat shock element showed that M-CSF activated the heat shock factor within 15 min, and the activation continued for at least 8 h. Northern-blot analysis with a cDNA probe for human HSP70 or HSC70 showed that accumulations of HSP70 and HSC70 mRNAs coincided with the inductions of the respective proteins. Oligonucleotides 34-49 colony stimulating factor 1 Homo sapiens 96-101 8723531-6 1996 We also found that macrophage-colony stimulating factor (M-CSF) and interleukin-2 (IL-2) augmented neopterin production from alveolar macrophage in both ILD patients (51.6 +/- 10.4 and 60.1 +/- 10.8 pmol/ml, respectively, P < 0.01) and control subjects (28.1 +/- 6.0 and 25.7 +/- 4.9 pmol/ml, respectively). Neopterin 99-108 colony stimulating factor 1 Homo sapiens 19-55 8723531-6 1996 We also found that macrophage-colony stimulating factor (M-CSF) and interleukin-2 (IL-2) augmented neopterin production from alveolar macrophage in both ILD patients (51.6 +/- 10.4 and 60.1 +/- 10.8 pmol/ml, respectively, P < 0.01) and control subjects (28.1 +/- 6.0 and 25.7 +/- 4.9 pmol/ml, respectively). Neopterin 99-108 colony stimulating factor 1 Homo sapiens 57-62 8723531-8 1996 These findings suggest that alveolar macrophages produce neopterin by M-CSF or IL-2. Neopterin 57-66 colony stimulating factor 1 Homo sapiens 70-75 8869967-3 1996 The effects of trans-retinoic acid (RA) on proliferation and cytokine gene expression in the human lung carcinoma Lu-CSF-1 are reported. Tretinoin 15-34 colony stimulating factor 1 Homo sapiens 117-122 8869967-3 1996 The effects of trans-retinoic acid (RA) on proliferation and cytokine gene expression in the human lung carcinoma Lu-CSF-1 are reported. Tretinoin 36-38 colony stimulating factor 1 Homo sapiens 117-122 7499838-10 1995 The glycosaminoglycan chain of the growth factor was not only shown to inhibit CSF-1 activity but also to increase the stability of the core protein when the CSF-1-producing osteosarcoma cells were maintained in a collagen lattice. Glycosaminoglycans 4-21 colony stimulating factor 1 Homo sapiens 158-163 8674843-3 1995 The present study investigates the growth of WEHI-3 monocytes/macrophages and the proliferative response of splenic macrophages to colony stimulating factor-1 when cultured in media containing high glucose concentrations. Glucose 198-205 colony stimulating factor 1 Homo sapiens 131-158 8599808-5 1995 Oxygen radicals act as second messenger for the activation of cytokines via NF-kappaB transcription factor, they stimulate the formation of TNF-alpha, IL-1, IL-6 and influence the expression of monocyte-specific cytokines (CSF-1 and MCP-1). Reactive Oxygen Species 0-15 colony stimulating factor 1 Homo sapiens 223-228 7595061-5 1995 Cycloheximide treatment of the cultures containing M-CSF and IFN-gamma inhibited the production of IL-1 beta and TNF-alpha. Cycloheximide 0-13 colony stimulating factor 1 Homo sapiens 51-56 7545471-7 1995 Although activation, phosphorylation, and turnover of the CSF-1 receptor and CSF-1-induced increase in diacylglycerol production remained normal, IFN-gamma blocked CSF-1-stimulated activation of mitogen-activated protein kinases, Raf-1 kinase, increase in GTP-bound Ras and tyrosine phosphorylation, and activation of protein kinase C delta (PKC-delta). Diglycerides 103-117 colony stimulating factor 1 Homo sapiens 77-82 7597091-6 1995 Dynamin interacts with the SH3 domains of Grb2 and exhibits M-CSF-dependent tyrosine phosphorylation in association with pp125FAK. Tyrosine 76-84 colony stimulating factor 1 Homo sapiens 60-65 8567816-7 1995 CSF-1 was found to increase [3H]thymidine uptake by trophoblast cultured on laminin for 72 h, but no such response was seen in trophoblast cultured on fibronectin, indicating that these extracellular matrix proteins have differential effects on the response of trophoblast to this cytokine. Tritium 29-31 colony stimulating factor 1 Homo sapiens 0-5 8567816-7 1995 CSF-1 was found to increase [3H]thymidine uptake by trophoblast cultured on laminin for 72 h, but no such response was seen in trophoblast cultured on fibronectin, indicating that these extracellular matrix proteins have differential effects on the response of trophoblast to this cytokine. Thymidine 32-41 colony stimulating factor 1 Homo sapiens 0-5 7561176-4 1995 MNC pretreated with M-CSF exhibited enhanced superoxide anion production in response to PMA (P = .026). Superoxides 45-61 colony stimulating factor 1 Homo sapiens 20-25 7624328-3 1995 Ectopic expression of c-myc or either of three D-type cyclin genes, but not cyclin E, resensitized these cells to the mitogenic effects of CSF-1, enabling them to proliferate continuously in liquid culture and to form colonies in agar in response to the growth factor. Agar 230-234 colony stimulating factor 1 Homo sapiens 139-144 7674895-5 1995 Results show that the differentiation of human monocytes/macrophages in the presence of physiological stimulating factors (M-CSF or GM-CSF) was associated with an increase in lactate production and glucose utilization. Lactic Acid 175-182 colony stimulating factor 1 Homo sapiens 123-128 7674895-5 1995 Results show that the differentiation of human monocytes/macrophages in the presence of physiological stimulating factors (M-CSF or GM-CSF) was associated with an increase in lactate production and glucose utilization. Glucose 198-205 colony stimulating factor 1 Homo sapiens 123-128 7634342-0 1995 Macrophage colony-stimulating factor (M-CSF) induction of enhanced anticryptococcal activity in human monocyte-derived macrophages: synergy with fluconazole for killing. Fluconazole 145-156 colony stimulating factor 1 Homo sapiens 0-36 7634342-0 1995 Macrophage colony-stimulating factor (M-CSF) induction of enhanced anticryptococcal activity in human monocyte-derived macrophages: synergy with fluconazole for killing. Fluconazole 145-156 colony stimulating factor 1 Homo sapiens 38-43 7634342-7 1995 Killing by FCZ was enhanced by HMM treated with M-CSF 5000 or 20,000 U/ml for 5 days compared to control HMM, 58% (P = 0.001) and 60% (P = 0.002) vs 48%, respectively. Fluconazole 11-14 colony stimulating factor 1 Homo sapiens 48-53 7634342-9 1995 M-CSF also induced in HMM enhancement of fungistasis by lower, fungistatic, concentrations of FCZ. Fluconazole 94-97 colony stimulating factor 1 Homo sapiens 0-5 7622526-0 1995 Nitric oxide inhibits macrophage-colony stimulating factor gene transcription in vascular endothelial cells. Nitric Oxide 0-12 colony stimulating factor 1 Homo sapiens 22-58 7622526-2 1995 Here we report that nitric oxide (NO) inhibits the expression of M-CSF in human vascular endothelial cells independent of guanylyl cyclase activation. Nitric Oxide 20-32 colony stimulating factor 1 Homo sapiens 65-70 7622526-3 1995 The induction of M-CSF mRNA expression by either oxidized low density lipoprotein (ox-LDL) or tumor necrosis factor-alpha (TNF alpha) was attenuated by NO donors, S-nitrosoglutathione (GSNO), sodium nitroprusside (SNP), and 3-morpholinosydnonimine, but not by cGMP analogues, glutathione, or nitrite. S-Nitrosoglutathione 163-183 colony stimulating factor 1 Homo sapiens 17-22 7622526-3 1995 The induction of M-CSF mRNA expression by either oxidized low density lipoprotein (ox-LDL) or tumor necrosis factor-alpha (TNF alpha) was attenuated by NO donors, S-nitrosoglutathione (GSNO), sodium nitroprusside (SNP), and 3-morpholinosydnonimine, but not by cGMP analogues, glutathione, or nitrite. S-Nitrosoglutathione 185-189 colony stimulating factor 1 Homo sapiens 17-22 7622526-3 1995 The induction of M-CSF mRNA expression by either oxidized low density lipoprotein (ox-LDL) or tumor necrosis factor-alpha (TNF alpha) was attenuated by NO donors, S-nitrosoglutathione (GSNO), sodium nitroprusside (SNP), and 3-morpholinosydnonimine, but not by cGMP analogues, glutathione, or nitrite. Nitroprusside 192-212 colony stimulating factor 1 Homo sapiens 17-22 7622526-3 1995 The induction of M-CSF mRNA expression by either oxidized low density lipoprotein (ox-LDL) or tumor necrosis factor-alpha (TNF alpha) was attenuated by NO donors, S-nitrosoglutathione (GSNO), sodium nitroprusside (SNP), and 3-morpholinosydnonimine, but not by cGMP analogues, glutathione, or nitrite. linsidomine 224-247 colony stimulating factor 1 Homo sapiens 17-22 7622526-3 1995 The induction of M-CSF mRNA expression by either oxidized low density lipoprotein (ox-LDL) or tumor necrosis factor-alpha (TNF alpha) was attenuated by NO donors, S-nitrosoglutathione (GSNO), sodium nitroprusside (SNP), and 3-morpholinosydnonimine, but not by cGMP analogues, glutathione, or nitrite. Cyclic GMP 260-264 colony stimulating factor 1 Homo sapiens 17-22 7622526-3 1995 The induction of M-CSF mRNA expression by either oxidized low density lipoprotein (ox-LDL) or tumor necrosis factor-alpha (TNF alpha) was attenuated by NO donors, S-nitrosoglutathione (GSNO), sodium nitroprusside (SNP), and 3-morpholinosydnonimine, but not by cGMP analogues, glutathione, or nitrite. Glutathione 172-183 colony stimulating factor 1 Homo sapiens 17-22 7622526-3 1995 The induction of M-CSF mRNA expression by either oxidized low density lipoprotein (ox-LDL) or tumor necrosis factor-alpha (TNF alpha) was attenuated by NO donors, S-nitrosoglutathione (GSNO), sodium nitroprusside (SNP), and 3-morpholinosydnonimine, but not by cGMP analogues, glutathione, or nitrite. Nitrites 292-299 colony stimulating factor 1 Homo sapiens 17-22 7622526-4 1995 Inhibition of endogenous NO production by N-monomethyl-L-arginine (L-NMA) also increased M-CSF expression in control and TNF alpha-stimulated cells. omega-N-Methylarginine 42-65 colony stimulating factor 1 Homo sapiens 89-94 7622526-4 1995 Inhibition of endogenous NO production by N-monomethyl-L-arginine (L-NMA) also increased M-CSF expression in control and TNF alpha-stimulated cells. l-nma 67-72 colony stimulating factor 1 Homo sapiens 89-94 8530162-8 1995 Moreover, DIF activation was observed during TPA-induced monocytic differentiation and after treatment of macrophages with the macrophage differentiation factor CSF-1. Tetradecanoylphorbol Acetate 45-48 colony stimulating factor 1 Homo sapiens 161-166 7643455-7 1995 Eight million units of human native M-CSF was administered intravenously for 14 days after the last BHAC-AMP therapy in case no 1, and for 5 days after the last modified B-triple V therapy in case no 2. bhac-amp 100-108 colony stimulating factor 1 Homo sapiens 36-41 7579059-0 1995 Regulation of macrophage growth responses to colony-stimulating factor-1 by 1,25-dihydroxyvitamin D3. Calcitriol 76-100 colony stimulating factor 1 Homo sapiens 45-72 7579059-2 1995 The effect of the vitamin D metabolite on the proliferative responses of macrophages to the cytokine colony-stimulating factor-1 (CSF-1) has been studied. Vitamin D 18-27 colony stimulating factor 1 Homo sapiens 101-128 7579059-2 1995 The effect of the vitamin D metabolite on the proliferative responses of macrophages to the cytokine colony-stimulating factor-1 (CSF-1) has been studied. Vitamin D 18-27 colony stimulating factor 1 Homo sapiens 130-135 7579059-3 1995 It was found that this substance was able to suppress the growth responses of macrophages to CSF-1 as assessed by macrophage-tritiated thymidine uptake and also by cell counts. tritiated 125-134 colony stimulating factor 1 Homo sapiens 93-98 7579059-3 1995 It was found that this substance was able to suppress the growth responses of macrophages to CSF-1 as assessed by macrophage-tritiated thymidine uptake and also by cell counts. Thymidine 135-144 colony stimulating factor 1 Homo sapiens 93-98 7643455-9 1995 These successful cases treated with M-CSF combining chemotherapy may suggest a new therapeutic strategy for APL in addition to all-trans retinoic acid. Tretinoin 137-150 colony stimulating factor 1 Homo sapiens 36-41 7591362-4 1995 GM-CSF and M-CSF demonstrated equipotency in the induction of monocyte phagocytosis of heat-killed baker"s yeast and in the regulation of the hexose-monophosphate shunt (NBT reduction). hexose monophosphate 142-162 colony stimulating factor 1 Homo sapiens 1-6 7546213-6 1995 Here we report studies indicating that the effect of protein and RNA synthesis inhibitors on prostanoid production, in cells incubated in the presence of CSF-1 (or FCS), can be correlated with an inductive event carried out by the growth factor, as demonstrated by the use of Western and Northern blotting procedures. Prostaglandins 93-103 colony stimulating factor 1 Homo sapiens 154-159 7546213-7 1995 However, while in human monocytes PGH-s and its mRNA are absent in controls and are expressed at high levels in CSF-1 stimulated cells, in U937 cells exposed to TPA, PGH-s mRNA was clearly detected by Northern blots, but its translation product was expressed at low level, and cells generated low amounts of TXA2 (13% of maximal production). pgh-s 34-39 colony stimulating factor 1 Homo sapiens 112-117 7546213-7 1995 However, while in human monocytes PGH-s and its mRNA are absent in controls and are expressed at high levels in CSF-1 stimulated cells, in U937 cells exposed to TPA, PGH-s mRNA was clearly detected by Northern blots, but its translation product was expressed at low level, and cells generated low amounts of TXA2 (13% of maximal production). pgh-s 166-171 colony stimulating factor 1 Homo sapiens 112-117 7591362-4 1995 GM-CSF and M-CSF demonstrated equipotency in the induction of monocyte phagocytosis of heat-killed baker"s yeast and in the regulation of the hexose-monophosphate shunt (NBT reduction). Nitroblue Tetrazolium 170-173 colony stimulating factor 1 Homo sapiens 1-6 7738650-8 1995 In the MCSF+R24 group, the increase of glucose metabolic rate on Days 3 and 10 was 35% and 31% above baseline on the average, but was not significant. Glucose 39-46 colony stimulating factor 1 Homo sapiens 7-11 7602192-5 1995 Combination therapy with M-CSF and amphotericin-B (AMPH-B) showed the therapy with either M-CSF or AMPH-B alone. Amphotericin B 35-49 colony stimulating factor 1 Homo sapiens 90-95 7602192-5 1995 Combination therapy with M-CSF and amphotericin-B (AMPH-B) showed the therapy with either M-CSF or AMPH-B alone. Amphotericin B 51-57 colony stimulating factor 1 Homo sapiens 25-30 7602192-5 1995 Combination therapy with M-CSF and amphotericin-B (AMPH-B) showed the therapy with either M-CSF or AMPH-B alone. Amphotericin B 51-57 colony stimulating factor 1 Homo sapiens 90-95 7602192-5 1995 Combination therapy with M-CSF and amphotericin-B (AMPH-B) showed the therapy with either M-CSF or AMPH-B alone. Amphotericin B 99-105 colony stimulating factor 1 Homo sapiens 25-30 7602192-7 1995 Furthermore, M-CSF promoted the production of superoxide and nitric oxide in macrophage. Superoxides 46-56 colony stimulating factor 1 Homo sapiens 13-18 7602192-7 1995 Furthermore, M-CSF promoted the production of superoxide and nitric oxide in macrophage. Nitric Oxide 61-73 colony stimulating factor 1 Homo sapiens 13-18 7627128-2 1995 Using oligonucleotide-directed mutagenesis of hM-CSF (1-149aa) cDNA, we have substituted Ser31 for Cys31 which forms intermolecular disulfide bond in native hM-CSF. Oligonucleotides 6-21 colony stimulating factor 1 Homo sapiens 46-52 7730365-8 1995 The activated colony stimulating factor-1 (CSF-1) receptor, which is known to associate with Src family kinases, has a sequence in its juxtamembrane region similar to that surrounding Tyr-579 of the PDGF receptor, and a phosphopeptide modeled on this sequence competed the association of Fyn with the receptor in vitro. Tyrosine 184-187 colony stimulating factor 1 Homo sapiens 14-41 7627128-2 1995 Using oligonucleotide-directed mutagenesis of hM-CSF (1-149aa) cDNA, we have substituted Ser31 for Cys31 which forms intermolecular disulfide bond in native hM-CSF. Oligonucleotides 6-21 colony stimulating factor 1 Homo sapiens 157-163 7627128-2 1995 Using oligonucleotide-directed mutagenesis of hM-CSF (1-149aa) cDNA, we have substituted Ser31 for Cys31 which forms intermolecular disulfide bond in native hM-CSF. Disulfides 132-141 colony stimulating factor 1 Homo sapiens 46-52 7627128-2 1995 Using oligonucleotide-directed mutagenesis of hM-CSF (1-149aa) cDNA, we have substituted Ser31 for Cys31 which forms intermolecular disulfide bond in native hM-CSF. Disulfides 132-141 colony stimulating factor 1 Homo sapiens 157-163 7890061-7 1995 In the levonorgestrel IUD-exposed endometria, the mean levels of IL-1 beta, TNF-alpha, and CSF-1 mRNA were similar to those in normal endometrium in the late secretory menstrual phase. Levonorgestrel 7-21 colony stimulating factor 1 Homo sapiens 91-96 7596682-9 1995 A possible role of female sex steroids was discussed in the regulation of M-CSF production by mammary gland epithelial cells. Steroids 30-38 colony stimulating factor 1 Homo sapiens 74-79 7538104-8 1995 We detected inhibitory activity toward L1210 growth in serum of mice administered with hM-CSF, and the degree of the inhibitory activity was correlated with the level of nitrite (NO2-) in the serum. Nitrites 170-177 colony stimulating factor 1 Homo sapiens 87-93 9815987-7 1995 High serum levels of serum CSF-1 were associated with elevated serum CA19-9 and CA-125 levels. ca19-9 69-75 colony stimulating factor 1 Homo sapiens 27-32 9815987-13 1995 These results therefore support the hypotheses that CSF-1 and CSF-1R are overexpressed in endometrial adenocarcinoma, that levels of expression significantly correlate with clinicopathological risk factors for poor outcome, and that CSF-1 in association with its receptor via autocrine, juxtacrine, and/or paracrine interactions has a causal role in endometrial adenocarcinoma development and proliferation. juxtacrine 287-297 colony stimulating factor 1 Homo sapiens 52-57 7538104-8 1995 We detected inhibitory activity toward L1210 growth in serum of mice administered with hM-CSF, and the degree of the inhibitory activity was correlated with the level of nitrite (NO2-) in the serum. Nitrogen Dioxide 179-183 colony stimulating factor 1 Homo sapiens 87-93 7538104-9 1995 When L1210 cells were co-cultured with peritoneal macrophages from mice intraperitoneally injected with hM-CSF, the uptake of [3H]thymidine in L1210 cells was inhibited. Tritium 127-129 colony stimulating factor 1 Homo sapiens 104-110 7538104-10 1995 The inhibition was abolished by the addition of NG-monomethyl-L-arginine, an inhibitor of NO2- synthesis, suggesting that the reactive nitrogen oxide intermediate is involved in hM-CSF-induced inhibition of L1210 growth. omega-N-Methylarginine 48-72 colony stimulating factor 1 Homo sapiens 178-184 7538104-10 1995 The inhibition was abolished by the addition of NG-monomethyl-L-arginine, an inhibitor of NO2- synthesis, suggesting that the reactive nitrogen oxide intermediate is involved in hM-CSF-induced inhibition of L1210 growth. Nitrogen Dioxide 90-93 colony stimulating factor 1 Homo sapiens 178-184 7538104-10 1995 The inhibition was abolished by the addition of NG-monomethyl-L-arginine, an inhibitor of NO2- synthesis, suggesting that the reactive nitrogen oxide intermediate is involved in hM-CSF-induced inhibition of L1210 growth. Nitrogen Oxides 135-149 colony stimulating factor 1 Homo sapiens 178-184 16695973-0 1995 Sites of M-CSF messenger RNA production in bone marrow trephine biopsy specimens and long term cultures demonstrated by nonisotopic in situ hybridisation. trephine 55-63 colony stimulating factor 1 Homo sapiens 9-14 7742005-6 1995 Tumour cell expression of CSF-1R is under the control of several steroid hormones (glucocorticoids and progestins) and tumour cell CSF-1 expression appears to be regulated by other hormones, some of which are involved in normal lactogenic differentiation. Steroids 65-81 colony stimulating factor 1 Homo sapiens 26-31 16695973-3 1995 Minor technical modifications were required to perform ISH with long term bone marrow cultures.Results-M-CSF mRNA was demonstrated successfully in trephine biopsy specimens and long term cultures. trephine 147-155 colony stimulating factor 1 Homo sapiens 103-108 16695973-8 1995 Weak M-CSF mRNA expression was also seen in stromal fibroblasts.Conclusions-ISH can be performed successfully with formic acid decalcified bone marrow trephine biopsy specimens and long term cultures. formic acid 115-126 colony stimulating factor 1 Homo sapiens 5-10 7994042-12 1994 The comparative stability of M-CSF mRNA from cord versus adult MNCs was next determined by actinomycin D decay studies. Dactinomycin 91-104 colony stimulating factor 1 Homo sapiens 29-34 7833270-6 1995 Analysis of the patient"s plasma and conditioned media prepared from peripheral blood mononuclear and granulocytic cell fractions for their ability to bind 125Iodine-labelled CSF-1 revealed the presence of a plasma CSF-1 binding factor. Iodine-125 156-165 colony stimulating factor 1 Homo sapiens 175-180 7833270-6 1995 Analysis of the patient"s plasma and conditioned media prepared from peripheral blood mononuclear and granulocytic cell fractions for their ability to bind 125Iodine-labelled CSF-1 revealed the presence of a plasma CSF-1 binding factor. Iodine-125 156-165 colony stimulating factor 1 Homo sapiens 215-220 7672777-1 1995 The effects of gonadal steroids on the secretion and gene expression of macrophage colony-stimulating factor (M-CSF) and on the secretion of transforming growth factor (TGF)-beta 1 and TGF-beta 2 by human endometrial stromal cells (ESCs) were examined by an in vitro system of ESC differentiation (decidualization). Steroids 23-31 colony stimulating factor 1 Homo sapiens 72-108 7672777-2 1995 M-CSF production by ESCs was dose-dependently enhanced by the addition of progesterone or testosterone, while estradiol treatment had no effect. Progesterone 74-86 colony stimulating factor 1 Homo sapiens 0-5 7672777-2 1995 M-CSF production by ESCs was dose-dependently enhanced by the addition of progesterone or testosterone, while estradiol treatment had no effect. Testosterone 90-102 colony stimulating factor 1 Homo sapiens 0-5 7751736-6 1995 Combination therapy with hM-CSF and fluconazole showed higher survival rate more than in the therapy with either hM-CSF or fluconazole alone. Fluconazole 36-47 colony stimulating factor 1 Homo sapiens 113-119 7751736-6 1995 Combination therapy with hM-CSF and fluconazole showed higher survival rate more than in the therapy with either hM-CSF or fluconazole alone. Fluconazole 123-134 colony stimulating factor 1 Homo sapiens 25-31 7751736-7 1995 Furthermore, hM-CSF enhanced the activity of RES organ, phagocytosis by macrophages and NBT reduction by macrophages, significantly. Nitroblue Tetrazolium 88-91 colony stimulating factor 1 Homo sapiens 13-19 7528686-2 1994 Upon removal of CSF-1 from bone marrow-derived macrophages (BMM), uPA mRNA decayed with a half-life of 2 h. If RNA synthesis inhibitors actinomycin D, 5,6-dichloro-1-beta-ribofuranosyl benzimidazole (DRB) or alpha-amanitin were added at the time as CSF-1 removal, the uPA message was stabilised. Dactinomycin 136-149 colony stimulating factor 1 Homo sapiens 16-21 7528686-2 1994 Upon removal of CSF-1 from bone marrow-derived macrophages (BMM), uPA mRNA decayed with a half-life of 2 h. If RNA synthesis inhibitors actinomycin D, 5,6-dichloro-1-beta-ribofuranosyl benzimidazole (DRB) or alpha-amanitin were added at the time as CSF-1 removal, the uPA message was stabilised. Dichlororibofuranosylbenzimidazole 200-203 colony stimulating factor 1 Homo sapiens 16-21 7528686-2 1994 Upon removal of CSF-1 from bone marrow-derived macrophages (BMM), uPA mRNA decayed with a half-life of 2 h. If RNA synthesis inhibitors actinomycin D, 5,6-dichloro-1-beta-ribofuranosyl benzimidazole (DRB) or alpha-amanitin were added at the time as CSF-1 removal, the uPA message was stabilised. Alpha-Amanitin 208-222 colony stimulating factor 1 Homo sapiens 16-21 7989771-10 1994 This resembles the situation after CSF-1-stimulation of macrophages, in which Raf-1 clearly transduces a signal generated by the CSF-1 receptor kinase, but is phosphorylated exclusively in serine. Serine 189-195 colony stimulating factor 1 Homo sapiens 35-40 7994042-16 1994 The increase of M-CSF mRNA induction by CHX was 2.5 times higher in cord MNCs compared with that in adult MNCs. Cycloheximide 40-43 colony stimulating factor 1 Homo sapiens 16-21 7528860-8 1994 Furthermore, ubenimex augmented the expression of M-CSF receptors by U937 cells and enhanced the tyrosine kinase activity of cellular pp60c-src. ubenimex 13-21 colony stimulating factor 1 Homo sapiens 50-55 7524738-4 1994 Interestingly, the anti-HIV activity of dextran sulfate and soluble-CD4 (two compounds that interfere with HIV-CD4 binding with different mechanisms) was reduced 100-fold and fivefold, respectively, in M-CSF-treated macrophages. Dextran Sulfate 40-55 colony stimulating factor 1 Homo sapiens 202-207 7524738-5 1994 Human blood concentrations of M-CSF are reported to be similar to those used in this work (1,000 U/mL); thus, it is conceivable that also in vivo this cytokine may modify the susceptibility of macrophages to HIV and the ability of dextran sulfate and soluble CD4 to inhibit HIV replication. Dextran Sulfate 231-246 colony stimulating factor 1 Homo sapiens 30-35 7889981-4 1994 In normal HL-60 cells retinoic acid is known to induce a colony-stimulating factor-1 (CSF-1)-dependent metabolic cascade culminating in G0 arrest and phenotypic conversion. Tretinoin 22-35 colony stimulating factor 1 Homo sapiens 57-84 7954814-1 1994 Cyclic AMP (cAMP) blocks the mitogenic effects of colony-stimulating factor 1 (CSF-1) in macrophages, inducing cell cycle arrest in mid-G1 phase. Cyclic AMP 0-10 colony stimulating factor 1 Homo sapiens 50-77 7954814-1 1994 Cyclic AMP (cAMP) blocks the mitogenic effects of colony-stimulating factor 1 (CSF-1) in macrophages, inducing cell cycle arrest in mid-G1 phase. Cyclic AMP 0-10 colony stimulating factor 1 Homo sapiens 79-84 7954814-1 1994 Cyclic AMP (cAMP) blocks the mitogenic effects of colony-stimulating factor 1 (CSF-1) in macrophages, inducing cell cycle arrest in mid-G1 phase. Cyclic AMP 12-16 colony stimulating factor 1 Homo sapiens 50-77 7954814-1 1994 Cyclic AMP (cAMP) blocks the mitogenic effects of colony-stimulating factor 1 (CSF-1) in macrophages, inducing cell cycle arrest in mid-G1 phase. Cyclic AMP 12-16 colony stimulating factor 1 Homo sapiens 79-84 7889981-4 1994 In normal HL-60 cells retinoic acid is known to induce a colony-stimulating factor-1 (CSF-1)-dependent metabolic cascade culminating in G0 arrest and phenotypic conversion. Tretinoin 22-35 colony stimulating factor 1 Homo sapiens 86-91 7814798-5 1994 In cirrhosis, levels of macrophage colony stimulating factor correlated positively with the serum alanine aminotransferase levels (p < 0.05), total bilirubin levels (p < 0.05), and indocyanine green clearance (p < 0.05). Bilirubin 151-160 colony stimulating factor 1 Homo sapiens 24-60 7929840-1 1994 We recently isolated a proteoglycan form of macrophage colony-stimulating factor (PG-M-CSF) that carries a chondroitin sulfate glycosaminoglycan chain. chondroitin sulfate glycosaminoglycan 107-144 colony stimulating factor 1 Homo sapiens 85-90 7929840-2 1994 Here, we examined the interaction of PG-M-CSF with low density lipoprotein (LDL). pg 37-39 colony stimulating factor 1 Homo sapiens 40-45 7929840-4 1994 When LDL was preincubated with chondroitin sulfate-free 85-kD M-CSF instead of PG-M-CSF, the elution profile of LDL remained unchanged, indicating specific interaction between PG-M-CSF and LDL. Chondroitin Sulfates 31-50 colony stimulating factor 1 Homo sapiens 62-67 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. Chondroitin Sulfates 26-45 colony stimulating factor 1 Homo sapiens 178-183 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. pg 91-93 colony stimulating factor 1 Homo sapiens 94-99 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. pg 91-93 colony stimulating factor 1 Homo sapiens 178-183 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. pg 91-93 colony stimulating factor 1 Homo sapiens 178-183 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. pg 175-177 colony stimulating factor 1 Homo sapiens 94-99 7929840-5 1994 The level of PG-M-CSF binding in the wells of a plastic microtitration plate precoated with LDL was significant, this binding being completely abolished by pretreatment of PG-M-CSF with chondroitinase AC, which degrades chondroitin sulfate. Chondroitin Sulfates 220-239 colony stimulating factor 1 Homo sapiens 16-21 7929840-5 1994 The level of PG-M-CSF binding in the wells of a plastic microtitration plate precoated with LDL was significant, this binding being completely abolished by pretreatment of PG-M-CSF with chondroitinase AC, which degrades chondroitin sulfate. Chondroitin Sulfates 220-239 colony stimulating factor 1 Homo sapiens 175-180 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. Chondroitin Sulfates 26-45 colony stimulating factor 1 Homo sapiens 94-99 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. Chondroitin Sulfates 26-45 colony stimulating factor 1 Homo sapiens 178-183 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. pg 175-177 colony stimulating factor 1 Homo sapiens 178-183 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. pg 175-177 colony stimulating factor 1 Homo sapiens 178-183 7929840-6 1994 The addition of exogenous chondroitin sulfate or apolipoprotein B inhibited the binding of PG-M-CSF to LDL in a dose-dependent manner, indicating that the interaction between PG-M-CSF and LDL was mediated by the binding of the chondroitin sulfate chain of PG-M-CSF to LDL apolipoprotein B. Chondroitin Sulfates 227-246 colony stimulating factor 1 Homo sapiens 94-99 7929840-8 1994 The in vitro interaction between PG-M-CSF and LDL thus appears to have physiological significance. pg 33-35 colony stimulating factor 1 Homo sapiens 36-41 7814798-5 1994 In cirrhosis, levels of macrophage colony stimulating factor correlated positively with the serum alanine aminotransferase levels (p < 0.05), total bilirubin levels (p < 0.05), and indocyanine green clearance (p < 0.05). Indocyanine Green 187-204 colony stimulating factor 1 Homo sapiens 24-60 7965406-2 1994 Preliminary results have already suggested a possible influence of steroids on FMS (M-CSF receptor) expression. Steroids 67-75 colony stimulating factor 1 Homo sapiens 84-89 8030755-8 1994 Furthermore, profound inhibition of microglial ramification was exerted by herbimycin A, a specific inhibitor of tyrosine kinase (a component of the signal cascade of c-fms), supporting the role of M-CSF/c-fms in the induction of microglial ramification. herbimycin 75-87 colony stimulating factor 1 Homo sapiens 198-203 9419789-7 1994 The probe for the AU-rich exon 10 of CSF-1 was prepared by amplification of the terminal 143 bp of the 3" UTR of human CSF-1 by polymerase chain reaction. Gold 18-20 colony stimulating factor 1 Homo sapiens 37-42 9419789-7 1994 The probe for the AU-rich exon 10 of CSF-1 was prepared by amplification of the terminal 143 bp of the 3" UTR of human CSF-1 by polymerase chain reaction. Gold 18-20 colony stimulating factor 1 Homo sapiens 119-124 8007983-0 1994 Tyrosine 569 in the c-Fms juxtamembrane domain is essential for kinase activity and macrophage colony-stimulating factor-dependent internalization. Tyrosine 0-8 colony stimulating factor 1 Homo sapiens 84-120 8020834-0 1994 Macrophage colony-stimulating factor enhances platelet recovery following cisplatin/carboplatin chemotherapy in ovarian cancer. Cisplatin 74-83 colony stimulating factor 1 Homo sapiens 0-36 8020834-0 1994 Macrophage colony-stimulating factor enhances platelet recovery following cisplatin/carboplatin chemotherapy in ovarian cancer. Carboplatin 84-95 colony stimulating factor 1 Homo sapiens 0-36 8027260-2 1994 In this study, we examined, by enzyme-linked immunosorbent assay, the supernatants of stromal cell-enriched fraction (SF) of human nonpregnant endometrium for the presence of M-CSF during culture with progesterone (P) or estrogen. Progesterone 201-213 colony stimulating factor 1 Homo sapiens 175-180 8007965-2 1994 To determine if c-fps/fes can mediate the action of the colony-stimulating factor 1 (CSF-1) receptor (CSF-1R) and to identify potential targets of c-fps/fes in macrophages, we have overexpressed c-fps/fes in a CSF-1-dependent macrophage cell line. CFP protocol 16-21 colony stimulating factor 1 Homo sapiens 56-83 8007965-2 1994 To determine if c-fps/fes can mediate the action of the colony-stimulating factor 1 (CSF-1) receptor (CSF-1R) and to identify potential targets of c-fps/fes in macrophages, we have overexpressed c-fps/fes in a CSF-1-dependent macrophage cell line. CFP protocol 16-21 colony stimulating factor 1 Homo sapiens 85-90 8007965-2 1994 To determine if c-fps/fes can mediate the action of the colony-stimulating factor 1 (CSF-1) receptor (CSF-1R) and to identify potential targets of c-fps/fes in macrophages, we have overexpressed c-fps/fes in a CSF-1-dependent macrophage cell line. Iron 22-25 colony stimulating factor 1 Homo sapiens 56-83 8007965-2 1994 To determine if c-fps/fes can mediate the action of the colony-stimulating factor 1 (CSF-1) receptor (CSF-1R) and to identify potential targets of c-fps/fes in macrophages, we have overexpressed c-fps/fes in a CSF-1-dependent macrophage cell line. Iron 22-25 colony stimulating factor 1 Homo sapiens 85-90 8199198-3 1994 Binding activity of 125I-M-CSF to THP-1 cells was higher than that in THP-1 cells elicited with TPA. Tetradecanoylphorbol Acetate 96-99 colony stimulating factor 1 Homo sapiens 25-30 8199198-4 1994 THP-1 cells incubated with M-CSF before TPA treatment were designated MT macrophages, and those incubated with M-CSF after TPA treatment were called TM macrophages. Tetradecanoylphorbol Acetate 123-126 colony stimulating factor 1 Homo sapiens 111-116 8199198-10 1994 These results suggested that beta-VLDL-induced cholesterol ester deposition in THP-1 cells-derived macrophages was suppressed by M-CSF, when M-CSF acted at the stage of monocytes (THP-1 cells), and that the reduction of cholesterol ester might be due to enhanced release of cholesterol from the cells with high neutral cholesterol esterase activity. Cholesterol Esters 47-64 colony stimulating factor 1 Homo sapiens 129-134 8199198-10 1994 These results suggested that beta-VLDL-induced cholesterol ester deposition in THP-1 cells-derived macrophages was suppressed by M-CSF, when M-CSF acted at the stage of monocytes (THP-1 cells), and that the reduction of cholesterol ester might be due to enhanced release of cholesterol from the cells with high neutral cholesterol esterase activity. Cholesterol Esters 47-64 colony stimulating factor 1 Homo sapiens 141-146 8199198-10 1994 These results suggested that beta-VLDL-induced cholesterol ester deposition in THP-1 cells-derived macrophages was suppressed by M-CSF, when M-CSF acted at the stage of monocytes (THP-1 cells), and that the reduction of cholesterol ester might be due to enhanced release of cholesterol from the cells with high neutral cholesterol esterase activity. Cholesterol Esters 220-237 colony stimulating factor 1 Homo sapiens 141-146 8199198-10 1994 These results suggested that beta-VLDL-induced cholesterol ester deposition in THP-1 cells-derived macrophages was suppressed by M-CSF, when M-CSF acted at the stage of monocytes (THP-1 cells), and that the reduction of cholesterol ester might be due to enhanced release of cholesterol from the cells with high neutral cholesterol esterase activity. Cholesterol 47-58 colony stimulating factor 1 Homo sapiens 129-134 8007965-6 1994 P130 and P75 may be direct substrates of c-fps/fes: P130 was tightly associated with NCP92, and the src homology 2 domain of NCP92 specifically bound phosphorylated P130 and P75 but not the CSF-1-induced phosphotyrosyl proteins, consistent with the possibility that P130 and P75 are physiological targets of c-fps/fes. CFP protocol 41-46 colony stimulating factor 1 Homo sapiens 190-195 8040620-10 1994 The mean M-CSF level in MLCS of the normal fertile group was 182.0 +/- 26.1 IU/ml, in contrast, it was not detected in MLCS of recurrent aborting couples or LCS of either group. lcs 25-28 colony stimulating factor 1 Homo sapiens 9-14 8161795-5 1994 These results indicated that M-CSF is required for 1 alpha,25(OH)2D3-stimulated monocyte proliferation. Calcitriol 51-68 colony stimulating factor 1 Homo sapiens 29-34 7513707-4 1994 An analysis of some potential signaling mechanisms associated with cytokine-mediated developmental decisions in GM-CFC revealed that M-CSF, but not SCF, was able to chronically stimulate phosphatidylcholine breakdown and diacylglycerol production, indicating that protein kinase C (PKC) may be involved in the action of M-CSF. Phosphatidylcholines 187-206 colony stimulating factor 1 Homo sapiens 133-138 7513707-4 1994 An analysis of some potential signaling mechanisms associated with cytokine-mediated developmental decisions in GM-CFC revealed that M-CSF, but not SCF, was able to chronically stimulate phosphatidylcholine breakdown and diacylglycerol production, indicating that protein kinase C (PKC) may be involved in the action of M-CSF. Diglycerides 221-235 colony stimulating factor 1 Homo sapiens 133-138 8161795-0 1994 Effects of 1 alpha,25-dihydroxyvitamin D3 on macrophage colony-stimulating factor production and proliferation of human monocytic cells. Calcitriol 11-41 colony stimulating factor 1 Homo sapiens 45-81 8161795-6 1994 In addition, 1 alpha,25(OH)2D3 stimulated M-CSF secretion from human circulating monocytes. Calcitriol 13-30 colony stimulating factor 1 Homo sapiens 42-47 8161795-2 1994 In the present study, we investigated a possible role of macrophage colony-stimulating factor (M-CSF) in 1 alpha,25(OH)2D3-induced proliferation of human circulating monocytes and the effects of 1 alpha,25(OH)2D3 on M-CSF production by human monocytic cells. 25(oh)2d3 113-122 colony stimulating factor 1 Homo sapiens 95-100 8161795-7 1994 Secretion and mRNA expression of M-CSF by 12-0-tetradecanoylphorbol-13-acetate (TPA)-treated THP-1 cells (human monocytic leukemia cell line) and TPA-treated HL-60 cells (human promyelocytic leukemia cell line) were also increased by 1 alpha,25(OH)2D3. 12-0-tetradecanoylphorbol-13-acetate 42-78 colony stimulating factor 1 Homo sapiens 33-38 8161795-7 1994 Secretion and mRNA expression of M-CSF by 12-0-tetradecanoylphorbol-13-acetate (TPA)-treated THP-1 cells (human monocytic leukemia cell line) and TPA-treated HL-60 cells (human promyelocytic leukemia cell line) were also increased by 1 alpha,25(OH)2D3. Tetradecanoylphorbol Acetate 80-83 colony stimulating factor 1 Homo sapiens 33-38 8161795-8 1994 M-CSF secretion from TPA-treated THP-1 cells was increased by 1 alpha,25(OH)2D3 in a dose-dependent and metabolite-specific manner. Tetradecanoylphorbol Acetate 21-24 colony stimulating factor 1 Homo sapiens 0-5 8161795-8 1994 M-CSF secretion from TPA-treated THP-1 cells was increased by 1 alpha,25(OH)2D3 in a dose-dependent and metabolite-specific manner. alpha,25(oh)2d3 64-79 colony stimulating factor 1 Homo sapiens 0-5 8155653-0 1994 Incorporation of norleucine at methionine positions in recombinant human macrophage colony stimulating factor (M-CSF, 4-153) expressed in Escherichia coli: structural analysis. Norleucine 17-27 colony stimulating factor 1 Homo sapiens 73-109 8161795-9 1994 The present study demonstrates that 1 alpha,25(OH)2D3 is a potent stimulator for M-CSF production by human monocytic cells and that the proliferative effect of 1 alpha,25(OH)2D3 on human monocytes may be attributed, at least in part, to the stimulated secretion of M-CSF. Calcitriol 36-53 colony stimulating factor 1 Homo sapiens 81-86 8155653-0 1994 Incorporation of norleucine at methionine positions in recombinant human macrophage colony stimulating factor (M-CSF, 4-153) expressed in Escherichia coli: structural analysis. Norleucine 17-27 colony stimulating factor 1 Homo sapiens 111-116 8161795-9 1994 The present study demonstrates that 1 alpha,25(OH)2D3 is a potent stimulator for M-CSF production by human monocytic cells and that the proliferative effect of 1 alpha,25(OH)2D3 on human monocytes may be attributed, at least in part, to the stimulated secretion of M-CSF. Calcitriol 36-53 colony stimulating factor 1 Homo sapiens 265-270 8155653-1 1994 Expression of the 17.5-kDa truncated form of human recombinant macrophage colony stimulating factor (rM-CSF, 4-153) in Escherichia coli is complicated by the replacement of methionine residues by norleucine. Methionine 173-183 colony stimulating factor 1 Homo sapiens 63-99 8155653-1 1994 Expression of the 17.5-kDa truncated form of human recombinant macrophage colony stimulating factor (rM-CSF, 4-153) in Escherichia coli is complicated by the replacement of methionine residues by norleucine. Norleucine 196-206 colony stimulating factor 1 Homo sapiens 63-99 8161795-9 1994 The present study demonstrates that 1 alpha,25(OH)2D3 is a potent stimulator for M-CSF production by human monocytic cells and that the proliferative effect of 1 alpha,25(OH)2D3 on human monocytes may be attributed, at least in part, to the stimulated secretion of M-CSF. Calcitriol 160-177 colony stimulating factor 1 Homo sapiens 265-270 8188522-2 1994 M-CSF promotes the growth of early gestation chorionic cells, hydatidiform mole cells, and a human term placenta cell line (tPA30-1). tpa30 124-129 colony stimulating factor 1 Homo sapiens 0-5 8150035-1 1994 Immunoblot analysis of macrophage colony-stimulating factor (M-CSF) in KM 102 cell-conditioned medium showed the presence of two M-CSF molecular types, one being 85-kd M-CSF, the other a proteoglycan form (PG-M-CSF) carrying a chondroitin sulfate chain of variable length. Chondroitin Sulfates 227-246 colony stimulating factor 1 Homo sapiens 61-66 8150035-2 1994 When KM 102 cells were stimulated by TNF-alpha, they produced more M-CSF than that produced in unstimulated condition, in which PG-M-CSF had a shorter chondroitin sulfate chain. Chondroitin Sulfates 151-170 colony stimulating factor 1 Homo sapiens 131-136 8150035-3 1994 Although PG-M-CSF has binding affinity for type V collagen, the PG-M-CSF with the shorter chondroitin sulfate chain shows lower affinity. pg 9-11 colony stimulating factor 1 Homo sapiens 12-17 8150035-3 1994 Although PG-M-CSF has binding affinity for type V collagen, the PG-M-CSF with the shorter chondroitin sulfate chain shows lower affinity. Chondroitin Sulfates 90-109 colony stimulating factor 1 Homo sapiens 67-72 8150035-4 1994 This spreads in type V collagen-containing agarose gel more easily than does PG-M-CSF with a longer chondroitin sulfate chain. Chondroitin Sulfates 100-119 colony stimulating factor 1 Homo sapiens 80-85 8120453-4 1994 In the presence of LPS, both M-CSF and GM-CSF were up-regulated by cyclooxygenase inhibition (indomethacin, 10(-5) M), while G-CSF was down-regulated. Indomethacin 94-106 colony stimulating factor 1 Homo sapiens 29-34 8120453-6 1994 In LPS-treated cells, in contrast to the different regulation by endogenous eicosanoid of M-CSF and GM-CSF formation and G-CSF formation, both interleukin-4 (IL-4, 250 pM) and the glucocorticoid dexamethasone (10(-7) M) lowered the amounts of all CSFs. Eicosanoids 76-86 colony stimulating factor 1 Homo sapiens 90-95 8297732-4 1994 Mean CSF-1 levels (n = 14) dropped significantly during six courses of platinum-based chemotherapy (P = 0.02). Platinum 71-79 colony stimulating factor 1 Homo sapiens 5-10 8106431-1 1994 The formation of membrane phospholipid is coordinated with the cell cycle in a colony-stimulating factor 1-dependent macrophage cell line. Phospholipids 26-38 colony stimulating factor 1 Homo sapiens 79-106 8119929-5 1994 Treatment of the same cells with other growth factors (colony-stimulating factor-1 and Steel factor) or phorbol esters induced the tyrosine phosphorylation and activation of p44erk-1 and p42erk-2 and stimulated p21ras activity. Tyrosine 131-139 colony stimulating factor 1 Homo sapiens 55-99 8199014-2 1994 The results demonstrate that on activation with the calcium ionophore A23187 both M-CSF and IL-6 mRNA are induced after 3 and 6 h respectively. Calcium 52-59 colony stimulating factor 1 Homo sapiens 82-87 8199014-3 1994 Co-stimulation with A23187 plus PMA resulted in an up-regulation of M-CSF mRNA and a down-regulation of IL-6 mRNA. Calcimycin 20-26 colony stimulating factor 1 Homo sapiens 68-73 8199014-3 1994 Co-stimulation with A23187 plus PMA resulted in an up-regulation of M-CSF mRNA and a down-regulation of IL-6 mRNA. Tetradecanoylphorbol Acetate 32-35 colony stimulating factor 1 Homo sapiens 68-73 8199014-4 1994 Conversely co-stimulation with A23187 plus DBcAMP resulted in a down-regulation of M-CSF mRNA and an up-regulation of IL-6 mRNA. Calcimycin 31-37 colony stimulating factor 1 Homo sapiens 83-88 8262907-8 1993 Our study shows that the disulfide-bond pairings of [-32-153]M-CSF that is expressed and post-translationally modified in mammalian cells are identical to those of Escherichia coli-derived [3-153]M-CSF with only one intermolecular disulfide bond, namely, Cys31-Cys31. Disulfides 25-34 colony stimulating factor 1 Homo sapiens 61-66 8301137-5 1994 The enhancement of M-CSF message levels in the presence of IL-1 beta was blocked by cycloheximide, suggesting that de novo protein synthesis was required. Cycloheximide 84-97 colony stimulating factor 1 Homo sapiens 19-24 8119865-6 1994 The combination of EM plus M-CSF significantly enhanced H2O2-producing capacity of those cells as compared with M-CSF alone. Hydrogen Peroxide 56-60 colony stimulating factor 1 Homo sapiens 27-32 8301552-7 1994 The rapidly declining phase was inhibited by carrageenan, indicating that saturable clearance might be due to metabolism of M-CSF by macrophages. Carrageenan 45-56 colony stimulating factor 1 Homo sapiens 124-129 7764334-3 1993 The average level of human M-CSF in urine from normal males (N = 71) and females (N = 46) was 3.94 +/- 1.78 ng/ml (2.85 +/- 1.15 micrograms/g creatinine), and 3.53 +/- 1.70 ng/ml (3.31 +/- 1.12 micrograms/g creatinine), respectively. Creatinine 142-152 colony stimulating factor 1 Homo sapiens 27-32 7764334-3 1993 The average level of human M-CSF in urine from normal males (N = 71) and females (N = 46) was 3.94 +/- 1.78 ng/ml (2.85 +/- 1.15 micrograms/g creatinine), and 3.53 +/- 1.70 ng/ml (3.31 +/- 1.12 micrograms/g creatinine), respectively. Creatinine 207-217 colony stimulating factor 1 Homo sapiens 27-32 8219218-7 1993 The addition of anti-M-CSF or anti-M-CSF receptor neutralizing antibodies dose-dependently inhibited the binding of [3H]-thymidine-labeled FDC-P2-MCSFR cells to KM102 cells. Tritium 117-119 colony stimulating factor 1 Homo sapiens 21-26 8219218-7 1993 The addition of anti-M-CSF or anti-M-CSF receptor neutralizing antibodies dose-dependently inhibited the binding of [3H]-thymidine-labeled FDC-P2-MCSFR cells to KM102 cells. Tritium 117-119 colony stimulating factor 1 Homo sapiens 35-40 8219218-7 1993 The addition of anti-M-CSF or anti-M-CSF receptor neutralizing antibodies dose-dependently inhibited the binding of [3H]-thymidine-labeled FDC-P2-MCSFR cells to KM102 cells. Thymidine 121-130 colony stimulating factor 1 Homo sapiens 21-26 8219218-7 1993 The addition of anti-M-CSF or anti-M-CSF receptor neutralizing antibodies dose-dependently inhibited the binding of [3H]-thymidine-labeled FDC-P2-MCSFR cells to KM102 cells. Thymidine 121-130 colony stimulating factor 1 Homo sapiens 35-40 8359233-10 1993 Taken together, our results suggest the existence of a labile mRNA regulatory protein or proteins, whose actions include destabilization of both c-fms and CSF-1 transcripts after inhibition of TPA-induced monocytic differentiation by dex or CsA. Tetradecanoylphorbol Acetate 193-196 colony stimulating factor 1 Homo sapiens 155-160 8359233-10 1993 Taken together, our results suggest the existence of a labile mRNA regulatory protein or proteins, whose actions include destabilization of both c-fms and CSF-1 transcripts after inhibition of TPA-induced monocytic differentiation by dex or CsA. Dexamethasone 234-237 colony stimulating factor 1 Homo sapiens 155-160 8359233-10 1993 Taken together, our results suggest the existence of a labile mRNA regulatory protein or proteins, whose actions include destabilization of both c-fms and CSF-1 transcripts after inhibition of TPA-induced monocytic differentiation by dex or CsA. Cyclosporine 241-244 colony stimulating factor 1 Homo sapiens 155-160 8347686-6 1993 Actinomycin D and cycloheximide inhibited both the basal and IL-1 alpha-induced production of M-CSF, suggesting a requirement for de novo RNA and protein synthesis. Dactinomycin 0-13 colony stimulating factor 1 Homo sapiens 94-99 8347686-6 1993 Actinomycin D and cycloheximide inhibited both the basal and IL-1 alpha-induced production of M-CSF, suggesting a requirement for de novo RNA and protein synthesis. Cycloheximide 18-31 colony stimulating factor 1 Homo sapiens 94-99 8347686-7 1993 Cytokine-induced M-CSF production was also inhibited by the antiinflammatory corticosteroid, dexamethasone, but not by the cyclooxygenase inhibitor, indomethacin. Dexamethasone 93-106 colony stimulating factor 1 Homo sapiens 17-22 8262907-8 1993 Our study shows that the disulfide-bond pairings of [-32-153]M-CSF that is expressed and post-translationally modified in mammalian cells are identical to those of Escherichia coli-derived [3-153]M-CSF with only one intermolecular disulfide bond, namely, Cys31-Cys31. Disulfides 231-240 colony stimulating factor 1 Homo sapiens 61-66 8269987-2 1994 Specifically, a glycosylphosphatidylinositol (GPI)-modified variant of the cytokine macrophage colony stimulating factor (M-CSF), designated M-CSF.GPI, was expressed on the surface of human bone marrow stromal cells. Glycosylphosphatidylinositols 16-44 colony stimulating factor 1 Homo sapiens 122-127 8269987-2 1994 Specifically, a glycosylphosphatidylinositol (GPI)-modified variant of the cytokine macrophage colony stimulating factor (M-CSF), designated M-CSF.GPI, was expressed on the surface of human bone marrow stromal cells. Glycosylphosphatidylinositols 16-44 colony stimulating factor 1 Homo sapiens 141-150 7508003-0 1993 [Effect of G-CSF and M-CSF on busulfan-induced marrow failure in a 91-year old patient with essential thrombocythemia]. Busulfan 30-38 colony stimulating factor 1 Homo sapiens 21-26 8267882-3 1993 Through the 3 stages of purification, i.e. concentration by DEAE-cellulose column chromatography, hydrophobic chromatography on phenyl-sepharose and Mono Q fast protein liquid chromatography, the recombinant truncated M-CSF was purified as to exhibit a specific activity of 1.02 x 10(7) units/mg of protein. DEAE-Cellulose 60-74 colony stimulating factor 1 Homo sapiens 218-223 8267882-3 1993 Through the 3 stages of purification, i.e. concentration by DEAE-cellulose column chromatography, hydrophobic chromatography on phenyl-sepharose and Mono Q fast protein liquid chromatography, the recombinant truncated M-CSF was purified as to exhibit a specific activity of 1.02 x 10(7) units/mg of protein. phenyl-sepharose 128-144 colony stimulating factor 1 Homo sapiens 218-223 8267882-4 1993 SDS-PAGE of this purified truncated M-CSF showed that its apparent molecular mass is 22 kDa under reducing conditions. Sodium Dodecyl Sulfate 0-3 colony stimulating factor 1 Homo sapiens 36-41 8359233-0 1993 Posttranscriptional regulation of colony-stimulating factor-1 (CSF-1) and CSF-1 receptor gene expression during inhibition of phorbol-ester-induced monocytic differentiation by dexamethasone and cyclosporin A: potential involvement of a destabilizing protein. Phorbol Esters 126-139 colony stimulating factor 1 Homo sapiens 63-68 8359233-0 1993 Posttranscriptional regulation of colony-stimulating factor-1 (CSF-1) and CSF-1 receptor gene expression during inhibition of phorbol-ester-induced monocytic differentiation by dexamethasone and cyclosporin A: potential involvement of a destabilizing protein. Dexamethasone 177-190 colony stimulating factor 1 Homo sapiens 63-68 8359233-0 1993 Posttranscriptional regulation of colony-stimulating factor-1 (CSF-1) and CSF-1 receptor gene expression during inhibition of phorbol-ester-induced monocytic differentiation by dexamethasone and cyclosporin A: potential involvement of a destabilizing protein. Cyclosporine 195-208 colony stimulating factor 1 Homo sapiens 63-68 8359233-3 1993 The present studies demonstrate that dexamethasone (dex) and cyclosporin A (CsA) resulted in inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced monocytic differentiation of HL60 cells, as well as TPA induction of c-fms and CSF-1 transcripts. Dexamethasone 37-50 colony stimulating factor 1 Homo sapiens 237-242 8359233-3 1993 The present studies demonstrate that dexamethasone (dex) and cyclosporin A (CsA) resulted in inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced monocytic differentiation of HL60 cells, as well as TPA induction of c-fms and CSF-1 transcripts. Dexamethasone 37-40 colony stimulating factor 1 Homo sapiens 237-242 8359233-3 1993 The present studies demonstrate that dexamethasone (dex) and cyclosporin A (CsA) resulted in inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced monocytic differentiation of HL60 cells, as well as TPA induction of c-fms and CSF-1 transcripts. Cyclosporine 61-74 colony stimulating factor 1 Homo sapiens 237-242 8359233-3 1993 The present studies demonstrate that dexamethasone (dex) and cyclosporin A (CsA) resulted in inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced monocytic differentiation of HL60 cells, as well as TPA induction of c-fms and CSF-1 transcripts. Cyclosporine 76-79 colony stimulating factor 1 Homo sapiens 237-242 8359233-3 1993 The present studies demonstrate that dexamethasone (dex) and cyclosporin A (CsA) resulted in inhibition of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced monocytic differentiation of HL60 cells, as well as TPA induction of c-fms and CSF-1 transcripts. Tetradecanoylphorbol Acetate 145-148 colony stimulating factor 1 Homo sapiens 237-242 8359233-8 1993 We observed, however, that the inhibition of protein synthesis by cycloheximide (CH) in this setting of early monocytic differentiation increased both c-fms and CSF-1 steady-state transcript levels. Cycloheximide 66-79 colony stimulating factor 1 Homo sapiens 161-166 8359233-8 1993 We observed, however, that the inhibition of protein synthesis by cycloheximide (CH) in this setting of early monocytic differentiation increased both c-fms and CSF-1 steady-state transcript levels. Cycloheximide 81-83 colony stimulating factor 1 Homo sapiens 161-166 8262568-4 1993 M-CSF-induced suppression was independent of TBH M phi prostaglandin E2 (PGE2) synthesis. tbh m phi prostaglandin e2 45-71 colony stimulating factor 1 Homo sapiens 0-5 8262568-7 1993 Although T-cell reactivity against NH syngeneic MHC class II molecules was additively increased by M-CSF and indomethacin (a PGE2 synthesis inhibitor) treatment, reactivity against TBH syngeneic MHC class II molecules increased solely through PGE2 synthesis inhibition. Dinoprostone 243-247 colony stimulating factor 1 Homo sapiens 99-104 7686754-7 1993 Both G-CSF and M-CSF were also effective in stimulating tyrosine phosphorylation. Tyrosine 56-64 colony stimulating factor 1 Homo sapiens 15-20 8513448-7 1993 Moreover, hM-CSF is effective against granulocytopenia due to bone marrow suppression caused by cisplatin. Cisplatin 96-105 colony stimulating factor 1 Homo sapiens 10-16 8394386-1 1993 Macrophage colony-stimulating factor (M-CSF) regulates cholesterol metabolism in vivo and in vitro. Cholesterol 55-66 colony stimulating factor 1 Homo sapiens 0-36 8394386-1 1993 Macrophage colony-stimulating factor (M-CSF) regulates cholesterol metabolism in vivo and in vitro. Cholesterol 55-66 colony stimulating factor 1 Homo sapiens 38-43 8340649-0 1993 [Induction of M-CSF and G-CSF receptor mRNA in peripheral blood mononuclear cells of gynecological cancer by sizofiran]. Sizofiran 109-118 colony stimulating factor 1 Homo sapiens 14-19 7681783-8 1993 When calcitriol was added, the following increases in day-20 TRAP-positive colonies occurred: with M-CSF, 189%; with IL-3, 109%; with the combination of M-CSF and IL-3, 52%; and with GM-CSF there was no change. Calcitriol 5-15 colony stimulating factor 1 Homo sapiens 99-104 7684496-6 1993 In both colony-stimulating factor 1- and stem cell factor-stimulated cells, there is a marginal increase in tyrosine phosphorylation of HCP. Tyrosine 108-116 colony stimulating factor 1 Homo sapiens 8-35 8513862-2 1993 Treatment of PEM with lipopolysaccharide (LPS) or tumor-promoting phorbol ester (12-O-tetradecanoylphorbol-13-acetate [TPA]) induces a rapid but transient loss of M-CSF receptors in PEM. Phorbol Esters 66-79 colony stimulating factor 1 Homo sapiens 163-168 8513862-2 1993 Treatment of PEM with lipopolysaccharide (LPS) or tumor-promoting phorbol ester (12-O-tetradecanoylphorbol-13-acetate [TPA]) induces a rapid but transient loss of M-CSF receptors in PEM. Tetradecanoylphorbol Acetate 81-117 colony stimulating factor 1 Homo sapiens 163-168 8513862-2 1993 Treatment of PEM with lipopolysaccharide (LPS) or tumor-promoting phorbol ester (12-O-tetradecanoylphorbol-13-acetate [TPA]) induces a rapid but transient loss of M-CSF receptors in PEM. Tetradecanoylphorbol Acetate 119-122 colony stimulating factor 1 Homo sapiens 163-168 8513862-4 1993 The loss of M-CSF receptors induced by LPS can be inhibited by neomycin and compound 48/80, two potent phospholipase C (PLC) inhibitors, but not by phospholipase A2, calpain, protein kinase C (PKC) or protease inhibitors. Neomycin 63-71 colony stimulating factor 1 Homo sapiens 12-17 8513862-5 1993 On the other hand, the loss of M-CSF receptors induced by TPA has been prevented by PKC inhibitors but not by PLC inhibitors. Tetradecanoylphorbol Acetate 58-61 colony stimulating factor 1 Homo sapiens 31-36 8513862-8 1993 Our results show that 1) TPA-induced M-CSF receptor loss is strictly dependent on PKC activation; 2) PLC activation alone also leads to downregulation of M-CSF receptors; and 3) LPS-induced M-CSF receptor downregulation in PEM is mediated primarily through a PLC-dependent pathway. Tetradecanoylphorbol Acetate 25-28 colony stimulating factor 1 Homo sapiens 37-42 8513862-8 1993 Our results show that 1) TPA-induced M-CSF receptor loss is strictly dependent on PKC activation; 2) PLC activation alone also leads to downregulation of M-CSF receptors; and 3) LPS-induced M-CSF receptor downregulation in PEM is mediated primarily through a PLC-dependent pathway. Tetradecanoylphorbol Acetate 25-28 colony stimulating factor 1 Homo sapiens 154-159 8513862-8 1993 Our results show that 1) TPA-induced M-CSF receptor loss is strictly dependent on PKC activation; 2) PLC activation alone also leads to downregulation of M-CSF receptors; and 3) LPS-induced M-CSF receptor downregulation in PEM is mediated primarily through a PLC-dependent pathway. Tetradecanoylphorbol Acetate 25-28 colony stimulating factor 1 Homo sapiens 154-159 7681783-8 1993 When calcitriol was added, the following increases in day-20 TRAP-positive colonies occurred: with M-CSF, 189%; with IL-3, 109%; with the combination of M-CSF and IL-3, 52%; and with GM-CSF there was no change. Calcitriol 5-15 colony stimulating factor 1 Homo sapiens 153-158 7681783-9 1993 In the presence of calcitriol, 75% of IL-3 plus M-CSF-induced TRAP-containing colonies demonstrated calcitonin receptors over their TRAP-positive cells, whereas with M-CSF, GM-CSF or IL-3 each alone, 0 to 25% of TRAP-containing colonies had calcitonin receptor over TRAP-positive cells. Calcitriol 19-29 colony stimulating factor 1 Homo sapiens 48-53 7681783-9 1993 In the presence of calcitriol, 75% of IL-3 plus M-CSF-induced TRAP-containing colonies demonstrated calcitonin receptors over their TRAP-positive cells, whereas with M-CSF, GM-CSF or IL-3 each alone, 0 to 25% of TRAP-containing colonies had calcitonin receptor over TRAP-positive cells. Calcitriol 19-29 colony stimulating factor 1 Homo sapiens 166-171 8445950-7 1993 The induction of c-fms transcripts by ATRA is associated with induction of M-CSF-binding ability, suggesting cell surface expression of the monocyte growth factor receptor. Tretinoin 38-42 colony stimulating factor 1 Homo sapiens 75-80 8384875-2 1993 Eleven synthetic 11-12-amino acid phosphopeptides containing YMXM or YVXM recognition motifs bound to a PI 3-kinase p85 SH2 domain with highest affinities, including sequences surrounding phosphorylated tyrosines of the PDGF, CSF-1/c-Fms, and kit-encoded receptors, IRS-1, and polyoma middle T antigens; matched, unphosphorylated sequences did not bind. 11-12-amino acid phosphopeptides 17-49 colony stimulating factor 1 Homo sapiens 226-231 8479820-0 1993 Combination macrophage-colony stimulating factor and interferon-gamma administration ameliorates the osteopetrotic condition in microphthalmic (mi/mi) mice. 2-methyl-4-isothiazolin-3-one 128-130 colony stimulating factor 1 Homo sapiens 12-48 8273598-1 1993 Six diphosphonates were examined for their ability to alter proliferative responses of mouse bone marrow cells to recombinant human M-CSF and recombinant murine GM-CSF. Diphosphonates 4-18 colony stimulating factor 1 Homo sapiens 132-137 8425498-3 1993 Since M-CSF has an undefined role in osteoclast development, we wished to examine the effect of 1,25-(OH)2D3, a strong promoter of osteoclast development, on the induction of M-CSF receptor. Calcitriol 96-108 colony stimulating factor 1 Homo sapiens 175-180 8425498-12 1993 1,25-(OH)2D3-induced phenotypic changes may, therefore, involve modulation of the M-CSF effect. Calcitriol 0-12 colony stimulating factor 1 Homo sapiens 82-87 8443602-6 1993 Peptide mapping and electrospray ionization mass spectrometry revealed that a folded monomeric species of M-CSF contained three of the four native disulfide bridges, and this folded monomer also showed some biological activity in a cell-based assay. Disulfides 147-156 colony stimulating factor 1 Homo sapiens 106-111 8457471-9 1993 M-CSF treatment of HCs also induced phosphorylation of c-fms, and a number of other proteins, on tyrosine. Tyrosine 97-105 colony stimulating factor 1 Homo sapiens 0-5 8422246-4 1993 Immunoblot analysis of urea-extracted bone M-CSF revealed the presence of PG-M-CSF. Urea 23-27 colony stimulating factor 1 Homo sapiens 43-48 8422246-4 1993 Immunoblot analysis of urea-extracted bone M-CSF revealed the presence of PG-M-CSF. Urea 23-27 colony stimulating factor 1 Homo sapiens 74-82 8217219-5 1993 The presence of the cyclooxygenase inhibitor, indomethacin, potentiated the action of IL-1 on M-CSF synthesis, suggesting that an endogenous cyclooxygenase product(s) can down-regulate M-CSF formation. Indomethacin 46-58 colony stimulating factor 1 Homo sapiens 94-99 8454579-1 1993 The recombinant human carboxy-terminal-truncated macrophage colony-stimulating factor ([3-153]M-CSF) consists of 302 amino acid residues and has a molecular mass of about 32 kDa, as estimated by SDS-PAGE. Sodium Dodecyl Sulfate 195-198 colony stimulating factor 1 Homo sapiens 94-99 8217219-5 1993 The presence of the cyclooxygenase inhibitor, indomethacin, potentiated the action of IL-1 on M-CSF synthesis, suggesting that an endogenous cyclooxygenase product(s) can down-regulate M-CSF formation. Indomethacin 46-58 colony stimulating factor 1 Homo sapiens 185-190 8217219-7 1993 The glucocorticoid, dexamethasone, and the retinoid, all-trans retinoic acid, stimulated M-CSF formation. Dexamethasone 20-33 colony stimulating factor 1 Homo sapiens 89-94 8217219-7 1993 The glucocorticoid, dexamethasone, and the retinoid, all-trans retinoic acid, stimulated M-CSF formation. Retinoids 43-51 colony stimulating factor 1 Homo sapiens 89-94 8217219-7 1993 The glucocorticoid, dexamethasone, and the retinoid, all-trans retinoic acid, stimulated M-CSF formation. Tretinoin 57-76 colony stimulating factor 1 Homo sapiens 89-94 8454579-8 1993 (2) The remaining disulfide linkage linked Cys 31 of one subunit to Cys 31 of the second subunit of M-CSF. Disulfides 18-27 colony stimulating factor 1 Homo sapiens 100-105 8454579-8 1993 (2) The remaining disulfide linkage linked Cys 31 of one subunit to Cys 31 of the second subunit of M-CSF. Cysteine 43-46 colony stimulating factor 1 Homo sapiens 100-105 8454579-8 1993 (2) The remaining disulfide linkage linked Cys 31 of one subunit to Cys 31 of the second subunit of M-CSF. Cysteine 68-71 colony stimulating factor 1 Homo sapiens 100-105 1455231-2 1992 The biologically active form of M-CSF is a disulfide-linked dimer that activates an intrinsic tyrosine kinase activity on the M-CSF receptor by inducing dimerization of the receptor molecules. Disulfides 43-52 colony stimulating factor 1 Homo sapiens 32-37 1334462-0 1992 Macrophage colony stimulating factor activates phosphatidylcholine hydrolysis by cytoplasmic phospholipase A2. Phosphatidylcholines 47-66 colony stimulating factor 1 Homo sapiens 0-36 1334462-2 1992 Previous studies have demonstrated that M-CSF stimulation is associated with phosphatidylcholine (PC) hydrolysis and increased formation of both diacylglycerol (DAG) and phosphorylcholine. Phosphatidylcholines 77-96 colony stimulating factor 1 Homo sapiens 40-45 1474134-6 1992 Anti-HIV activity of zidovudine (AZT) was also comparatively evaluated in M-CSF- and normal monocyte-macrophage cells both using the MTT assay and by measuring HIV-p24 antigen production in supernatants of monocyte-macrophage cells cultures, and similar results obtained with both methods. Zidovudine 21-31 colony stimulating factor 1 Homo sapiens 74-79 1385421-0 1992 Protein tyrosine phosphatase-1C is rapidly phosphorylated in tyrosine in macrophages in response to colony stimulating factor-1. Tyrosine 8-16 colony stimulating factor 1 Homo sapiens 100-127 1385421-1 1992 An approximately 64-kDa cytoplasmic protein is rapidly phosphorylated in tyrosine in the response of macrophages to colony stimulating factor-1. Tyrosine 73-81 colony stimulating factor 1 Homo sapiens 116-143 1334462-2 1992 Previous studies have demonstrated that M-CSF stimulation is associated with phosphatidylcholine (PC) hydrolysis and increased formation of both diacylglycerol (DAG) and phosphorylcholine. Phosphatidylcholines 98-100 colony stimulating factor 1 Homo sapiens 40-45 1334462-2 1992 Previous studies have demonstrated that M-CSF stimulation is associated with phosphatidylcholine (PC) hydrolysis and increased formation of both diacylglycerol (DAG) and phosphorylcholine. Diglycerides 145-159 colony stimulating factor 1 Homo sapiens 40-45 1334462-2 1992 Previous studies have demonstrated that M-CSF stimulation is associated with phosphatidylcholine (PC) hydrolysis and increased formation of both diacylglycerol (DAG) and phosphorylcholine. Diglycerides 161-164 colony stimulating factor 1 Homo sapiens 40-45 1334462-2 1992 Previous studies have demonstrated that M-CSF stimulation is associated with phosphatidylcholine (PC) hydrolysis and increased formation of both diacylglycerol (DAG) and phosphorylcholine. Phosphorylcholine 170-187 colony stimulating factor 1 Homo sapiens 40-45 1334462-3 1992 The present work extends those results by demonstrating that treatment of human monocytes with M-CSF is associated with increases in a cytoplasmic Ca(2+)-dependent activity which hydrolyzes 1-palmitoyl,2-arachidonoyl PC to arachidonic acid. 1-palmitoyl, 190-202 colony stimulating factor 1 Homo sapiens 95-100 1334462-3 1992 The present work extends those results by demonstrating that treatment of human monocytes with M-CSF is associated with increases in a cytoplasmic Ca(2+)-dependent activity which hydrolyzes 1-palmitoyl,2-arachidonoyl PC to arachidonic acid. 2-arachidonoyl pc 202-219 colony stimulating factor 1 Homo sapiens 95-100 1334462-3 1992 The present work extends those results by demonstrating that treatment of human monocytes with M-CSF is associated with increases in a cytoplasmic Ca(2+)-dependent activity which hydrolyzes 1-palmitoyl,2-arachidonoyl PC to arachidonic acid. Arachidonic Acid 223-239 colony stimulating factor 1 Homo sapiens 95-100 1334462-4 1992 The finding that this hydrolysis of PC is associated with increases in production of lysophosphatidylcholine indicates that M-CSF stimulates a cytoplasmic phospholipase A2 (cPLA2) activity. Phosphatidylcholines 36-38 colony stimulating factor 1 Homo sapiens 124-129 1334462-4 1992 The finding that this hydrolysis of PC is associated with increases in production of lysophosphatidylcholine indicates that M-CSF stimulates a cytoplasmic phospholipase A2 (cPLA2) activity. Lysophosphatidylcholines 85-108 colony stimulating factor 1 Homo sapiens 124-129 1334462-10 1992 In this regard, levels of both PGE2 and PGF2 alpha were increased in response to M-CSF. Dinoprostone 31-35 colony stimulating factor 1 Homo sapiens 81-86 1334462-10 1992 In this regard, levels of both PGE2 and PGF2 alpha were increased in response to M-CSF. Dinoprost 40-44 colony stimulating factor 1 Homo sapiens 81-86 1334462-11 1992 Taken together, these results indicate that M-CSF stimulates PC hydrolysis in human monocytes by inducing cPLA2 activity and thereby formation of eicosanoids. Eicosanoids 146-157 colony stimulating factor 1 Homo sapiens 44-49 1455231-2 1992 The biologically active form of M-CSF is a disulfide-linked dimer that activates an intrinsic tyrosine kinase activity on the M-CSF receptor by inducing dimerization of the receptor molecules. Disulfides 43-52 colony stimulating factor 1 Homo sapiens 126-131 1455231-3 1992 The structure of a recombinant human M-CSF dimer, determined at 2.5 angstroms by x-ray crystallography, contains two bundles of four alpha helices laid end-to-end, with an interchain disulfide bond. Disulfides 183-192 colony stimulating factor 1 Homo sapiens 37-42 1334711-6 1992 Additions of IFN-gamma, macrophage colony-stimulating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF), which prime monocyte activation and induce O2- production, were also affected by the reciprocal effect of vIL-10. Superoxides 174-176 colony stimulating factor 1 Homo sapiens 62-67 1520704-6 1992 The fractions eluted by 0.3-0.6 M NaCl, which were shown to contain only PG-M-CSF on immunoblot analysis, also have macrophage-colony-stimulating activity. Sodium Chloride 34-38 colony stimulating factor 1 Homo sapiens 73-81 1587305-5 1992 Unexpectedly, the combination of IL-1 plus M-CSF (q24 h, days 1-4) followed by M-CSF (q24 h, days 5-14) resulted in a more than additive stimulation of progenitor recovery in both the marrow and the spleen that was observed as early as day 3 following 5-FU treatment. Fluorouracil 252-256 colony stimulating factor 1 Homo sapiens 43-48 1505643-0 1992 Induction of human monocyte cell line U937 differentiation and CSF-1 production by phorbol ester. Phorbol Esters 83-96 colony stimulating factor 1 Homo sapiens 63-68 1504058-6 1992 Furthermore, IL-2-induced LAMs were found to produce cytotoxic factors in the culture medium when they were cocultured with tumor cells, and the cytotoxic activity in the culture supernatant of LAMs was also increased by the incubation of LAMs with CSF-1. lipoarabinomannan 26-30 colony stimulating factor 1 Homo sapiens 249-254 1504058-6 1992 Furthermore, IL-2-induced LAMs were found to produce cytotoxic factors in the culture medium when they were cocultured with tumor cells, and the cytotoxic activity in the culture supernatant of LAMs was also increased by the incubation of LAMs with CSF-1. lipoarabinomannan 194-198 colony stimulating factor 1 Homo sapiens 249-254 1504058-8 1992 It is suggested from these results that the cytotoxicity of LAMs is regulated by CSF-1, IL-1, IFN-gamma, and TNF, and that the production of cytotoxic molecules is involved in cell-mediated killing by LAMs. lipoarabinomannan 60-64 colony stimulating factor 1 Homo sapiens 81-86 1433977-5 1992 This type of M-CSF has a molecular weight of greater than 200 kDa and consists of a 43 kDa subunit and a 150-200 kDa subunit, the latter of which contains chondroitin sulfate glycosaminoglycan. Chondroitin Sulfates 155-174 colony stimulating factor 1 Homo sapiens 13-18 1433977-5 1992 This type of M-CSF has a molecular weight of greater than 200 kDa and consists of a 43 kDa subunit and a 150-200 kDa subunit, the latter of which contains chondroitin sulfate glycosaminoglycan. Glycosaminoglycans 175-192 colony stimulating factor 1 Homo sapiens 13-18 1433977-6 1992 This proteoglycan type M-CSF binds to extra-cellular matrix at the part of glycosaminoglycan. Glycosaminoglycans 75-92 colony stimulating factor 1 Homo sapiens 23-28 1351091-4 1992 Inhibitors of BMM proliferation (LPS, TNF-alpha, IFN-gamma, and cAMP elevating agents) suppressed CSF-1-induced expression of M1, M2, and PCNA mRNA measured at 22 h. This suppression occurred even when added up to 12 h after the CSF-1, a period coinciding with the G1/S-phase boundary. Cyclic AMP 64-68 colony stimulating factor 1 Homo sapiens 98-103 1351091-4 1992 Inhibitors of BMM proliferation (LPS, TNF-alpha, IFN-gamma, and cAMP elevating agents) suppressed CSF-1-induced expression of M1, M2, and PCNA mRNA measured at 22 h. This suppression occurred even when added up to 12 h after the CSF-1, a period coinciding with the G1/S-phase boundary. Cyclic AMP 64-68 colony stimulating factor 1 Homo sapiens 229-234 1587305-5 1992 Unexpectedly, the combination of IL-1 plus M-CSF (q24 h, days 1-4) followed by M-CSF (q24 h, days 5-14) resulted in a more than additive stimulation of progenitor recovery in both the marrow and the spleen that was observed as early as day 3 following 5-FU treatment. Fluorouracil 252-256 colony stimulating factor 1 Homo sapiens 79-84 1587305-6 1992 Furthermore, in the absence of protracted M-CSF administration on days 5-14, the 4-day rescue with a combination of IL-1 plus M-CSF also resulted in a more than additive effect on the recovery from 5-FU-induced neutropenia. Fluorouracil 198-202 colony stimulating factor 1 Homo sapiens 126-131 1587305-7 1992 Collectively, these observations demonstrated that IL-1 and M-CSF can interact synergistically to stimulate granulopoietic recovery in the 5-FU-treated animal. Fluorouracil 139-143 colony stimulating factor 1 Homo sapiens 60-65 1579589-1 1992 Recently, we reported that human monocyte colony-stimulating factor (M-CSF) stimulates the clearance of lipoproteins containing apoB100 via both low density lipoprotein receptor-dependent and -independent pathways in target cells of M-CSF, and reduces plasma cholesterol level (Journal of Biological Chemistry, 265:12869-12875, 1990). Cholesterol 259-270 colony stimulating factor 1 Homo sapiens 33-67 1613390-9 1992 In an [3H]thymidine incorporation assay with BM cells collected at different times of culture, d3 or d4 BM cells responded to human recombinant M-CSF, human recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF), bovine GM-CSF, murine M-CSF or murine M-CSF-containing supernatants, and bovine interleukin 1 beta (IL-1 beta) in decreasing order of magnitude. Thymidine 10-19 colony stimulating factor 1 Homo sapiens 144-149 1579589-3 1992 Furthermore, we found a significant role of M-CSF in cholesterol metabolism of human monocyte-derived macrophages. Cholesterol 53-64 colony stimulating factor 1 Homo sapiens 44-49 1579589-1 1992 Recently, we reported that human monocyte colony-stimulating factor (M-CSF) stimulates the clearance of lipoproteins containing apoB100 via both low density lipoprotein receptor-dependent and -independent pathways in target cells of M-CSF, and reduces plasma cholesterol level (Journal of Biological Chemistry, 265:12869-12875, 1990). Cholesterol 259-270 colony stimulating factor 1 Homo sapiens 69-74 1579589-4 1992 M-CSF enhanced not only the uptake of acetylated low density lipoprotein and oxidized low density lipoprotein in macrophages, but also the efflux of cholesterol from cholesterol-loaded macrophages. Cholesterol 149-160 colony stimulating factor 1 Homo sapiens 0-5 1579589-4 1992 M-CSF enhanced not only the uptake of acetylated low density lipoprotein and oxidized low density lipoprotein in macrophages, but also the efflux of cholesterol from cholesterol-loaded macrophages. Cholesterol 166-177 colony stimulating factor 1 Homo sapiens 0-5 1373232-3 1992 MC and monocytes from adult and neonatal subjects produced mRNA for GM-CSF, G-CSF, and M-CSF, whereas T cells produced only GM-CSF mRNA. Methylcholanthrene 0-2 colony stimulating factor 1 Homo sapiens 69-74 1579589-5 1992 To elucidate in vivo effects of M-CSF on cholesterol efflux from tissues, we administered an intravenous injection of 3H-cholesterol (150 microCi) into WHHL rabbits 1 month before starting M-CSF treatment. Cholesterol 41-52 colony stimulating factor 1 Homo sapiens 32-37 1579589-6 1992 We observed an increased cholesterol efflux from tissues to plasma high density lipoprotein after M-CSF treatment when cholesterol efflux was estimated as the change in specific radioactivity of plasma high density lipoprotein-cholesterol. Cholesterol 25-36 colony stimulating factor 1 Homo sapiens 98-103 1579589-6 1992 We observed an increased cholesterol efflux from tissues to plasma high density lipoprotein after M-CSF treatment when cholesterol efflux was estimated as the change in specific radioactivity of plasma high density lipoprotein-cholesterol. Cholesterol 119-130 colony stimulating factor 1 Homo sapiens 98-103 1579589-7 1992 This result suggests that M-CSF can enhance the excretion of cholesterol from target cells of M-CSF, such as cholesterol-loaded macrophages in the arterial wall, and reduce the rate of atherogenesis. Cholesterol 61-72 colony stimulating factor 1 Homo sapiens 26-31 1579589-7 1992 This result suggests that M-CSF can enhance the excretion of cholesterol from target cells of M-CSF, such as cholesterol-loaded macrophages in the arterial wall, and reduce the rate of atherogenesis. Cholesterol 61-72 colony stimulating factor 1 Homo sapiens 94-99 1579589-7 1992 This result suggests that M-CSF can enhance the excretion of cholesterol from target cells of M-CSF, such as cholesterol-loaded macrophages in the arterial wall, and reduce the rate of atherogenesis. Cholesterol 109-120 colony stimulating factor 1 Homo sapiens 26-31 1579589-7 1992 This result suggests that M-CSF can enhance the excretion of cholesterol from target cells of M-CSF, such as cholesterol-loaded macrophages in the arterial wall, and reduce the rate of atherogenesis. Cholesterol 109-120 colony stimulating factor 1 Homo sapiens 94-99 1315505-4 1992 Similarly, IL-1-induced CSF-1 production was inhibited by cholera toxin and this inhibition was reversed by an arginine analog, p-methoxy-benzylaminodecamethylene guanidine sulfate. Arginine 111-119 colony stimulating factor 1 Homo sapiens 24-29 1315505-4 1992 Similarly, IL-1-induced CSF-1 production was inhibited by cholera toxin and this inhibition was reversed by an arginine analog, p-methoxy-benzylaminodecamethylene guanidine sulfate. p-methoxy-benzylaminodecamethylene guanidine sulfate 128-180 colony stimulating factor 1 Homo sapiens 24-29 1315505-5 1992 Dibutyryl-cAMP as well as other cAMP elevating agents such as theophylline and forskolin also suppressed IL-1-induced CSF-1 production, suggesting that cAMP concentrations inversely regulate the biosynthesis of CSF-1. Bucladesine 0-14 colony stimulating factor 1 Homo sapiens 118-123 1315505-5 1992 Dibutyryl-cAMP as well as other cAMP elevating agents such as theophylline and forskolin also suppressed IL-1-induced CSF-1 production, suggesting that cAMP concentrations inversely regulate the biosynthesis of CSF-1. Bucladesine 0-14 colony stimulating factor 1 Homo sapiens 211-216 1315505-5 1992 Dibutyryl-cAMP as well as other cAMP elevating agents such as theophylline and forskolin also suppressed IL-1-induced CSF-1 production, suggesting that cAMP concentrations inversely regulate the biosynthesis of CSF-1. Cyclic AMP 10-14 colony stimulating factor 1 Homo sapiens 118-123 1315505-5 1992 Dibutyryl-cAMP as well as other cAMP elevating agents such as theophylline and forskolin also suppressed IL-1-induced CSF-1 production, suggesting that cAMP concentrations inversely regulate the biosynthesis of CSF-1. Cyclic AMP 10-14 colony stimulating factor 1 Homo sapiens 211-216 1315505-5 1992 Dibutyryl-cAMP as well as other cAMP elevating agents such as theophylline and forskolin also suppressed IL-1-induced CSF-1 production, suggesting that cAMP concentrations inversely regulate the biosynthesis of CSF-1. Theophylline 62-74 colony stimulating factor 1 Homo sapiens 118-123 1315505-5 1992 Dibutyryl-cAMP as well as other cAMP elevating agents such as theophylline and forskolin also suppressed IL-1-induced CSF-1 production, suggesting that cAMP concentrations inversely regulate the biosynthesis of CSF-1. Theophylline 62-74 colony stimulating factor 1 Homo sapiens 211-216 1315505-5 1992 Dibutyryl-cAMP as well as other cAMP elevating agents such as theophylline and forskolin also suppressed IL-1-induced CSF-1 production, suggesting that cAMP concentrations inversely regulate the biosynthesis of CSF-1. Colforsin 79-88 colony stimulating factor 1 Homo sapiens 118-123 1315505-5 1992 Dibutyryl-cAMP as well as other cAMP elevating agents such as theophylline and forskolin also suppressed IL-1-induced CSF-1 production, suggesting that cAMP concentrations inversely regulate the biosynthesis of CSF-1. Colforsin 79-88 colony stimulating factor 1 Homo sapiens 211-216 1315505-7 1992 IL-1-induced CSF-1 production was not suppressed by the protein kinase C (PKC) inhibitor, H7, under conditions in which 12-O-tetradecanoylphorbol-13-acetate-induced CSF-1 production was completely abolished. Tetradecanoylphorbol Acetate 120-156 colony stimulating factor 1 Homo sapiens 13-18 1315505-7 1992 IL-1-induced CSF-1 production was not suppressed by the protein kinase C (PKC) inhibitor, H7, under conditions in which 12-O-tetradecanoylphorbol-13-acetate-induced CSF-1 production was completely abolished. Tetradecanoylphorbol Acetate 120-156 colony stimulating factor 1 Homo sapiens 165-170 1392404-1 1992 The ability of peripheral blood monocytes, granulocytes and resident peritoneal macrophages to generate hydrogen peroxide in response to concanavalin A was enhanced by a single intravenous injection of macrophage colony-stimulating factor (M-CSF) of recombinant human type in AKR mice. Hydrogen Peroxide 104-121 colony stimulating factor 1 Homo sapiens 202-238 1392404-1 1992 The ability of peripheral blood monocytes, granulocytes and resident peritoneal macrophages to generate hydrogen peroxide in response to concanavalin A was enhanced by a single intravenous injection of macrophage colony-stimulating factor (M-CSF) of recombinant human type in AKR mice. Hydrogen Peroxide 104-121 colony stimulating factor 1 Homo sapiens 240-245 1590829-6 1992 The accumulation of cholesterol ester was remarkably decreased in the aortae of M-CSF-treated animals (0.60 +/- 0.32 mg/g tissue), as compared to those of controls (4.32 +/- 0.61 mg/g tissue). Cholesterol Esters 20-37 colony stimulating factor 1 Homo sapiens 80-85 1312371-0 1992 Rapid priming of human monocytes by human hematopoietic growth factors: granulocyte-macrophage colony-stimulating factor (CSF), macrophage-CSF, and interleukin-3 selectively enhance superoxide release triggered by receptor-mediated agonists. Superoxides 182-192 colony stimulating factor 1 Homo sapiens 128-142 1312371-7 1992 These findings show that GM-CSF, M-CSF, and IL-3 selectively enhance O2- release in human monocytes triggered by receptor-mediated agonists after short-term preincubation. Superoxides 69-71 colony stimulating factor 1 Homo sapiens 26-31 1533785-7 1992 After exposure of leukaemic cells to phorbol myristate acetate (PMA), release of M-CSF protein was documented in three of five patients studied. Tetradecanoylphorbol Acetate 37-62 colony stimulating factor 1 Homo sapiens 81-86 1533785-7 1992 After exposure of leukaemic cells to phorbol myristate acetate (PMA), release of M-CSF protein was documented in three of five patients studied. Tetradecanoylphorbol Acetate 64-67 colony stimulating factor 1 Homo sapiens 81-86 1373232-6 1992 Neonatal MC also accumulated similar amounts of G-CSF mRNA and somewhat more M-CSF mRNA than did adult MC; results with monocytes were similar to those with MC. Methylcholanthrene 9-11 colony stimulating factor 1 Homo sapiens 77-82 1540160-2 1992 The human CSF-1 gene has previously been assigned to chromosome 5 using somatic cell hybrids, and further localized to 5q33 by in situ hybridization with a 3H labelled cDNA probe. Tritium 156-158 colony stimulating factor 1 Homo sapiens 10-15 1739124-9 1992 In contrast, phorbol 12-myristate 13-acetate (PMA) was a less potent inducer of MCSF gene expression and iron-oxidized low-density lipoproteins (ox-LDL) did not increase consistently MCSF mRNA or the synthesis and secretion of immunoreactive protein. Tetradecanoylphorbol Acetate 13-44 colony stimulating factor 1 Homo sapiens 80-84 1739124-9 1992 In contrast, phorbol 12-myristate 13-acetate (PMA) was a less potent inducer of MCSF gene expression and iron-oxidized low-density lipoproteins (ox-LDL) did not increase consistently MCSF mRNA or the synthesis and secretion of immunoreactive protein. Tetradecanoylphorbol Acetate 46-49 colony stimulating factor 1 Homo sapiens 80-84 1739124-10 1992 Northern analysis of mRNA isolated from the atheromatous aorta of rabbits fed a 1% cholesterol diet for 10 weeks showed elevated MCSF mRNA compared with controls. Cholesterol 83-94 colony stimulating factor 1 Homo sapiens 129-133 1370208-8 1992 M-CSF RNA and protein levels were maintained even when dexamethasone (1 mumol/L) was present for the whole duration of a 48-hour TNF stimulation. Dexamethasone 55-68 colony stimulating factor 1 Homo sapiens 0-5 1372669-6 1992 The combination of retinoic acid with interferon gamma was most effective in reducing CFU-L recovering (8 responsive/15 AML cases), G-CSF and M-CSF displayed either inhibitory or stimulatory activity in different AML cases. Tretinoin 19-32 colony stimulating factor 1 Homo sapiens 142-147 1740646-4 1992 In contrast, CSF-1-derived BMDMs produced nitrite in response to lipopolysaccharide (LPS) alone, whereas GM-CSF-derived BMDMs required interferon gamma plus LPS treatment. Nitrites 42-49 colony stimulating factor 1 Homo sapiens 13-18 1380308-2 1992 IL-3, GM-CSF, and IL-5 enhanced basophil histamine release and in-vitro survival, while G-CSF, M-CSF, and IL-4 had no enhancing activities at all. Histamine 41-50 colony stimulating factor 1 Homo sapiens 7-12 1660466-5 1991 Here we show that eluates of antiphosphotyrosine affinity purified lysates of colony-stimulating factor 1-stimulated cells contain elevated levels of phosphatidylcholine-specific phospholipase C activity. antiphosphotyrosine 29-48 colony stimulating factor 1 Homo sapiens 78-105 1660466-8 1991 The phosphatidylcholine phospholipase C activity in isolated membranes of colony-stimulating factor 1-treated cells was also reduced by pertussis toxin treatment and stimulated by guanosine 5"-3-O-(thio)triphosphate. Guanosine 5'-O-(3-Thiotriphosphate) 180-215 colony stimulating factor 1 Homo sapiens 74-101 1299376-5 1992 Inhibition of prostaglandin E2 (PGE2) synthesis reversed M-CSF-induced suppression of autoreactivity to NH M phi and, to a lesser extent, to TBH M phi. Dinoprostone 14-30 colony stimulating factor 1 Homo sapiens 57-62 1299376-5 1992 Inhibition of prostaglandin E2 (PGE2) synthesis reversed M-CSF-induced suppression of autoreactivity to NH M phi and, to a lesser extent, to TBH M phi. Dinoprostone 32-36 colony stimulating factor 1 Homo sapiens 57-62 1299376-5 1992 Inhibition of prostaglandin E2 (PGE2) synthesis reversed M-CSF-induced suppression of autoreactivity to NH M phi and, to a lesser extent, to TBH M phi. tbh 141-144 colony stimulating factor 1 Homo sapiens 57-62 1311060-3 1992 However, the extent of GAP tyrosine phosphorylation induced by CSF-1 was approximately 10% of that induced by PDGF-BB in the NIH3T3 fibroblasts. Tyrosine 27-35 colony stimulating factor 1 Homo sapiens 63-68 1311060-5 1992 Taken together, our findings provide evidence for a possible role of tyrosine phosphorylation of GAP and GAP-associated phosphoproteins in regulating transduction of CSF-1-induced mitogenic signals through p21ras activation. Tyrosine 69-77 colony stimulating factor 1 Homo sapiens 166-171 1660466-5 1991 Here we show that eluates of antiphosphotyrosine affinity purified lysates of colony-stimulating factor 1-stimulated cells contain elevated levels of phosphatidylcholine-specific phospholipase C activity. Phosphatidylcholines 150-169 colony stimulating factor 1 Homo sapiens 78-105 1824254-4 1991 IFN-gamma also inhibited M-CSF-, GM-CSF-, or IL-3-stimulated [3H]-thymidine incorporation in highly enriched GM-CFC. Tritium 62-64 colony stimulating factor 1 Homo sapiens 25-30 1783426-0 1991 Human recombinant macrophage colony-stimulating factor (M-CSF) increases Cl-esterase inhibitor (Cl-INH) synthesis by human monocytes. cl-inh 96-102 colony stimulating factor 1 Homo sapiens 18-54 1783426-0 1991 Human recombinant macrophage colony-stimulating factor (M-CSF) increases Cl-esterase inhibitor (Cl-INH) synthesis by human monocytes. cl-inh 96-102 colony stimulating factor 1 Homo sapiens 56-61 1836352-0 1991 The gene expressions of macrophage colony-stimulating factor (MCSF) and MCSF receptor in the human myometrium during pregnancy: regulation by sex steroid hormones. Steroids 146-162 colony stimulating factor 1 Homo sapiens 24-60 1836352-0 1991 The gene expressions of macrophage colony-stimulating factor (MCSF) and MCSF receptor in the human myometrium during pregnancy: regulation by sex steroid hormones. Steroids 146-162 colony stimulating factor 1 Homo sapiens 62-66 1836352-0 1991 The gene expressions of macrophage colony-stimulating factor (MCSF) and MCSF receptor in the human myometrium during pregnancy: regulation by sex steroid hormones. Steroids 146-162 colony stimulating factor 1 Homo sapiens 72-76 1836352-1 1991 We investigated the biological effect of sex-steroid hormones, secreted from the corpus luteum and placenta, on the induction of mRNA encoding macrophage colony-stimulating factor (MCSF) and c-fms proto-oncogene (MCSF receptor) in the human uterine myometrium. Steroids 45-52 colony stimulating factor 1 Homo sapiens 143-179 1836352-1 1991 We investigated the biological effect of sex-steroid hormones, secreted from the corpus luteum and placenta, on the induction of mRNA encoding macrophage colony-stimulating factor (MCSF) and c-fms proto-oncogene (MCSF receptor) in the human uterine myometrium. Steroids 45-52 colony stimulating factor 1 Homo sapiens 181-185 1836352-1 1991 We investigated the biological effect of sex-steroid hormones, secreted from the corpus luteum and placenta, on the induction of mRNA encoding macrophage colony-stimulating factor (MCSF) and c-fms proto-oncogene (MCSF receptor) in the human uterine myometrium. Steroids 45-52 colony stimulating factor 1 Homo sapiens 213-217 1836352-5 1991 The mRNAs of both MCSF and c-fms proto-oncogene were induced in the uterine myometrium of non-pregnant women under pseudopregnant therapy of mestranol and norethindrone. Mestranol 141-150 colony stimulating factor 1 Homo sapiens 18-22 1836352-5 1991 The mRNAs of both MCSF and c-fms proto-oncogene were induced in the uterine myometrium of non-pregnant women under pseudopregnant therapy of mestranol and norethindrone. Norethindrone 155-168 colony stimulating factor 1 Homo sapiens 18-22 1836352-6 1991 These results indicate that sex steroid hormone secreted from the corpus luteum of pregnancy and/or placenta may be deeply involved in the hypertrophic change of uterus during pregnancy by inducing MCSF and MCSF receptor (c-fms proto-oncogene protein product) in the myometrium. Steroids 32-39 colony stimulating factor 1 Homo sapiens 198-202 1836352-6 1991 These results indicate that sex steroid hormone secreted from the corpus luteum of pregnancy and/or placenta may be deeply involved in the hypertrophic change of uterus during pregnancy by inducing MCSF and MCSF receptor (c-fms proto-oncogene protein product) in the myometrium. Steroids 32-39 colony stimulating factor 1 Homo sapiens 207-211 1824254-4 1991 IFN-gamma also inhibited M-CSF-, GM-CSF-, or IL-3-stimulated [3H]-thymidine incorporation in highly enriched GM-CFC. Thymidine 66-75 colony stimulating factor 1 Homo sapiens 25-30 1824254-7 1991 However, the effect of IFN-gamma on intracellular pH and DNA synthesis was transient and pretreatment with IFN markedly inhibited the ability of GM-CSF, M-CSF, and IL-3 to activate the sodium/hydrogen antiport. Sodium 185-191 colony stimulating factor 1 Homo sapiens 146-151 1824254-7 1991 However, the effect of IFN-gamma on intracellular pH and DNA synthesis was transient and pretreatment with IFN markedly inhibited the ability of GM-CSF, M-CSF, and IL-3 to activate the sodium/hydrogen antiport. Hydrogen 192-200 colony stimulating factor 1 Homo sapiens 146-151 1687728-1 1991 In a patient with a debulked mullerian adenocarcinoma involving the ovary, an elevated serum concentration of macrophage-colony stimulating factor (M-CSF) (5.3 ng/ml) was lowered into the range of the age- and gender-matched controls by a 24-hour infusion of 135 mg/m2 of taxol, as was a Ca125 of 1480 U/ml by three such taxol courses given at 3-week intervals (to 14 U/ml). Paclitaxel 272-277 colony stimulating factor 1 Homo sapiens 110-146 1687728-1 1991 In a patient with a debulked mullerian adenocarcinoma involving the ovary, an elevated serum concentration of macrophage-colony stimulating factor (M-CSF) (5.3 ng/ml) was lowered into the range of the age- and gender-matched controls by a 24-hour infusion of 135 mg/m2 of taxol, as was a Ca125 of 1480 U/ml by three such taxol courses given at 3-week intervals (to 14 U/ml). Paclitaxel 272-277 colony stimulating factor 1 Homo sapiens 148-153 1687728-1 1991 In a patient with a debulked mullerian adenocarcinoma involving the ovary, an elevated serum concentration of macrophage-colony stimulating factor (M-CSF) (5.3 ng/ml) was lowered into the range of the age- and gender-matched controls by a 24-hour infusion of 135 mg/m2 of taxol, as was a Ca125 of 1480 U/ml by three such taxol courses given at 3-week intervals (to 14 U/ml). Paclitaxel 321-326 colony stimulating factor 1 Homo sapiens 110-146 1687728-1 1991 In a patient with a debulked mullerian adenocarcinoma involving the ovary, an elevated serum concentration of macrophage-colony stimulating factor (M-CSF) (5.3 ng/ml) was lowered into the range of the age- and gender-matched controls by a 24-hour infusion of 135 mg/m2 of taxol, as was a Ca125 of 1480 U/ml by three such taxol courses given at 3-week intervals (to 14 U/ml). Paclitaxel 321-326 colony stimulating factor 1 Homo sapiens 148-153 1831804-4 1991 The expression of M-CSF mRNA in Ishikawa cells increased about 2.3 times following treatment with R5020 at 10(-7) M. Induction of M-CSF mRNA by R5020 was antagonized by anti-progestin RU486 in a dose-dependent manner. Mifepristone 184-189 colony stimulating factor 1 Homo sapiens 18-23 1833648-4 1991 Unlike cells bearing wild-type receptors, mouse NIH3T3 cells expressing mutant CSF-1R(Phe 809) were unable to grow in serum-free medium containing human recombinant CSF-1 and did not form colonies in semi-solid medium in its presence. Phenylalanine 86-89 colony stimulating factor 1 Homo sapiens 79-84 1831804-4 1991 The expression of M-CSF mRNA in Ishikawa cells increased about 2.3 times following treatment with R5020 at 10(-7) M. Induction of M-CSF mRNA by R5020 was antagonized by anti-progestin RU486 in a dose-dependent manner. Mifepristone 184-189 colony stimulating factor 1 Homo sapiens 130-135 1831804-8 1991 On the other hand, accumulation of glycogen granules in cytoplasm detected by periodicacid-Schiff staining was observed in Ishikawa cells treated with M-CSF. Glycogen 35-43 colony stimulating factor 1 Homo sapiens 151-156 1831804-8 1991 On the other hand, accumulation of glycogen granules in cytoplasm detected by periodicacid-Schiff staining was observed in Ishikawa cells treated with M-CSF. Periodic Acid 78-90 colony stimulating factor 1 Homo sapiens 151-156 1831804-8 1991 On the other hand, accumulation of glycogen granules in cytoplasm detected by periodicacid-Schiff staining was observed in Ishikawa cells treated with M-CSF. schiff 91-97 colony stimulating factor 1 Homo sapiens 151-156 1872833-1 1991 Human macrophage colony-stimulating factor (hM-CSF) concentration-dependently enhanced the secretion of human chorionic gonadotropin (hCG) by primary cultured human cytotrophoblastic cells and a human placental cell line, 3A-SubE (tPA30-1). tpa30 231-236 colony stimulating factor 1 Homo sapiens 44-50 1838015-3 1991 M-CSF was also expressed by H-RS cells in lymph nodes from patients with Hodgkin"s disease. h-rs 28-32 colony stimulating factor 1 Homo sapiens 0-5 1828037-1 1991 Mouse NIH 3T3 fibroblasts transfected with human colony stimulating factor-1 receptor produced diacylglycerol in response to CSF1 and this correlated with elevated phosphatidylcholine hydrolyzing activity measured in an in vitro assay. Diglycerides 95-109 colony stimulating factor 1 Homo sapiens 125-129 1713254-3 1991 Treatment of cells with antisense oligodeoxynucleotides (oligos) to exons 1 and 2, but not 4, 5, or 6, of the CD45 gene, or with monoclonal anti-CD45, significantly decreased CFU-GM colony formation stimulated with GM-CSF, IL-3, fusion protein, and GM-CSF + MGF, but not with G-CSF or M-CSF. Oligodeoxyribonucleotides 34-55 colony stimulating factor 1 Homo sapiens 216-221 2071899-1 1991 The regulation of macrophage colony-stimulating factor (M-CSF) gene expression by phorbol esters and calcium ionophore (A23187) was studied in HL-60 cells. Calcimycin 120-126 colony stimulating factor 1 Homo sapiens 18-54 2071899-1 1991 The regulation of macrophage colony-stimulating factor (M-CSF) gene expression by phorbol esters and calcium ionophore (A23187) was studied in HL-60 cells. Calcimycin 120-126 colony stimulating factor 1 Homo sapiens 56-61 2071899-7 1991 However, cells treated with A23187 for 6 h and CHX for 1, 3, or 6 h transcribed more M-CSF than cells treated with A23187 alone for 6 h. CHX also regulates M-CSF expression by message stabilization. Calcimycin 28-34 colony stimulating factor 1 Homo sapiens 85-90 2071899-7 1991 However, cells treated with A23187 for 6 h and CHX for 1, 3, or 6 h transcribed more M-CSF than cells treated with A23187 alone for 6 h. CHX also regulates M-CSF expression by message stabilization. Calcimycin 28-34 colony stimulating factor 1 Homo sapiens 156-161 2071899-7 1991 However, cells treated with A23187 for 6 h and CHX for 1, 3, or 6 h transcribed more M-CSF than cells treated with A23187 alone for 6 h. CHX also regulates M-CSF expression by message stabilization. Calcimycin 115-121 colony stimulating factor 1 Homo sapiens 156-161 2071899-8 1991 The t1/2 of M-CSF mRNA was 45 min in cells treated with A23187 for 6 h or in cells treated with PdBu for 24 h, was over 2 h in HL-60 cells treated with A23187 for 6 h and CHX for 1 h, and was 3 h in cells treated with PdBu for 24 h and CHX for 1 h. We conclude that M-CSF gene expression can be differentially regulated in HL-60 cells and that new protein synthesis plays an important role in both the transcriptional and posttranscriptional regulation. Calcimycin 56-62 colony stimulating factor 1 Homo sapiens 12-17 2071899-8 1991 The t1/2 of M-CSF mRNA was 45 min in cells treated with A23187 for 6 h or in cells treated with PdBu for 24 h, was over 2 h in HL-60 cells treated with A23187 for 6 h and CHX for 1 h, and was 3 h in cells treated with PdBu for 24 h and CHX for 1 h. We conclude that M-CSF gene expression can be differentially regulated in HL-60 cells and that new protein synthesis plays an important role in both the transcriptional and posttranscriptional regulation. Calcimycin 56-62 colony stimulating factor 1 Homo sapiens 266-271 2071899-8 1991 The t1/2 of M-CSF mRNA was 45 min in cells treated with A23187 for 6 h or in cells treated with PdBu for 24 h, was over 2 h in HL-60 cells treated with A23187 for 6 h and CHX for 1 h, and was 3 h in cells treated with PdBu for 24 h and CHX for 1 h. We conclude that M-CSF gene expression can be differentially regulated in HL-60 cells and that new protein synthesis plays an important role in both the transcriptional and posttranscriptional regulation. Calcimycin 152-158 colony stimulating factor 1 Homo sapiens 12-17 2071899-8 1991 The t1/2 of M-CSF mRNA was 45 min in cells treated with A23187 for 6 h or in cells treated with PdBu for 24 h, was over 2 h in HL-60 cells treated with A23187 for 6 h and CHX for 1 h, and was 3 h in cells treated with PdBu for 24 h and CHX for 1 h. We conclude that M-CSF gene expression can be differentially regulated in HL-60 cells and that new protein synthesis plays an important role in both the transcriptional and posttranscriptional regulation. Calcimycin 152-158 colony stimulating factor 1 Homo sapiens 266-271 2029576-3 1991 A single band with a MW of 43 Kd, which reacted with anti-recombinant hM-CSF IgG but not with control IgG, was found when serum and urine from normal adults underwent electrophoresis on reduced sodium dodecyl sulfate-polyacrylamide gel and subsequent immunoblotting. Sodium Dodecyl Sulfate 194-216 colony stimulating factor 1 Homo sapiens 70-76 2029576-3 1991 A single band with a MW of 43 Kd, which reacted with anti-recombinant hM-CSF IgG but not with control IgG, was found when serum and urine from normal adults underwent electrophoresis on reduced sodium dodecyl sulfate-polyacrylamide gel and subsequent immunoblotting. polyacrylamide 217-231 colony stimulating factor 1 Homo sapiens 70-76 2071899-1 1991 The regulation of macrophage colony-stimulating factor (M-CSF) gene expression by phorbol esters and calcium ionophore (A23187) was studied in HL-60 cells. Phorbol Esters 82-96 colony stimulating factor 1 Homo sapiens 18-54 2071899-1 1991 The regulation of macrophage colony-stimulating factor (M-CSF) gene expression by phorbol esters and calcium ionophore (A23187) was studied in HL-60 cells. Phorbol Esters 82-96 colony stimulating factor 1 Homo sapiens 56-61 2071899-1 1991 The regulation of macrophage colony-stimulating factor (M-CSF) gene expression by phorbol esters and calcium ionophore (A23187) was studied in HL-60 cells. Calcium 101-108 colony stimulating factor 1 Homo sapiens 18-54 2071899-1 1991 The regulation of macrophage colony-stimulating factor (M-CSF) gene expression by phorbol esters and calcium ionophore (A23187) was studied in HL-60 cells. Calcium 101-108 colony stimulating factor 1 Homo sapiens 56-61 1828037-1 1991 Mouse NIH 3T3 fibroblasts transfected with human colony stimulating factor-1 receptor produced diacylglycerol in response to CSF1 and this correlated with elevated phosphatidylcholine hydrolyzing activity measured in an in vitro assay. Phosphatidylcholines 164-183 colony stimulating factor 1 Homo sapiens 125-129 1828037-2 1991 Treatment of cells with the isoflavone derivative genistein attenuated PC hydrolysis in vitro suggesting a role for CSF1R tyrosine kinase activity. Isoflavones 28-38 colony stimulating factor 1 Homo sapiens 116-120 1828037-2 1991 Treatment of cells with the isoflavone derivative genistein attenuated PC hydrolysis in vitro suggesting a role for CSF1R tyrosine kinase activity. Genistein 50-59 colony stimulating factor 1 Homo sapiens 116-120 1826853-5 1991 However, the loss of M-CSF receptors in marrow cells was prevented by dexamethasone (Dex) treatment before rhuIL-1 administration. Dexamethasone 70-83 colony stimulating factor 1 Homo sapiens 21-26 1826853-5 1991 However, the loss of M-CSF receptors in marrow cells was prevented by dexamethasone (Dex) treatment before rhuIL-1 administration. Dexamethasone 85-88 colony stimulating factor 1 Homo sapiens 21-26 1826853-6 1991 The fact that Dex treatment also reduced the level of circulating M-CSF after rhuIL-1 administration suggests that the inhibitory effects of IL-1 are mediated through locally produced M-CSF. Dexamethasone 14-17 colony stimulating factor 1 Homo sapiens 66-71 1826853-6 1991 The fact that Dex treatment also reduced the level of circulating M-CSF after rhuIL-1 administration suggests that the inhibitory effects of IL-1 are mediated through locally produced M-CSF. Dexamethasone 14-17 colony stimulating factor 1 Homo sapiens 184-189 2030912-0 1991 Proteolytic processing of a plasma membrane-bound precursor to human macrophage colony-stimulating factor (CSF-1) is accelerated by phorbol ester. Phorbol Esters 132-145 colony stimulating factor 1 Homo sapiens 69-105 1708091-3 1991 Immune complexes formed with anti-KI1, anti-A, or a peptide antiserum to the CSF-1R carboxyl terminus (anti-C-ter) coprecipitated CSF-1R complexed to a phosphatidylinositol 3-kinase (PtdIns 3-K) from CSF-1-stimulated cells, whereas anti-KI2 serum did not. Phosphatidylinositols 183-189 colony stimulating factor 1 Homo sapiens 77-82 2030912-0 1991 Proteolytic processing of a plasma membrane-bound precursor to human macrophage colony-stimulating factor (CSF-1) is accelerated by phorbol ester. Phorbol Esters 132-145 colony stimulating factor 1 Homo sapiens 107-112 2030912-2 1991 Incubation in the presence of phorbol ester resulted in rapid cleavage of the plasma membrane-bound precursor and release of soluble CSF-1. Phorbol Esters 30-43 colony stimulating factor 1 Homo sapiens 133-138 2030912-5 1991 Phorbol ester-accelerated processing of the cell surface CSF-1 precursor was abrogated by long-term exposure to phorbol, but was not inhibited by pretreatment with cycloheximide or incubation in serum-free medium. Phorbol Esters 0-13 colony stimulating factor 1 Homo sapiens 57-62 2030912-5 1991 Phorbol ester-accelerated processing of the cell surface CSF-1 precursor was abrogated by long-term exposure to phorbol, but was not inhibited by pretreatment with cycloheximide or incubation in serum-free medium. phorbol 112-119 colony stimulating factor 1 Homo sapiens 57-62 2030912-5 1991 Phorbol ester-accelerated processing of the cell surface CSF-1 precursor was abrogated by long-term exposure to phorbol, but was not inhibited by pretreatment with cycloheximide or incubation in serum-free medium. Cycloheximide 164-177 colony stimulating factor 1 Homo sapiens 57-62 2030912-6 1991 These results suggest that the enhanced post-translational processing of the CSF-1 precursor resulted from activation of a pre-existing cellular protease via a mechanism involving phorbol ester-mediated stimulation of protein kinase C. Phorbol Esters 180-193 colony stimulating factor 1 Homo sapiens 77-82 2009973-4 1991 The action of these proteins to induce M-CSF transcript levels was dependent on synthesis of new proteins and was not mediated by protein kinase C (PKC) stimulation as depletion of cellular PKC pools by prolonged exposure of fibroblasts to phorbolester TPA did not prevent factor induced synthesis of M-CSF transcripts. Tetradecanoylphorbol Acetate 253-256 colony stimulating factor 1 Homo sapiens 39-44 1880126-6 1991 SDS-PAGE of the purified truncated M-CSF gave a single band at 17 kDa under reducing conditions and at 32 kDa under non-reducing conditions. Sodium Dodecyl Sulfate 0-3 colony stimulating factor 1 Homo sapiens 35-40 1998593-5 1991 Exposure to hM-CSF in vivo did not directly stimulate the monocyte respiratory burst, but increased the percentage of monocytes responding to f-met-leu-phe from 9.8 +/- 2.5 to 16.6 +/- 4.2 (P less than 0.01). N-Formylmethionine Leucyl-Phenylalanine 142-155 colony stimulating factor 1 Homo sapiens 12-18 1825054-2 1991 Addition of CSF-1 to cells stimulates or stabilizes non-covalent CSF-1R dimerization resulting in activation of the CSF-1R kinase and the tyrosine phosphorylation of the receptor and certain cytoplasmic proteins. Tyrosine 138-146 colony stimulating factor 1 Homo sapiens 12-17 1825054-2 1991 Addition of CSF-1 to cells stimulates or stabilizes non-covalent CSF-1R dimerization resulting in activation of the CSF-1R kinase and the tyrosine phosphorylation of the receptor and certain cytoplasmic proteins. Tyrosine 138-146 colony stimulating factor 1 Homo sapiens 65-70 1713637-6 1991 In contrast, IL-1 beta, TNF, and TPA equally stimulated increased levels of M-CSF, GM-CSF, IL-1 beta and IL-6 RNAs. Tetradecanoylphorbol Acetate 33-36 colony stimulating factor 1 Homo sapiens 76-81 22359048-3 1991 Improvement of M-CSF productivity upon TRC-29SF cell line was performed by M-CSF gene amplification with dhfr-MTX system and by truncation of membrane-binding amino acid sequence by recombinant DNA technique. dhfr-mtx 105-113 colony stimulating factor 1 Homo sapiens 15-20 1367256-3 1991 Improvement of M-CSF productivity upon TRC-29SF cell line was performed by M-CSF gene amplification with dhfr-MTX system and by truncation of membrane-binding amino acid sequence by recombinant DNA technique. dhfr-mtx 105-113 colony stimulating factor 1 Homo sapiens 15-20 1883525-8 1991 Inhibition of PKC by the isoquinoline derivative H7 abolishes induction of M-CSF by M-CSF. isoquinoline 25-37 colony stimulating factor 1 Homo sapiens 75-80 1883525-8 1991 Inhibition of PKC by the isoquinoline derivative H7 abolishes induction of M-CSF by M-CSF. isoquinoline 25-37 colony stimulating factor 1 Homo sapiens 84-89 2281603-9 1990 ASFV-infection of P-MM, placed in culture medium with CSF-1, caused a pronounced transient increase in total 3H-TdR incorporation at the early onset of CPE and HAd. Tritium 109-111 colony stimulating factor 1 Homo sapiens 54-59 1843210-1 1991 The receptor for colony-stimulating factor-1 (CSF-1) is a 165-kDa tyrosine kinase phosphorylated on serine residues in quiescent macrophages. Serine 100-106 colony stimulating factor 1 Homo sapiens 46-51 1843210-4 1991 CSF-1 induced a rapid (2-4 min) initial increase in tyrosine phosphorylation of the 165-kDa subunits of the noncovalent 380-kDa homodimer. Tyrosine 52-60 colony stimulating factor 1 Homo sapiens 0-5 1707631-5 1990 Northern blot hybridization on the endometrium of a pseudopregnant uterus revealed that the expression of endometrial M-CSF and c-fms mRNAs is regulated by synergistic action of female sex steroid hormones. Steroids 189-196 colony stimulating factor 1 Homo sapiens 118-123 1701353-7 1990 Colony-forming capacity of NKM-1 cells in semisolid agar was also enhanced with the addition of 10 ng/ml of G-CSF or M-CSF but decreased at higher concentrations. Agar 52-56 colony stimulating factor 1 Homo sapiens 117-122 1698619-1 1990 The serine/threonine kinase RAF-1 is phosphorylated in intact macrophages in response to CSF-1 at 37 degrees C The augmented phosphorylation of RAF-1 and a concomitant increase in RAF-1 associated serine/threonine kinase activity are kinetically later events than CSF-1 induced protein tyrosine phosphorylation. Tyrosine 286-294 colony stimulating factor 1 Homo sapiens 89-94 1698619-3 1990 In contrast to CSF-1 induced protein tyrosine phosphorylation, RAF-1 phosphorylation and activation are temperature dependent and do not occur at 4 degrees C. Furthermore, coprecipitation experiments failed to reveal any noncovalent association of RAF-1 with the CSF-1 receptor. Tyrosine 37-45 colony stimulating factor 1 Homo sapiens 15-20 2281603-11 1990 For P-MM that were cultured without CSF-1 and for MM-CSF, that were kept in culture with CSF-1, transient increases in 3H-TdR incorporation at the onset of CPE and HAd by ASFV-infection were evident, but were much less pronounced. Tritium 119-121 colony stimulating factor 1 Homo sapiens 89-94 2214871-1 1990 The c-fms proto-oncogene product, which is the receptor for the macrophage colony-stimulating factor CSF-1, is always found expressed in acute myeloid leukemia cells, irrespective of their stage of differentiation according to the FAB classification (Dubreuil P, Torres H, Courcoul M, Birg F, Mannoni P. mannoni p 293-302 colony stimulating factor 1 Homo sapiens 101-106 2147374-0 1990 Steroid hormones induce macrophage colony-stimulating factor (MCSF) and MCSF receptor mRNAs in the human endometrium. Steroids 0-16 colony stimulating factor 1 Homo sapiens 24-60 2147374-0 1990 Steroid hormones induce macrophage colony-stimulating factor (MCSF) and MCSF receptor mRNAs in the human endometrium. Steroids 0-16 colony stimulating factor 1 Homo sapiens 62-66 2147374-0 1990 Steroid hormones induce macrophage colony-stimulating factor (MCSF) and MCSF receptor mRNAs in the human endometrium. Steroids 0-16 colony stimulating factor 1 Homo sapiens 72-76 2147374-1 1990 We investigated the biological effects of sex-steroid hormones, secreted from the corpus luteum and placenta, on the induction of mRNAs encoding macrophage colony-stimulating factor (MCSF) and c-fms proto-oncogene (MCSF receptor) in human endometrium. Steroids 46-62 colony stimulating factor 1 Homo sapiens 145-181 2147374-1 1990 We investigated the biological effects of sex-steroid hormones, secreted from the corpus luteum and placenta, on the induction of mRNAs encoding macrophage colony-stimulating factor (MCSF) and c-fms proto-oncogene (MCSF receptor) in human endometrium. Steroids 46-62 colony stimulating factor 1 Homo sapiens 183-187 2147374-1 1990 We investigated the biological effects of sex-steroid hormones, secreted from the corpus luteum and placenta, on the induction of mRNAs encoding macrophage colony-stimulating factor (MCSF) and c-fms proto-oncogene (MCSF receptor) in human endometrium. Steroids 46-62 colony stimulating factor 1 Homo sapiens 215-219 2147374-3 1990 Results showed: (1) that MCSF mRNA was expressed in the placenta and endometrium of the pregnant uterus, (2) that c-fms proto-oncogene mRNA was also expressed in the placenta and endometrium of the pregnant uterus, and (3) that exogenous sex-steroid hormones could induce the expression of MCSF and c-fms proto-oncogene mRNAs in the endometrium of non-pregnant women. Steroids 242-258 colony stimulating factor 1 Homo sapiens 25-29 2147374-4 1990 These results indicate that sex-steroid hormones secreted by the corpus luteum and/or placenta influence endometrial and placental growth and differentiation via a mechanism of action involving local production of MCSF and its receptor. Steroids 32-39 colony stimulating factor 1 Homo sapiens 214-218 2201680-7 1990 It was evident that M-CSF enhanced cholesterol esterification to a greater extent than the cellular uptake of acetyl-LDL (24.1- versus 7.5-fold). Cholesterol 35-46 colony stimulating factor 1 Homo sapiens 20-25 2171188-9 1990 Moreover, human CSF-1 caused a rapid tyrosine phosphorylation of v-fms molecules detectable within 5 min after addition of the growth factor. Tyrosine 37-45 colony stimulating factor 1 Homo sapiens 16-21 2201680-6 1990 Cellular cholesterol esterification in the presence of 10 micrograms/ml acetyl-LDL was enhanced 24.1-fold (n = 13) by 128 ng/ml M-CSF. Cholesterol 9-20 colony stimulating factor 1 Homo sapiens 128-133 2201680-9 1990 We conclude that M-CSF enhances the uptake of both acetyl-LDL and LDL by increasing their receptor number, and further enhances the process of cholesterol esterification, resulting in a remarkable increase in cholesterol esterification in macrophages. Cholesterol 143-154 colony stimulating factor 1 Homo sapiens 17-22 2201680-9 1990 We conclude that M-CSF enhances the uptake of both acetyl-LDL and LDL by increasing their receptor number, and further enhances the process of cholesterol esterification, resulting in a remarkable increase in cholesterol esterification in macrophages. Cholesterol 209-220 colony stimulating factor 1 Homo sapiens 17-22 2201680-10 1990 These findings strongly suggest the significant involvement of cytokines such as M-CSF in cholesterol metabolism of macrophages. Cholesterol 90-101 colony stimulating factor 1 Homo sapiens 81-86 2164469-3 1990 A tyrosine kinase defective CSF-1R mutant (CSF-1R[met616]), containing a mutated ATP binding site, lacked associated PtdIns 3-kinase activity in immune complexes recovered from CSF-1-stimulated cells. Adenosine Triphosphate 81-84 colony stimulating factor 1 Homo sapiens 28-33 2198280-8 1990 The data suggest that M-CSF stimulates the clearance of lipoproteins containing apolipoprotein B-100 via both LDL receptor-dependent and -independent pathways in target cells of M-CSF and reduces plasma cholesterol. Cholesterol 203-214 colony stimulating factor 1 Homo sapiens 22-27 2196173-7 1990 Moreover, the results indicate that CSF-1 stimulation is associated with decreases in PC, but not in phosphatidylinositol (PI), levels. Phosphatidylcholines 86-88 colony stimulating factor 1 Homo sapiens 36-41 2196173-9 1990 In contrast, CSF-1 stimulation was associated with increased hydrolysis of PC to phosphorylcholine and diacylglycerol (DAG) in both intact monocytes and cell-free assays. Phosphatidylcholines 75-77 colony stimulating factor 1 Homo sapiens 13-18 2141686-4 1990 Furthermore, we treated the HL-60 cells with M-CSF (macrophage-colony stimulating factor or CSF-1) anti-sense N degrees 2 (see Figure 1) in the presence of PMA, hrGM-CSF, 1-alpha-25-(OH)2D3 and DMSO. Calcitriol 171-189 colony stimulating factor 1 Homo sapiens 45-50 2196173-9 1990 In contrast, CSF-1 stimulation was associated with increased hydrolysis of PC to phosphorylcholine and diacylglycerol (DAG) in both intact monocytes and cell-free assays. Phosphorylcholine 81-98 colony stimulating factor 1 Homo sapiens 13-18 2196173-9 1990 In contrast, CSF-1 stimulation was associated with increased hydrolysis of PC to phosphorylcholine and diacylglycerol (DAG) in both intact monocytes and cell-free assays. Diglycerides 103-117 colony stimulating factor 1 Homo sapiens 13-18 2196173-9 1990 In contrast, CSF-1 stimulation was associated with increased hydrolysis of PC to phosphorylcholine and diacylglycerol (DAG) in both intact monocytes and cell-free assays. Diglycerides 119-122 colony stimulating factor 1 Homo sapiens 13-18 2196173-11 1990 The results also demonstrate that the induction of Na+ influx by CSF-1 is inhibited by the protein kinase C inhibitors staurosporine and the isoquinoline derivative H7, but not by HA1004. Staurosporine 119-132 colony stimulating factor 1 Homo sapiens 65-70 2196173-11 1990 The results also demonstrate that the induction of Na+ influx by CSF-1 is inhibited by the protein kinase C inhibitors staurosporine and the isoquinoline derivative H7, but not by HA1004. isoquinoline 141-153 colony stimulating factor 1 Homo sapiens 65-70 1695110-0 1990 Enhanced stimulation of human bone marrow macrophage colony formation in vitro by recombinant human macrophage colony-stimulating factor in agarose medium and at low oxygen tension. Sepharose 140-147 colony stimulating factor 1 Homo sapiens 100-136 2141686-4 1990 Furthermore, we treated the HL-60 cells with M-CSF (macrophage-colony stimulating factor or CSF-1) anti-sense N degrees 2 (see Figure 1) in the presence of PMA, hrGM-CSF, 1-alpha-25-(OH)2D3 and DMSO. Dimethyl Sulfoxide 194-198 colony stimulating factor 1 Homo sapiens 45-50 2141686-4 1990 Furthermore, we treated the HL-60 cells with M-CSF (macrophage-colony stimulating factor or CSF-1) anti-sense N degrees 2 (see Figure 1) in the presence of PMA, hrGM-CSF, 1-alpha-25-(OH)2D3 and DMSO. Dimethyl Sulfoxide 194-198 colony stimulating factor 1 Homo sapiens 92-97 2141686-6 1990 It was further demonstrated that the M-CSF (or CSF-1) and c-fms antisense oligomers acted synergistically on inhibition of macrophage formation induced by PMA and hrGM-CSF, but had no inhibitory effect on the macrophage formation induced by 1-alpha-25-(OH)2D3. Tetradecanoylphorbol Acetate 155-158 colony stimulating factor 1 Homo sapiens 37-42 2141686-6 1990 It was further demonstrated that the M-CSF (or CSF-1) and c-fms antisense oligomers acted synergistically on inhibition of macrophage formation induced by PMA and hrGM-CSF, but had no inhibitory effect on the macrophage formation induced by 1-alpha-25-(OH)2D3. Tetradecanoylphorbol Acetate 155-158 colony stimulating factor 1 Homo sapiens 47-52 2141686-6 1990 It was further demonstrated that the M-CSF (or CSF-1) and c-fms antisense oligomers acted synergistically on inhibition of macrophage formation induced by PMA and hrGM-CSF, but had no inhibitory effect on the macrophage formation induced by 1-alpha-25-(OH)2D3. Calcitriol 241-259 colony stimulating factor 1 Homo sapiens 37-42 2141686-6 1990 It was further demonstrated that the M-CSF (or CSF-1) and c-fms antisense oligomers acted synergistically on inhibition of macrophage formation induced by PMA and hrGM-CSF, but had no inhibitory effect on the macrophage formation induced by 1-alpha-25-(OH)2D3. Calcitriol 241-259 colony stimulating factor 1 Homo sapiens 47-52 2157138-3 1990 By using an antipeptide serum that specifically reacts with epitopes deleted from the enzymatically competent truncation mutant, cross-phosphorylation of CSF-1R[met 616] on tyrosine was demonstrated, both in immune-complex kinase reactions and in intact cells stimulated with CSF-1. Tyrosine 173-181 colony stimulating factor 1 Homo sapiens 154-159 1691932-4 1990 Accelerated turnover of the human CSF-1 receptor was observed in response to CSF-1 and phorbol esters, but not after stimulation with IL-3 or bacterial lipopolysaccharide. Phorbol Esters 87-101 colony stimulating factor 1 Homo sapiens 34-39 1691932-5 1990 Although both CSF-1 and IL-3 induced tyrosine phosphorylation of heterologous substrates in the dually responsive cells, differences in the patterns of substrate phosphorylation were observed in response to the two hematopoietins. Tyrosine 37-45 colony stimulating factor 1 Homo sapiens 14-19 2323362-12 1990 Calcitriol at 10 nM caused TRAP-negative colonies to increase in number and proportion when GM-CSF was present, but in the presence of M-CSF, the same dose of calcitriol caused a decline in numbers of TRAP-negative colonies. Calcitriol 0-10 colony stimulating factor 1 Homo sapiens 93-98 2105339-4 1990 The combination of a protein synthesis inhibitor, cycloheximide, and TNF increased levels of CSF-1 mRNA compared with treatment by TNF alone. Cycloheximide 50-63 colony stimulating factor 1 Homo sapiens 93-98 1689760-2 1990 Human monocytes allowed to adhere express high levels of M-CSF transcripts and secreted protein at 24 h in the presence but not in the absence of indomethacin (Indo), an inhibitor of prostaglandin E (PGE) production. Prostaglandins E 200-203 colony stimulating factor 1 Homo sapiens 57-62 1689760-5 1990 Exogenous addition of PGE-2 to LPS-induced monocytes down-modulates the expression of M-CSF and GM-CSF transcripts. Dinoprostone 22-27 colony stimulating factor 1 Homo sapiens 86-91 1689760-10 1990 PGE-2 added with LPS during the 24-48 h induction blocks M-CSF and TNF production, but appears to enhance M-CSF message expression, in contrast to its effect on 0 h inductions. Dinoprostone 0-5 colony stimulating factor 1 Homo sapiens 57-62 1689760-10 1990 PGE-2 added with LPS during the 24-48 h induction blocks M-CSF and TNF production, but appears to enhance M-CSF message expression, in contrast to its effect on 0 h inductions. Dinoprostone 0-5 colony stimulating factor 1 Homo sapiens 106-111 2179231-0 1990 Macrophage-colony-stimulating factor (CSF-1) modulates a differentiation-specific inward-rectifying potassium current in human leukemic (HL-60) cells. Potassium 100-109 colony stimulating factor 1 Homo sapiens 38-43 2105339-6 1990 Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-1 transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA. 4-bromophenacyl bromide 5-28 colony stimulating factor 1 Homo sapiens 119-124 2105339-6 1990 Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-1 transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA. 4-bromophenacyl bromide 5-28 colony stimulating factor 1 Homo sapiens 307-312 2105339-6 1990 Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-1 transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA. Quinacrine 33-43 colony stimulating factor 1 Homo sapiens 119-124 2105339-6 1990 Both 4-bromophenacyl bromide and quinacrine, inhibitors of phospholipase A2 activity, blocked TNF-induced increases in CSF-1 transcripts in a concentration-dependent manner, while caffeic acid and nordihydroguaiaretic acid, inhibitors of the 5-lipoxygenase pathway, had no detectable effect on induction of CSF-1 RNA. Quinacrine 33-43 colony stimulating factor 1 Homo sapiens 307-312 2105339-7 1990 PGE2 or dibutyryl cAMP treatment of HL-60 cells in the presence of TNF blocked the expression of CSF-1 mRNA in a dose-dependent manner. Dinoprostone 0-4 colony stimulating factor 1 Homo sapiens 97-102 2105339-7 1990 PGE2 or dibutyryl cAMP treatment of HL-60 cells in the presence of TNF blocked the expression of CSF-1 mRNA in a dose-dependent manner. Cyclic AMP 18-22 colony stimulating factor 1 Homo sapiens 97-102 2105339-8 1990 These findings suggest that the increase in CSF-1 RNA observed during TNF treatment is regulated, at least in part, by both transcriptional and posttranscriptional mechanisms, and that PGE2 and cAMP regulate transcriptional activation of the CSF-1 gene by TNF. Dinoprostone 185-189 colony stimulating factor 1 Homo sapiens 242-247 2105339-8 1990 These findings suggest that the increase in CSF-1 RNA observed during TNF treatment is regulated, at least in part, by both transcriptional and posttranscriptional mechanisms, and that PGE2 and cAMP regulate transcriptional activation of the CSF-1 gene by TNF. Cyclic AMP 194-198 colony stimulating factor 1 Homo sapiens 242-247 2183578-6 1990 The hypothesis that prostanoids may be considered as second messengers of platelet CSF-1 like factor, as well as of other growth factors and that PGHs induction plays a pivotal role in this process, will be illustrated. Prostaglandins 20-31 colony stimulating factor 1 Homo sapiens 83-88 2171969-8 1990 In CSF-1-dependent cells, the steroid produces doubling of expression of the mannose receptor, a macrophage-specific membrane protein, which is also expressed by differentiated osteoclasts. Steroids 30-37 colony stimulating factor 1 Homo sapiens 3-8 2193582-0 1990 Plasma cholesterol-lowering activity of monocyte colony-stimulating factor (M-CSF). Cholesterol 7-18 colony stimulating factor 1 Homo sapiens 40-74 2193582-0 1990 Plasma cholesterol-lowering activity of monocyte colony-stimulating factor (M-CSF). Cholesterol 7-18 colony stimulating factor 1 Homo sapiens 76-81 2193582-1 1990 We investigated the action of monocyte colony-stimulating factor (M-CSF) on plasma cholesterol metabolism. Cholesterol 83-94 colony stimulating factor 1 Homo sapiens 30-64 2193582-1 1990 We investigated the action of monocyte colony-stimulating factor (M-CSF) on plasma cholesterol metabolism. Cholesterol 83-94 colony stimulating factor 1 Homo sapiens 66-71 2193582-5 1990 The effect of M-CSF on the LDL-receptor-deficient animal in vivo and evidence from Northern blot analysis of liver suggested that M-CSF lowers plasma cholesterol level through activated uptake of lipoproteins containing apo B 100 via pathways other than the hepatic LDL receptor. Cholesterol 150-161 colony stimulating factor 1 Homo sapiens 130-135 2193582-6 1990 We have started a clinical study to evaluate the plasma cholesterol-lowering effect of M-CSF in patients with familial hypercholesterolemia, and have observed a decreased in total plasma cholesterol level in one of three patients treated with M-CSF. Cholesterol 56-67 colony stimulating factor 1 Homo sapiens 87-92 2193582-6 1990 We have started a clinical study to evaluate the plasma cholesterol-lowering effect of M-CSF in patients with familial hypercholesterolemia, and have observed a decreased in total plasma cholesterol level in one of three patients treated with M-CSF. Cholesterol 56-67 colony stimulating factor 1 Homo sapiens 243-248 2193582-6 1990 We have started a clinical study to evaluate the plasma cholesterol-lowering effect of M-CSF in patients with familial hypercholesterolemia, and have observed a decreased in total plasma cholesterol level in one of three patients treated with M-CSF. Cholesterol 124-135 colony stimulating factor 1 Homo sapiens 87-92 2193582-7 1990 M-CSF may provide new insight into plasma cholesterol metabolism and a possible new tool to treat patients with hypercholesterolemia and atherosclerosis. Cholesterol 42-53 colony stimulating factor 1 Homo sapiens 0-5 2156660-3 1990 Introduction of human CSF-1R enables mouse NIH-3T3 cells to form colonies in agar in response to human CSF-1 and to proliferate in serum-free medium supplemented with CSF-1, albumin, transferrin and insulin. Agar 77-81 colony stimulating factor 1 Homo sapiens 22-27 2156660-3 1990 Introduction of human CSF-1R enables mouse NIH-3T3 cells to form colonies in agar in response to human CSF-1 and to proliferate in serum-free medium supplemented with CSF-1, albumin, transferrin and insulin. Agar 77-81 colony stimulating factor 1 Homo sapiens 103-108 2156660-3 1990 Introduction of human CSF-1R enables mouse NIH-3T3 cells to form colonies in agar in response to human CSF-1 and to proliferate in serum-free medium supplemented with CSF-1, albumin, transferrin and insulin. Agar 77-81 colony stimulating factor 1 Homo sapiens 103-108 2180644-3 1990 Both early progenitor cell growth factors, such as IL-3, and late-acting factors, such as CSF-1, stimulate tyrosine and serine/threonine substrate phosphorylations. Tyrosine 107-115 colony stimulating factor 1 Homo sapiens 90-95 2180644-3 1990 Both early progenitor cell growth factors, such as IL-3, and late-acting factors, such as CSF-1, stimulate tyrosine and serine/threonine substrate phosphorylations. Serine 120-126 colony stimulating factor 1 Homo sapiens 90-95 2180644-3 1990 Both early progenitor cell growth factors, such as IL-3, and late-acting factors, such as CSF-1, stimulate tyrosine and serine/threonine substrate phosphorylations. Threonine 127-136 colony stimulating factor 1 Homo sapiens 90-95 33033302-3 2020 The impact of M-CSF and RANKL in the common OC co-culture was assessed for OB, FB and OK via MTT assay via DAPI control. oc 44-46 colony stimulating factor 1 Homo sapiens 14-19 2159762-3 1990 CSF-1 increased [3H]thymidine incorporation in serum-starved cells and potentiated the mitogenic effects of FGF and thrombin. Tritium 17-19 colony stimulating factor 1 Homo sapiens 0-5 2159762-3 1990 CSF-1 increased [3H]thymidine incorporation in serum-starved cells and potentiated the mitogenic effects of FGF and thrombin. Thymidine 20-29 colony stimulating factor 1 Homo sapiens 0-5 2159762-5 1990 Activation of the CSF-1 receptor by its ligand was evidenced by the rapid activation of the Na+/H+ exchanger resulting in amiloride-sensitive cytoplasmic alkalinization (0.1-0.2 pH units) within minutes after stimulation. Amiloride 122-131 colony stimulating factor 1 Homo sapiens 18-23 2157180-7 1990 Expression of CSF-1 receptors bearing activating mutations led to increased phosphorylation of cellular substrates on tyrosine, suggesting that cell transformation resulted from constitutive receptor kinase activity. Tyrosine 118-126 colony stimulating factor 1 Homo sapiens 14-19 33805444-4 2021 Currently, inhibition of CSF-1/CSF-1R interaction by therapeutic antibody to deplete TAMs and their pro-tumor functions is becoming a prevalent strategy in cancer therapy. tams 85-89 colony stimulating factor 1 Homo sapiens 25-30 1698425-6 1990 Previous work suggested that TNF induces M-CSF gene expression through activation of phospholipase A2 and eicosanoid production. Eicosanoids 106-116 colony stimulating factor 1 Homo sapiens 41-46 2090881-2 1990 Binding of CSF-1 activates the receptor kinase, leading to "autophosphorylation" of receptor subunits and the concomitant phosphorylation of a series of cellular proteins on tyrosine residues. Tyrosine 174-182 colony stimulating factor 1 Homo sapiens 11-16 34948130-4 2021 To confirm whether gal-3 contributes to the regulatory effects of 1alpha,25-(OH)2D3 on osteoclastogenesis, osteoclast precursors (OCPs) were induced by macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor kappaB ligand (RANKL). Calcitriol 66-83 colony stimulating factor 1 Homo sapiens 190-195 34244727-6 2021 Moreover, GPR151 in DRG neurons was required for CCI-induced neuronal hyperexcitability and upregulation of colony-stimulating factor 1 (CSF1), which is necessary for microglial activation in the spinal cord after nerve injury. CCI 49-52 colony stimulating factor 1 Homo sapiens 108-135 34244727-6 2021 Moreover, GPR151 in DRG neurons was required for CCI-induced neuronal hyperexcitability and upregulation of colony-stimulating factor 1 (CSF1), which is necessary for microglial activation in the spinal cord after nerve injury. CCI 49-52 colony stimulating factor 1 Homo sapiens 137-141 34244727-10 2021 Furthermore, knockdown of P2X3 in DRGs reversed CCI-induced CSF1 upregulation, spinal microglial activation, and neuropathic pain-like behavior. CCI 48-51 colony stimulating factor 1 Homo sapiens 60-64 34764771-6 2021 Results: DPMSC-CM augmented invasion, adhesion, multi-drug resistance, DNA repair, and mitochondrial repair in AW13516 through upregulation of growth factors Ang-2, EGF, M-CSF, PDGF-AA, PDGF-BB, pro-inflammatory cytokines TNF-alpha, IL-2, downregulation of anti-inflammatory cytokine TGF-beta1, and pro-inflammatory cytokine IL-4. aw13516 111-118 colony stimulating factor 1 Homo sapiens 170-175 34288020-14 2021 CONCLUSIONS: IL-1beta-induced SLC7A11 overexpression upregulated PD-L1 and CSF1 through alphaKG/HIF1alpha axis, which promoted TAMs and MDSCs infiltration. tams 127-131 colony stimulating factor 1 Homo sapiens 75-79 34433663-0 2021 Vimseltinib: A precision CSF1R therapy for tenosynovial giant cell tumors and diseases promoted by macrophages. Vimseltinib 0-11 colony stimulating factor 1 Homo sapiens 25-29 34433663-7 2021 Vimseltinib (DCC-3014) is an oral, switch control tyrosine kinase inhibitor specifically designed to selectively and potently inhibit CSF1R by exploiting unique features of the switch control region that regulates kinase conformational activation. Vimseltinib 0-11 colony stimulating factor 1 Homo sapiens 134-138 34433663-7 2021 Vimseltinib (DCC-3014) is an oral, switch control tyrosine kinase inhibitor specifically designed to selectively and potently inhibit CSF1R by exploiting unique features of the switch control region that regulates kinase conformational activation. Vimseltinib 13-21 colony stimulating factor 1 Homo sapiens 134-138 34969774-12 2021 This study further indicated that M-CSF secreted by OvCa cells drived the polarization of M2-TAMs. tams 93-97 colony stimulating factor 1 Homo sapiens 34-39 34969774-13 2021 Therefore, a CCL18-ZEB1-M-CSF interacting loop between OvCa cells and TAMs in the spheroids was identified. tams 70-74 colony stimulating factor 1 Homo sapiens 24-29 34129862-5 2021 ZOL@CNPs was actively recruited to TMZ-resistant GBM region by CX3CL1/CX3CR1 and CSF-1/CSF-1R signal axis, and the release of ZOL from ZOL@CNPs was triggered by glutathione in GBM cells. Temozolomide 35-38 colony stimulating factor 1 Homo sapiens 81-86 34586485-3 2022 Pexidartinib (trade name Turalio ), a colony-stimulating factor-1 (CSF-1) inhibitor, was shown in a recent phase III trial to effectively treat diffuse TSGCT and is FDA approved for the treatment of adult patients with symptomatic diffuse TSGCT associated with severe morbidity or functional limitations and not amenable to improvement with surgery. pexidartinib 0-12 colony stimulating factor 1 Homo sapiens 38-65 34586485-3 2022 Pexidartinib (trade name Turalio ), a colony-stimulating factor-1 (CSF-1) inhibitor, was shown in a recent phase III trial to effectively treat diffuse TSGCT and is FDA approved for the treatment of adult patients with symptomatic diffuse TSGCT associated with severe morbidity or functional limitations and not amenable to improvement with surgery. pexidartinib 0-12 colony stimulating factor 1 Homo sapiens 67-72 34680177-5 2021 NMP at concentrations as low as 1 micromol/L reduced the stimulated expression of several pro-inflammatory mediators, including C-C Motif chemokine ligand (CCL)-2, C-X-C Motif chemokine ligand (CXCL)-10, and intercellular adhesion Molecule (ICAM)-1, but left the induction of prostaglandin G/H synthase (PTGS)2, interleukin (IL)-1beta, and colony stimulating factor (CSF)1 unaffected. 1-methylpyridinium 0-3 colony stimulating factor 1 Homo sapiens 340-372 34901550-5 2022 Simultaneously, ASP VI significantly reduced the differentiation of mononuclear osteoclasts in the process of osteoclast formation induced by M-CSF and RANKL. akebia saponin D 16-22 colony stimulating factor 1 Homo sapiens 142-147 34133181-4 2021 TAMM could deplete the CSF1 secreted by tumor cells in the tumor microenvironment (TME), blocking the interaction between TAM and cancer cells. Tetrakis(acetoxymercuri)methane 0-4 colony stimulating factor 1 Homo sapiens 23-27 34133181-4 2021 TAMM could deplete the CSF1 secreted by tumor cells in the tumor microenvironment (TME), blocking the interaction between TAM and cancer cells. Tamoxifen 122-125 colony stimulating factor 1 Homo sapiens 23-27 35366939-9 2022 TAb2 tumor cells drastically expanded F4/80+ TAMs from bone marrow precursors, requiring CSF1 and VEGF. tams 45-49 colony stimulating factor 1 Homo sapiens 89-93 34149707-0 2021 Continuous Exposure to Non-Soluble beta-Glucans Induces Trained Immunity in M-CSF-Differentiated Macrophages. beta-Glucans 35-47 colony stimulating factor 1 Homo sapiens 76-81 34069563-0 2021 Tumor-Associated Macrophage Promotes the Survival of Cancer Cells upon Docetaxel Chemotherapy via the CSF1/CSF1R-CXCL12/CXCR4 Axis in Castration-Resistant Prostate Cancer. Docetaxel 71-80 colony stimulating factor 1 Homo sapiens 102-106 34069563-2 2021 Previously, we found that tumor-associated macrophages (TAM) can be recruited by CSF-1 secreted by docetaxel-treated prostate cancer cells and promote the survival of cancer cells in response to chemotherapy. Docetaxel 99-108 colony stimulating factor 1 Homo sapiens 81-86 34069563-5 2021 Here, for the first time, we found that the enhanced survival of cancer cells achieved by TAM was mainly mediated by CXCR4 activation from the increased secretion of CXCL12 from CSF-1 activated TAM. tam 90-93 colony stimulating factor 1 Homo sapiens 178-183 34069563-5 2021 Here, for the first time, we found that the enhanced survival of cancer cells achieved by TAM was mainly mediated by CXCR4 activation from the increased secretion of CXCL12 from CSF-1 activated TAM. tam 194-197 colony stimulating factor 1 Homo sapiens 178-183 34298983-6 2021 Further investigations showed that CSF1R-CSF1 signaling is involved in the induction of cell metabolic reprogramming, triggering glycolysis to produce high amounts of lactate, a novel suppressive mechanism of T cell proliferation, recently found in autologous tolerogenic dendritic cells (ATDCs). Lactic Acid 167-174 colony stimulating factor 1 Homo sapiens 41-45 35597882-6 2022 The expressions of M-CSFR ligands (interleukin-34 and M-CSF) were also increased by co-culture with HMDMs. hmdms 100-105 colony stimulating factor 1 Homo sapiens 54-59 35527392-7 2022 NaCl significantly upregulated chemotactic cytokines, most markedly CCL26, CCL2 and CSF1. Sodium Chloride 0-4 colony stimulating factor 1 Homo sapiens 84-88 35527392-9 2022 In contrast urea, the main medullary osmolyte in catabolism, dampened tubular epithelial CCL26 and CSF1 expression. Urea 12-16 colony stimulating factor 1 Homo sapiens 99-103 35479318-5 2022 In addition, mupirocin at 0.1 mM significantly stimulated the production of hepatocyte growth factor and M-CSF in HaCat cells, whereas at 0.2 mM, PDGF-AA and EPO were increased. Mupirocin 13-22 colony stimulating factor 1 Homo sapiens 105-110 35096812-11 2021 Metformin inhibited osteoclast formation and accordingly downregulated the genes involved in osteoclastogenesis: RANKL, macrophage colony stimulating factor (M-CSF) and osteoclast fusion gene DC-STAMP. Metformin 0-9 colony stimulating factor 1 Homo sapiens 120-156 34995730-7 2022 RESULTS: The stronger correlations in the obese without T2D or reference group was between ICAM1 and HbA1c; HP and TC and LDL while in the obese with diabetes or case group the correlation occurred between CSF1 and BMI. Technetium 115-117 colony stimulating factor 1 Homo sapiens 206-210 35219791-10 2022 Notably, Go6976, a protein kinase inhibitor, and lenvatinib, a multi-kinase inhibitor, reset the tumor microenvironment and restore sensitivity to anti-PD1 by blocking the PKCalpha/ZFP64/CSF1 axis. Go 6976 9-15 colony stimulating factor 1 Homo sapiens 187-191 35219791-10 2022 Notably, Go6976, a protein kinase inhibitor, and lenvatinib, a multi-kinase inhibitor, reset the tumor microenvironment and restore sensitivity to anti-PD1 by blocking the PKCalpha/ZFP64/CSF1 axis. lenvatinib 49-59 colony stimulating factor 1 Homo sapiens 187-191 35219791-11 2022 CONCLUSIONS: We propose that PKCalpha/ZFP64/CSF1 axis is critical for triggering immune evasion and anti-PD1 tolerance, and that inhibiting this axis with Go6976 or lenvatinib overcame anti-PD1 resistance in HCC. Go 6976 155-161 colony stimulating factor 1 Homo sapiens 44-48 35219791-11 2022 CONCLUSIONS: We propose that PKCalpha/ZFP64/CSF1 axis is critical for triggering immune evasion and anti-PD1 tolerance, and that inhibiting this axis with Go6976 or lenvatinib overcame anti-PD1 resistance in HCC. lenvatinib 165-175 colony stimulating factor 1 Homo sapiens 44-48 35386453-2 2022 Therefore, a multi-functional oxygen delivery nanoplatform was rationally constructed based on an oxygen-saturated perfluorohexane (PFH)-cored liposome, with the CXCR4 antagonist LFC131 peptides modifying on the surface to simultaneously deliver sorafenib and the CSF1/CSF1R inhibitor PLX3397 (named PFH@LSLP) for sorafenib-resistant HCC treatment. Oxygen 30-36 colony stimulating factor 1 Homo sapiens 264-268 35386453-2 2022 Therefore, a multi-functional oxygen delivery nanoplatform was rationally constructed based on an oxygen-saturated perfluorohexane (PFH)-cored liposome, with the CXCR4 antagonist LFC131 peptides modifying on the surface to simultaneously deliver sorafenib and the CSF1/CSF1R inhibitor PLX3397 (named PFH@LSLP) for sorafenib-resistant HCC treatment. Oxygen 98-104 colony stimulating factor 1 Homo sapiens 264-268 35096812-11 2021 Metformin inhibited osteoclast formation and accordingly downregulated the genes involved in osteoclastogenesis: RANKL, macrophage colony stimulating factor (M-CSF) and osteoclast fusion gene DC-STAMP. Metformin 0-9 colony stimulating factor 1 Homo sapiens 158-163 35096812-12 2021 Osteoclast formation on both plastic and bone as well as bone resorption was inhibited by metformin in M-CSF and RANKL stimulated monocyte cultures, probably by reduction of RANK expression. Metformin 90-99 colony stimulating factor 1 Homo sapiens 103-108