ライフサイエンスコーパス: CSF1R

1 CSF1R inhibition is a promising new target for the treat

2 CSF1R is a representative of this signature, and its exp

3 CSF1R was not upregulated in hTERT immortalized epitheli

4 CSF1R(+) myeloid-primed embryonic ProB cells are relevan

5 CSF1R-FRed was expressed in monocytes and macrophages an

6 A CSF1R inhibitor, Plexxikon (PLX) 5622, was administered

7 (APPswe, PSEN1dE9; APP/PS1 mice) we define a CSF1R-dependent progressive increase in microglial proli

8 ison to insulin in 3T3-L1 cells expressing a CSF1R/IR mutated at Tyr960 (CSF1R/IRA960).

9 Here, we show that application of a CSF1R inhibitor eliminated virtually all microglia from

10 rt the development and characterization of a CSF1R reporter mouse.

11 the 25 d lesion, we administered PLX3397, a CSF1R inhibitor, for 30 d to eliminate microglia.

12 timulating factor 1 receptor (CSF1R) using a CSF1R inhibitor-NO-NR system leads to enhanced efficacy

13 Moreover, microglial depletion with a CSF1R antagonist prior to stress prevented the recruitme

14 r 1 receptor (CSF1R), we treated mice with a CSF1R inhibitor, PLX5622.

15 hibiting CSF1/CSF1-receptor signaling with a CSF1R kinase inhibitor reduces resident macrophage proli

16 this model, depletion of macrophages with a CSF1R-blocking antibody reduced the efficacy of 5AZA-C +

17 human leukemic cells expressing ABL1, ABL2, CSF1R, and PDGFRB fusions were sensitive in vitro to das

18 lude ABL-class fusions involving ABL1, ABL2, CSF1R, and PDGFRB that phenocopy BCR-ABL1 and alteration

19 ed targetable ABL-class fusions (ABL1, ABL2, CSF1R, and PDGFRB) in 14.1%, EPOR rearrangements or JAK2

20 Expression of ABL1, ABL2, CSF1R, JAK2, and PDGFRB fusions resulted in cytokine-ind

21 ollow-up sequencing identified an additional CSF1R mutation in an individual diagnosed with corticoba

22 mApple transgene, suggesting that additional CSF1R transcriptional regulatory elements are required b

23 the microglial homeostatic population after CSF1R signaling returns.

24 repopulate the central nervous system after CSF1R inhibition, these changes have practical implicati

25 s and clinically relevant genes such as ALK, CSF1R, and CD274/PD-L1 The over 1,000 genetic alteration

26 CSF1R deficiency and implied that bi-allelic CSF1R mutations cause a spectrum of neurological and ske

27 three unrelated families who had bi-allelic CSF1R mutations.

28 Here we investigated whether an alternative CSF1R ligand, interleukin 34 (IL-34), is responsible for

29 mutated genes were NOTCH3, EIF2B5, AARS2 and CSF1R.

30 ed group, tumors following BRAFi, aPDL1, and CSF1R-blocking antibody combination therapy did not show

31 Gene expression of CD68, CD11b, and CSF1R but not Mphi was correlated negatively with glucos

32 e-specific gene expression (CD68, CD11b, and CSF1R), were correlated with percent body fat, age, and

33 cells co-expressing F4/80, CD103, CD207, and CSF1R acquired parasites during the liver stage of malar

34 human breast tumors expressing both CSF1 and CSF1R, invasion in vivo is dependent both on a paracrine

35 monocytes expressed KUL01, class II MHC, and CSF1R-mApple uniformly.

36 essed in PDX tumors, e.g. PDGFRA, PDGFRB and CSF1R.

37 increased inflammatory cell recruitment and CSF1R signal transduction in both macrophages and endoth

38 In the liver, TIM4 and CSF1R reporters distinguished Kupffer cells from an abun

39 Treatment with anti-CSF1R preferentially depleted macrophages with an inflam

40 As CSF1R is a crucial mediator of microglial proliferation

41 As CSF1R regulates microglia this mutation implies that dys

42 Abrogation of autocrine CSF1R signaling in MDA-MB-231 xenografts (a claudin-low

43 Our results suggest that autocrine CSF1R signaling is essential in maintaining low claudin

44 n about the mechanism by which the autocrine CSF1R signaling contributes to tumor progression.

45 te enhancer factor 2D) and five genes (BCL9, CSF1R, DAZAP1, HNRNPUL1 and SS18) in 22 B progenitor ALL

46 aded the peripheral nerve of ALS mice before CSF1R-induced microgliosis occurred.

47 t, highly selective, and orally bioavailable CSF1R inhibitor, IACS-9439 (1).

48 a unique human skeletal phenotype caused by CSF1R deficiency and implied that bi-allelic CSF1R mutat

49 ny stimulating factor 1 receptor (encoded by CSF1R) in 14 families with HDLS.

50 artly caused by the monocytopenia induced by CSF1R inhibition.

51 ion and invasion are oppositely regulated by CSF1R downstream of TGFbeta only in claudin-low cell lin

52 th typical features of ALSP who do not carry CSF1R mutations.

53 The HLA-DR(-) subset coexpressed CD163(+)CSF1R(+) at higher levels than CD68(+)HLA-DR(+) macropha

54 factor-1 receptor/insulin receptor chimera (CSF1R/IR)) connecting the extracellular, ligand-binding

55 factor-1 receptor/insulin receptor chimera (CSF1R/IR).

56 of nonlymphoid tissues in mice with combined CSF1R-FRed/Csf1r-EGFP confirmed the restriction of CSF1R

57 Combining CSF1R inhibitor with a CXCR2 antagonist blocked granuloc

58 By contrast, CSF1R-mApple was detected in liver TIM4(lo) and TIM4(-)

59 rearrangements involving ABL1, ABL2, CRLF2, CSF1R, EPOR, JAK2, NTRK3, PDGFRB, PTK2B, TSLP, or TYK2 a

60 93A) mice, indicating the importance of CSF1-CSF1R signalling in microgliosis in ALS.

61 The CSF1-CSF1R pathway has a critical role in trafficking allerge

62 The inhibition of the CSF1-CSF1R signaling pathway effectively suppresses sensitiza

63 The CSF1-CSF1R signaling pathway modulates the production, differ

64 Our results highlight the importance of CSF1/CSF1R signaling in the recruitment of TIMs that can limi

65 o acid deletion of the juxtamembrane domain (CSF1R/IRDelta960).

66 Finally, although both elevated CSF1R and IL-4Ralpha signaling triggered proliferation a

67 These early embryonic CSF1R(+)CD19(+) ProB cells also express multiple other m

68 of coincident expression with the endogenous CSF1R protein.

69 cells, whereas the majority of cells express CSF1R but not CSF1, suggesting a tumor-landscaping effec

70 eurons in the hippocampus and cortex express CSF1R under physiological conditions and that kainic aci

71 These cells expressed CSF1R alongside high levels of FLT3, MHCII, XCR1, and ot

72 Although they expressed CSF1R mRNA, Kupffer cells did not express the CSF1R-mApp

73 or for macrophage colony-stimulating factor, CSF1R.

74 e colony-stimulating factor receptor family (CSF1R/IL34/CSF1) respectively.

75 We identified five CSF1R mutations that were homozygous or compound heteroz

76 ific sensitivity to down-regulation of FLT1, CSF1R, PDGFR, ROR1, EPHA4/5, JAK1/3, LMTK3, LYN, FYN, PT

77 tem cells, arguing against a direct role for CSF1R in myeloid lineage commitment.

78 tifying an evolutionarily conserved role for CSF1R signaling in production or maintenance of CUX1(+)

79 eukodystrophies and that genetic testing for CSF1R mutations is essential in adult patients presentin

80 esent in CSF1-deficient mice but absent from CSF1R-deficient mice.

81 ce analysis of cDNA generated by 5'RACE from CSF1R coding sequences identified a novel fusion of the

82 e Colony-Stimulating Factor 1 Receptor gene (CSF1R).

83 were also reduced in sections of homozygous CSF1R mutant human brain, identifying an evolutionarily

84 rt two unrelated individuals with homozygous CSF1R mutations whose presentation was distinct from ALS

85 ue of Cancer Cell, Kumar et al. describe how CSF1R blockade induces not only an expected deprivation

86 This study identifies CSF1R as a novel therapeutic target of AML and provides

87 crosstalk enforces aggressive CD44(+)IGF1R(+)CSF1R(+) LC phenotypes, including extranodal invasion an

88 and immune cell differentiation (eg, IL10RA, CSF1R) decreased.

89 deletion of FIRE in mice selectively impacts CSF1R expression and tissue macrophage development in sp

90 DNA from this subject displayed chimerism in CSF1R acquired after haematopoietic stem cell transplant

91 d a novel, heterozygous missense mutation in CSF1R [c.1990G > A p.(E664K)] by exome sequencing in fiv

92 study, we uncovered activating mutations in CSF1R and rearrangements in RET and ALK that conferred d

93 We identified 12 probands with mutations in CSF1R.

94 encephalopathies discussed in detail include CSF1R, AARS2, cerebral arteriopathy with subcortical inf

95 GW2580 significantly attenuated MPTP-induced CSF1R activation and Iba1-positive cell proliferation, w

96 et M2 macrophages and simultaneously inhibit CSF1R and SHP2 pathways.

97 is a novel monoclonal antibody that inhibits CSF1R activation.

98 by Western blotting revealed that the intact CSF1R/IR co-precipitates with IRS-2 from CSF-1-treated c

99 brain injury and neurodegeneration involving CSF1R expression on neurons.

100 y other RTKs, including PDGFRs, VEGFRs, KIT, CSF1R, FLT3, TEK, and TIE, are also subject to regulatio

101 To determine whether the other known CSF1R ligand IL34 is expressed in gliomas, we examined e

102 As in mammals, CSF1R-reporter genes were specifically expressed at high

103 In bone marrow, CSF1R-FRed was absent in lineage-negative hematopoietic

104 In sections of bone marrow, CSF1R-FRed was also detected in osteoclasts, CD169(+) re

105 Antibody-mediated CSF1R blocking prevented the cold-induced recruitment of

106 of a therapeutic strategy aimed at modifying CSF1R activation as a promising approach to tackle micro

107 Thus, small-molecule CSF1R inhibition is not restricted to microglia, causing

108 he kinase domain of wild-type but not mutant CSF1R, suggesting that HDLS may result from partial loss

109 ent to initiate involution in the absence of CSF1R(+) macrophages.

110 t some macrophages persist in the absence of CSF1R.

111 y the pathway regulated by the activation of CSF1R and the transcription factors PU.1 and C/EBPalpha

112 We show that targeting the activity of CSF1R inhibits microglial proliferation and slows neuron

113 Moreover, analysis of CSF1R-deficient mice establishes a distinct role of CSF1

114 Comparison of CSF1R-expressing cells in AML vs healthy donors by mass

115 We have studied the contribution of CSF1R signalling to inflammation in ALS, as a pathway pr

116 Selective deletion of CSF1R in forebrain neurons in mice exacerbated excitotox

117 Depletion of CSF1R(+) macrophages resulted in delayed mammary involut

118 the cleavage of the intracellular domain of CSF1R.

119 Downstream of CSF1R, we found that the microglial membrane adaptor pro

120 The insertion had no effect of CSF1R expression or function.

121 ied the mechanism that limited the effect of CSF1R targeted therapy.

122 s provide the first proof of the efficacy of CSF1R inhibition in models of Alzheimer's disease, and v

123 's disease and validation of the efficacy of CSF1R-inhibiting strategies have not yet been reported.

124 genic mice correlates with the expression of CSF1R and its ligand CSF1.

125 r, we described increased mRNA expression of CSF1R in human telomerase reverse transcriptase (hTERT)

126 Additionally, the high expression of CSF1R on tumor cells has been associated with poor survi

127 Reducing the expression of CSF1R using short hairpin interfering RNA abolished thes

128 e have significantly increased expression of CSF1R.

129 sults give an indication of the frequency of CSF1R mutations in a European leukodystrophy series and

130 indicate potential for human PET imaging of CSF1R and the microglial component of neuroinflammation.

131 These data highlight the importance of CSF1R signaling in the recruitment and function of disti

132 gly supports the potential for inhibition of CSF1R as a target for the treatment of Alzheimer's disea

133 systemic short- and long-term inhibition of CSF1R by oral administration leads to a robust decline i

134 Prolonged inhibition of CSF1R in APP/PS1 mice by an orally available tyrosine ki

135 tiphoton imaging revealed that inhibition of CSF1R in the tumor cells leads to decreased in vivo moti

136 Inhibition of CSF1R using small molecule inhibitors such as imatinib,

137 hages by an orally administered inhibitor of CSF1R may offer a highly efficacious and safe treatment

138 use the selective pharmacologic inhibitor of CSF1R signaling, GW2580, to demonstrate that CSF-1 regul

139 ed to radiotherapy, a selective inhibitor of CSF1R suppressed tumor growth more effectively than irra

140 mpletely blocked by a selective inhibitor of CSF1R.

141 l cell lines showed rapid internalization of CSF1R with concomitant down-modulation and colocalizatio

142 ic LPS treatment, mRNA and protein levels of CSF1R and CSF-1 were significantly increased.

143 pulation in old mice expressed low levels of CSF1R and granulin and failed to promote tumor outgrowth

144 ng that HDLS may result from partial loss of CSF1R function.

145 Mono-allelic mutations of CSF1R are known to cause hereditary diffuse leukoencepha

146 analysis supported the ancestral pairings of CSF1R/IL34 and CSF3R/CSF3, and the emergence of CSF1 lat

147 The quantity of CSF1R-expressing cells correlated with GW-2580 sensitivi

148 verexpress CSF1, resulting in recruitment of CSF1R-bearing macrophages that are polyclonal and make u

149 SF1R) activation leads to the recruitment of CSF1R-expressing cells of the mononuclear phagocyte line

150 d macrophages and an autocrine regulation of CSF1R in the tumor cells themselves.

151 FRed/Csf1r-EGFP confirmed the restriction of CSF1R expression to MPS cells.

152 eficient mice establishes a distinct role of CSF1R in fetal B-lymphopoiesis.

153 However, the role of CSF1R signaling in microglial homeostasis in the adult b

154 issue M2 macrophages, suggesting the role of CSF1R signaling in the process.

155 A combined score of CSF1R in situ hybridization and CD68 immunohistochemistr

156 uencing in a family and Sanger sequencing of CSF1R.

157 rring allergens and novel delivery system of CSF1R inhibitor encapsulated nanoprobe.

158 Pharmacological targeting of CSF1R in APP/PS1 mice resulted in an improved performanc

159 in ALS, supporting therapeutic targeting of CSF1R in this disease.

160 was inserted in-frame with the C terminus of CSF1R, separated by a T2A-cleavable linker.

161 Use of CSF1R inhibitors to target TAM is therapeutically appeal

162 heimer's disease brain are also dependent on CSF1R signalling, and if so, how these cells contribute

163 The majority of microglia rely on CSF1R signaling for survival.

164 Targeting CCR2 or CSF1R improves chemotherapeutic efficacy, inhibits metas

165 550 in combination with either checkpoint or CSF1R blockade caused additive antitumor activity with c

166 evidence of ALSP who do not carry pathogenic CSF1R mutations.

167 nthesized a highly selective brain-penetrant CSF1R inhibitor (PLX5622) allowing for extended and spec

168 We conclude that pharmacological CSF1R inhibitors afford the most extensive versatility i

169 whereas select combinations involving PI3K, CSF1R, or bromodomain inhibitors showed preferential ben

170 (ABL1 fusion-positive, ABL2 fusion-positive, CSF1R fusion-positive, and PDGFRB fusion-positive) B-cel

171 n of the macrophage differentiation protein, CSF1R.

172 Expression of the RBM6-CSF1R fusion protein conferred interleukin-3 (IL-3)-inde

173 naling by the myeloid growth factor receptor CSF1R can functionally reprogram macrophage responses th

174 ia/macrophage cytokine CSF1 and its receptor CSF1R are overexpressed in human high-grade gliomas.

175 of the colony stimulating factor 1 receptor (CSF1R) by immunotherapy was confirmed to inhibit macroph

176 in the colony stimulating factor-1 receptor (CSF1R) gene.

177 s, but colony stimulating factor-1 receptor (CSF1R) has emerged as a primary factor.

178 in the colony stimulating factor 1 receptor (CSF1R) have recently been discovered as causal for hered

179 Colony-stimulating factor 1 receptor (CSF1R) inhibition has been proposed as a method for micr

180 th the colony stimulating factor 1 receptor (CSF1R) inhibitor PLX5622.

181 sing a colony stimulating factor 1 receptor (CSF1R) inhibitor, Plexxikon 5622.

182 nib, a colony-stimulating factor 1 receptor (CSF1R) inhibitor, to reduce TAM density.

183 The colony-stimulating factor 1 receptor (CSF1R) is a key regulator of myeloid lineage cells.

184 ophage colony-stimulating factor 1 receptor (CSF1R) is a product of the proto-oncogene c-fms and a me

185 ingly, colony stimulating factor-1 receptor (CSF1R) is significantly increased following implantation

186 ivated colony-stimulating factor 1 receptor (CSF1R) kinase in the acute megakaryoblastic leukemia (AM

187 of the colony stimulating factor 1 receptor (CSF1R) locus.

188 eptors colony-stimulating factor-1 receptor (CSF1R) or chemokine (C-C motif) receptor 2 (CCR2) decrea

189 Colony stimulating factor 1 receptor (CSF1R) plays key roles in regulating development and fun

190 ent on colony-stimulating factor 1 receptor (CSF1R) signaling for survival in the healthy adult brain

191 ent on colony stimulating factor 1 receptor (CSF1R) signaling for their survival.

192 ent on colony-stimulating factor 1 receptor (CSF1R) signaling for their survival.

193 CSF-1 receptor (CSF1R) signaling is important for the recruitment of CD1

194 end on colony-stimulating factor 1 receptor (CSF1R) signalling for survival, and pharmacological inhi

195 22) of colony stimulating factor-1 receptor (CSF1R) to deplete microglia post-irradiation.

196 ion of colony stimulating factor 1 receptor (CSF1R) using a CSF1R inhibitor-NO-NR system leads to enh

197 essing colony stimulating factor 1 receptor (CSF1R) was initiated just prior to weaning in the Mafia

198 of the colony-stimulating factor 1 receptor (CSF1R) which is a tyrosine kinase receptor essential for

199 quires Colony Stimulating Factor 1 Receptor (CSF1R), a gene previously associated with a dominant adu

200 equire colony-stimulating factor 1 receptor (CSF1R), but some macrophages persist in the absence of C

201 ss the colony-stimulating factor-1 receptor (CSF1R), previously thought to be expressed, and play a l

202 ophage colony-stimulating factor 1 receptor (CSF1R), the expression of which is essentially restricte

203 of the colony-stimulating factor 1 receptor (CSF1R), thus providing a target that may prevent the pro

204 ent on colony-stimulating factor 1 receptor (CSF1R), we treated mice with a CSF1R inhibitor, PLX5622.

205 of the colony stimulating factor 1 receptor (CSF1R).

206 lizing colony stimulating factor 1 receptor (CSF1R).

207 ons in colony stimulating factor 1 receptor (CSF1R).

208 urvival pathway we used a chimeric receptor (CSF1R/IR) consisting of the ligand-binding domain of the

209 ntrolled by signals from the M-CSF receptor (CSF1R).

210 CSF1 receptor (CSF1R) activation leads to the recruitment of CSF1R-expr

211 are functional ligands of the CSF1 receptor (CSF1R) and thus are key regulators of the monocyte/macro

212 re it targeted the microglial CSF1 receptor (CSF1R).

213 ment of therapy targeting the CSF1 receptor (CSF1R).

214 colony-stimulating factor 1 (CSF1) receptor (CSF1R), a receptor tyrosine kinase responsible for survi

215 timulating factor-1 (CSF1) and its receptor (CSF1R) have critical roles during breast cancer progress

216 tors of CSF1 signaling through its receptor, CSF1R, were tested in combination with ABT, demonstratin

217 res the growth factor CSF1 and its receptor, CSF1R.

218 isorders, probably depending on the residual CSF1R function.

219 old 5xfAD mice were treated with a selective CSF1R inhibitor for 1 month, resulting in the eliminatio

220 Administration of GW2580, a selective CSF1R inhibitor, reduced microglial cell proliferation i

221 -GW nanoprobe containing GW2580, a selective CSF1R inhibitor, showed favorable pharmacokinetics for i

222 of TAMs; however, the discovery of selective CSF1R inhibitors devoid of type III kinase activity has

223 this end, we tested the effects of selective CSF1R inhibitors on microglia in adult mice.

224 y research, we generated a potent, selective CSF1R inhibitor, PLX3397, that traps the kinase in the a

225 udy, we tested the efficacy of the selective CSF1R inhibitor JNJ-40346527 (JNJ-527) in the P301S mous

226 athobiology of treatment failure and suggest CSF1R as a drug target of at-risk CHL.

227 heir progenitors in bone marrow lack surface CSF1R.

228 s indistinguishable from those that survived CSF1R inhibition, supporting the notion that MAC2+ proge

229 Suspending CSF1R blockade following ablation enabled spontaneous ma

230 Targeting CSF1R has been proposed as a potential therapy to reduce

231 DSCs, and validate the benefits of targeting CSF1R signaling in combination with antiangiogenic drugs

232 Our results indicate that targeting CSF1R may allow for a more selective method of fibrosis

233 roglial depletion, suggesting that targeting CSF1R signaling may be a viable neuroprotective strategy

234 of breast cancer cell lines, we confirm that CSF1R expression is elevated and regulated by TGFbeta sp

235 We now demonstrate that CSF1R antagonist-mediated microglial depletion in transg

236 Here, we further describe that CSF1R is upregulated at both the mRNA and protein level

237 Using flow cytometry, we discovered that CSF1R is not expressed on the majority of leukemic blast

238 The discovery that CSF1R mutations cause ALSP led to more accurate prognosi

239 We estimate that CSF1R mutations account for 10% of idiopathic adult onse

240 Overall, our findings provide evidence that CSF1R signalling regulates inflammation in the central a

241 nvestigations of this response revealed that CSF1R blockade also upregulated T-cell checkpoint molecu

242 panel of recombinant cytokines revealed that CSF1R inhibitor sensitivity correlated with a growth res

243 Here, we show that CSF1R inhibition by PLX5622 indeed affects the myeloid a

244 A and a small-molecule inhibitor showed that CSF1R is essential for the growth and survival of MKPL-1

245 Our study shows that CSF1R mutations are responsible for a significant propor

246 Our results suggest that CSF1R is required for human brain development and establ

247 the basis of these findings, we suggest that CSF1R may be a critical factor facilitating hTERT immort

248 Our results suggest that CSF1R-expressing cells support the bulk leukemia populat

249 The CSF1R and AARS2 proteins have different cellular functio

250 The CSF1R-FRed mouse provides a novel reporter with exquisit

251 Upon activation with CSF-1, the CSF1R/IR phosphorylates itself and intracellular substra

252 epleted microglia (99%) by administering the CSF1R (colony-stimulating factor 1 receptor) antagonist

253 Upon stimulation by the CSF1R ligand CSF1, the immortalized epithelial cell line

254 In contrast, the CSF1R/IRA960 co-precipitates poorly with IRS-2.

255 ition of apoptosis, activation of either the CSF1R/IR or the CSF1R/IRDelta960 rapidly induced membran

256 SF1R mRNA, Kupffer cells did not express the CSF1R-mApple transgene, suggesting that additional CSF1R

257 F-1 treatment protected cells expressing the CSF1R/IR from staurosporine-induced apoptosis.

258 CSF-1-treated adipocytes expressing the CSF1R/IRA960 were impaired in their ability to phosphory

259 other's blood and saliva were mosaic for the CSF1R mutation.

260 aused by autosomal dominant mutations in the CSF1R (colony-stimulating factor 1) gene.

261 s and colleagues identified mutations in the CSF1R gene as the cause of hereditary diffuse leukoencep

262 Genetic loss of the CSF1R blocks the normal population of resident microglia

263 mma to inhibit expression of RANK and of the CSF1R gene that encodes c-Fms, and to synergistically in

264 it has been known since the discovery of the CSF1R gene that there are patients with typical clinical

265 y data, we found that mRNA expression of the CSF1R ligand, CSF-1, is increased in the brain of PD pat

266 However, the impact of the CSF1R signaling pathway on other TIM subsets, including

267 n line with an increased upregulation of the CSF1R-dependent pro-mitogenic cascade, correlating with

268 The anti-apoptotic action of the CSF1R/IRDelta960 was reversed by dominant-inhibitory Rac

269 is, activation of either the CSF1R/IR or the CSF1R/IRDelta960 rapidly induced membrane ruffling in Ra

270 In this study, we sequenced the CSF1R gene in a cohort of 48 patients from the UK, Greec

271 of maximal accumulation and response to the CSF1R inhibitor, and revealed differences between microe

272 Treatment with the CSF1R inhibitor GW2580 significantly attenuated MPTP-ind

273 Notably, these CSF1R(+) myeloid-primed ProB cells are uniquely present

274 strate that elimination of microglia through CSF1R inhibition can ameliorate radiation-induced cognit

275 Thus, CSF1R inhibition could have therapeutic potential for a

276 In lymphoid tissues, CSF1R-FRed highlighted diverse MPS populations, includin

277 such inhibitors and monoclonal antibodies to CSF1R are putative drugs that may play an important role

278 on of the RNA binding motif 6 (RBM6) gene to CSF1R gene generated presumably by a t(3;5)(p21;q33) tra

279 ET tracer to quickly monitor the response to CSF1R inhibitors and other therapeutic strategies target

280 itivity correlated with a growth response to CSF1R ligand, CSF1, and other cytokines, including hepat

281 Sensitivity to CSF1R inhibitor GW-2580 was found preferentially in de n

282 indings suggest that expression of wild-type CSF1R in some cells, whether achieved by mosaicism or ch

283 ngrafting myeloid cells with donor wild-type CSF1R to repopulate the microglial niche.

284 lls expressing a CSF1R/IR mutated at Tyr960 (CSF1R/IRA960).

285 e heterogeneous microglial populations under CSF1R inhibition, including microglia with reduced homeo

286 portantly, MAC2/Lgals3 was upregulated under CSF1R inhibition, and shared striking similarities with

287 ult brain are physiologically dependent upon CSF1R signaling.

288 oval of neurotoxic microglia after TBI using CSF1R inhibitors markedly reduce chronic neuroinflammati

289 multiple recurrences, systemic therapy using CSF1R inhibitors may help delay or avoid surgical proced

290 at the ablation of choroidal macrophages via CSF1R blockade was associated with choroidal vascular at

291 We show that, both in vitro and in vivo, CSF1R inhibition results in a reversal of claudin-low ma

292 3%) were ABL1 fusion-positive, ten (8%) were CSF1R fusion-positive, and eight (7%) were ABL2 fusion-p

293 phenotypic B-myeloid phenotype, and in which CSF1R-rearrangements have recently been reported.

294 ogic, or pathologic features of ALSP in whom CSF1R mutations had been excluded previously by sequenci

295 growth, but that combining these agents with CSF1R blockade potently elicited tumor regressions, even

296 d anti-chicken TIM4 mAbs in combination with CSF1R reporter transgenes to dissect the function of TIM

297 The few recently reported families with CSF1R mutations had been previously labelled "hereditary

298 Treatment with CSF1R inhibitors disrupted this crosstalk and triggered

299 ms intronic regulatory element (FIRE) within CSF1R is shown to be highly conserved in amniotes and ab

300 icroglia in mouse brains can survive without CSF1R signaling and reestablish the microglial homeostat