CSFR (Phospho-Tyr708) Antibody
- Known as:
- CSFR (Phospho-Tyr708) Antibody
- Catalog number:
- 11832
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Signalway
- Gene target:
- CSFR (Phospho-Tyr708) Antibody
Related genes to: CSFR (Phospho-Tyr708) Antibody
- Gene:
- CSF1R NIH gene
- Name:
- colony stimulating factor 1 receptor
- Previous symbol:
- FMS
- Synonyms:
- C-FMS, CSFR, CD115
- Chromosome:
- 5q32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-09-11
- Gene:
- CSF3R NIH gene
- Name:
- colony stimulating factor 3 receptor
- Previous symbol:
- CD114
- Synonyms:
- GCSFR
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-12-10
- Date modifiied:
- 2019-04-23
Related products to: CSFR (Phospho-Tyr708) Antibody
Related articles to: CSFR (Phospho-Tyr708) Antibody
- Uterine sarcomas are rare, heterogeneous malignancies with distinct pathological behaviors. This study aimed to identify clinicopathological characteristics, prognostic risk factors, and potential therapeutic targets to enhance clinical management. - Source: PubMed
Publication date: 2026/05/22
Huang TingXie XinyuDu XinqiaoSun XiulingZhang GuoWang Jianliu - Traumatic brain injury (TBI) initiates complex neuroinflammatory cascades that significantly influence recovery outcomes. Although sex differences in neuroinflammation have been reported previously, findings remain inconclusive as the role of the female estrous cycle in post-injury responses is not well understood. In this study, we aimed to characterize sex-based differences in neuroinflammatory, vascular, and behavioral outcomes following TBI, with particular emphasis on the different phases of the estrous cycle in female mice. Male and female mice were subjected to controlled cortical impact (CCI) and subsequently assessed for behavioral deficits, cerebral blood flow (CBF), immune cell infiltration, and inflammatory genes expression. Although TBI induced robust neuroinflammation and reduction in CBF in both sexes, female mice showed significantly increased myeloid, microglial and T-cell presence, as well as elevated expression of key inflammatory transcripts (Btk, Inpp5d, and Tmem173), while downregulation in Grm2 expressions. Stratified cohort of female mice as per phases in estrous cycle (proestrus, estrus, metestrus, and diestrus) before injury showed alterations in Inpp5d, Csf3r, Csf1r, CD84, Tmem173, Homer1, Grm2 and Supt7l. Notably, female injured mice showed differential improvements in select parameters, although estrous cycle phase at the time of impact had limited but phase-dependent impact on CBF. Female mice did not show significant changes in the behavioral tests as compared to male or different estrous phenotypes. However, female mice showed higher frequency to visit center in an open arena. These findings highlight sex-specific neuroinflammatory and transcriptional responses to TBI, with moderate modulation by estrous cycle. Our study further suggests that one estrous phase could be more vulnerable to neuroinflammation or neurovascular injury than others on cellular and molecular level. However, this interphase difference might be masked in the studies including randomly cycled female population. Thus, our results underscore the importance of incorporating sex, estrous and hormonal status into sex-dependent studies on TBI and other brain diseases research to inform the development of targeted therapeutic strategies. - Source: PubMed
Publication date: 2026/03/04
Royal TabithaAhluwalia PankajGulhane MayuriSalles Evila LopesGaur PankajAhluwalia MeenakshiRandhawa TajmanSunil ShreyaBudim SriramAkter KhadijaKhan Mohammad BadruzzamanGhosh SantuBaban BabakHess David CVale Fernando LDhandapani Krishnan MKolhe RavindraVaibhav Kumar - Acute administration of MK-801 (dizocilpine), an N-methyl-D-aspartate receptor (NMDAR) antagonist, can establish animal models of psychiatric disorders. However, the roles of microglia and inflammation-related genes in these animal models of psychiatric disorders remain unknown. Here, we found rapid elimination of microglia in the prefrontal cortex (PFC) and hippocampus (HPC) of mice following administration of the dual colony-stimulating factor 1 receptor (CSF1R)/c-Kit kinase inhibitor PLX3397 (pexidartinib) in drinking water. Single administration of MK-801 induced hyperactivity in the open-field test (OFT). Importantly, PLX3397-induced depletion of microglia prevented the hyperactivity and schizophrenia-like behaviors induced by MK-801. However, neither repopulation of microglia nor inhibition of microglial activation by minocycline affected MK-801-induced hyperactivity. Importantly, microglial density in the PFC and HPC was significantly correlated with behavioral changes. In addition, common and distinct glutamate-, GABA-, and inflammation-related gene (116 genes) expression patterns were observed in the brains of PLX3397- and/or MK-801-treated mice. Moreover, 10 common inflammation-related genes ( , , , , , , , , , and ) with very strong correlations were identified in the brain using hierarchical clustering analysis. Further correlation analysis demonstrated that the behavioral changes in the OFT were most significantly associated with the expression of inflammation-related genes ( , , , , , and ), but not glutamate- or GABA-related genes in PLX3397- and MK-801-treated mice. Thus, our results suggest that microglial depletion via a CSF1R/c-Kit kinase inhibitor can ameliorate the hyperactivity induced by an NMDAR antagonist, which is associated with modulation of immune-related genes in the brain. - Source: PubMed
Ni Rong-JunWang Yi-YanGao Tian-HaoWang Qi-RunWei Jin-XueZhao Lian-ShengMa Yang-RuiMa Xiao-HongLi Tao - Chicken bone marrow-derived macrophages (BMMΦ) and dendritic cells (BMDC) are utilized as models to study the mononuclear phagocytic system (MPS). A widely used method to generate macrophages and DC is to culture bone marrow cells in the presence of colony-stimulating factor-1 (CSF1) to differentiate BMMΦ and granulocyte-macrophage-CSF (GM-CSF, CSF2) and interleukin-4 (IL-4) to differentiate BMDC, while CSF2 alone can lead to the development of granulocyte-macrophage-CSF-derived DC (GMDC). However, in chickens, the MPS cell lineages and their functions represented by these cultures are poorly understood. Here, we decipher the phenotypical, functional and transcriptional differences between chicken BMMΦ and BMDC along with examining differences in DC cultures grown in the absence of IL-4 on days 2, 4, 6 and 8 of culture. BMMΦ cultures develop into a morphologically homogenous cell population in contrast to the BMDC and GMDC cultures, which produce morphologically heterogeneous cell cultures. At a phenotypical level, all cultures contained similar cell percentages and expression levels of MHCII, CD11c and -transgene, whilst MRC1L-B expression decreased over time in BMMΦ. All cultures were efficiently able to uptake 0.5 µm beads, but poorly phagocytosed 1 µm beads. Little difference was observed in the kinetics of phagosomal acidification across the cultures on each day of analysis. Temporal transcriptomic analysis indicated that all cultures expressed high levels of , , , and , genes associated with macrophages in mammals. In contrast, low levels of , and , genes associated with DC, were expressed at day 2 in BMDC and GMDC after which expression levels decreased. Collectively, chicken CSF2 + IL-4- and CSF2-dependent BM cultures represent cells of the macrophage lineage rather than inducing conventional DC. - Source: PubMed
Publication date: 2022/12/21
Borowska DominikaSives SamanthaVervelde LonnekeSutton Kate M - Colony Stimulating Factor 1 Receptor (CSF1R) is a potential target for anti-epileptic drugs. However, inhibition of CSF1R is not well tolerated by patients, thereby prompting the need for alternative targets. To develop a framework for identification of such alternatives, we here develop a mathematical model of a pro-inflammatory gene regulatory network (GRN) involved in epilepsy and centered around CSF1R. This GRN comprises validated transcriptional and post-transcriptional regulations involving STAT1, STAT3, NFκB, IL6R, CSF3R, IRF8, PU1, C/EBPα, TNFR1, CSF1 and CSF1R. The model was calibrated on mRNA levels of all GRN components in lipopolysaccharide (LPS)-treated mouse microglial BV-2 cells, and allowed to predict that STAT1 and STAT3 have the strongest impact on the expression of the other GRN components. Microglial BV-2 cells were selected because, the modules from which the GRN was deduced are enriched for microglial marker genes. The function of STAT1 and STAT3 in the GRN was experimentally validated in BV-2 cells. Further, in silico analysis of the GRN dynamics predicted that a pro-inflammatory stimulus can induce irreversible bistability whereby the expression level of GRN components occurs as two distinct states. The irreversibility of the switch may enforce the need for chronic inhibition of the CSF1R GRN in order to achieve therapeutic benefit. The cell-to-cell heterogeneity driven by the bistability may cause variable therapeutic response. In conclusion, our modeling approach uncovered a GRN controlling CSF1R that is predominantly regulated by STAT1 and STAT3. Irreversible inflammation-induced bistability and cell-to-cell heterogeneity of the GRN provide a theoretical foundation to the need for chronic GRN control and the limited potential for disease modification via inhibition of CSF1R. - Source: PubMed
Publication date: 2021/04/05
Gérard ClaudeDe Mot LauraneCordi Sabinevan Eyll JonathanLemaigre Frédéric P