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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Colony stimulating factor 3 receptor

The protein encoded by this gene is the receptor for colony stimulating factor 3, a cytokine that controls the production, differentiation, and function of granulocytes. The encoded protein, which is a member of the family of cytokine receptors, may also function in some cell surface adhesion or recognition processes. Alternatively spliced transcript variants have been described. Mutations in this gene are a cause of Kostmann syndrome, also known as severe congenital neutropenia. [provided by RefSeq, Aug 2010] (from NCBI)
Top mentioned proteins: CsF, G-CSF, CAN, HAD, STAT3
Papers using G-CSFR antibodies
Mutations associated with neutropenia in dogs and humans disrupt intracellular transport of neutrophil elastase
Avalos Belinda R et al., In Journal of Inflammation (London, England), 2002
... Anti-G-CSFR antibodies recognizing the extracellular region of the human G-CSFR were obtained from BD Biosciences (Palo Alto, CA) ...
Papers on G-CSFR
Autocrine protective mechanisms of human granulocyte colony-stimulating factor (G-CSF) on retinal ganglion cells after optic nerve crush.
Tsai et al., Taipei, Taiwan. In Exp Eye Res, Feb 2016
We observed that both G-CSF and G-CSF receptor (G-CSFR) are expressed in normal rat retina.
Protective role of G-CSF in dextran sulfate sodium-induced acute colitis through generating gut-homing macrophages.
Kim et al., London, Canada. In Cytokine, Feb 2016
Here, we examined the role of G-CSF in dextran sulfate sodium (DSS)-induced acute colitis using G-CSF receptor-deficient (G-CSFR(-/-)) mice.
Chronic Neutrophilic Leukemia 2016: Update on diagnosis, molecular genetics, prognosis and management.
Tefferi et al., In Am J Hematol, Jan 2016
Such a pathogenic clonal marker has now been identified as a somatic activating mutation of CSF3R, most commonly CSF3R T618I, thus demanding revision of the current WHO diagnostic classification to include the molecular criterion of mutated CSF3R.
What's different about atypical CML and chronic neutrophilic leukemia?
Tyner et al., Portland, United States. In Hematology Am Soc Hematol Educ Program, Jan 2016
The discovery of CSF3R mutations in aCML and CNL have prompted a more comprehensive genetic profiling of these disorders.
Game of clones: the genomic evolution of severe congenital neutropenia.
Touw, Rotterdam, Netherlands. In Hematology Am Soc Hematol Educ Program, Jan 2016
Expansion of hematopoietic clones with acquired mutations in the gene encoding the G-CSF receptor (CSF3R) is regularly seen in SCN patients and AML usually descends from one of these CSF3R mutant clones.
Chronic neutrophilic leukemia with overexpression of EVI-1, and concurrent CSF3R and SETBP1 mutations: A case report.
Zhao et al., Tianjin, China. In Oncol Lett, Sep 2015
The present study describes a case that fulfilled the World Health Organization diagnostic criteria for CNL, and was associated with overexpression of EVI-1, as well as novel concurrent mutations of colony stimulating factor 3 receptor (CSF3R) and SET binding protein-1 (SETBP1).
Pathogenesis of myeloproliferative neoplasms.
Grisouard et al., Basel, Switzerland. In Exp Hematol, Aug 2015
Mutations in one of four genes-JAK2, MPL, CALR, and CSF3R-can be found in the vast majority of patients with MPN and represent driver mutations that can induce the MPN phenotype.
Chronic neutrophilic leukemia: a clinical perspective.
Cigudosa et al., Madrid, Spain. In Onco Targets Ther, 2014
Chronic neutrophilic leukemia (CNL) is a rare myeloproliferative neoplasm (MPN) that includes only 150 patients described to date meeting the latest World Health Organization (WHO) criteria and the recently reported CSF3R mutations.
The importance of the granulocyte-colony stimulating factor in oncology.
Oprean et al., Cluj-Napoca / Kolozsvár, Romania. In Clujul Med, 2014
The receptor for G-CSF (G-CSFR) is part of the cytokine and hematopoietin receptor superfamily and G-CSFR mutations cause severe congenital neutropenia.
Expressions of CD96 and CD123 in Bone Marrow Cells of Patients with Myelodysplastic Syndromes.
Liu et al., In Clin Lab, 2014
CD114 (GCSFR), EPOR, and CD110 (TPOR) expression on their CD34+CD38-CD96+ and CD34+CD38-CD96- BMC and these cells' apoptosis (Annexin V) were also detected by FACS.
Oncogenic CSF3R mutations in chronic neutrophilic leukemia and atypical CML.
Tyner et al., Portland, United States. In N Engl J Med, 2013
RESULTS: We identified activating mutations in the gene encoding the receptor for colony-stimulating factor 3 (CSF3R) in 16 of 27 patients (59%) with CNL or atypical CML.
An acquired CSF3R mutation in an adult chronic idiopathic neutropenia patient who developed acute myeloid leukaemia.
Kadota et al., In Br J Haematol, 2012
An acquired CSF3R mutation in an adult chronic idiopathic neutropenia patient who developed acute myeloid leukaemia.
A truncation mutant of Csf3r cooperates with PML-RARα to induce acute myeloid leukemia in mice.
Link et al., Saint Louis, United States. In Exp Hematol, 2011
Expression of truncated G-CSFR significantly shortens the latency of AML in a G-CSF-dependent fashion and it is associated with a distinct AML presentation characterized by higher blast counts and more severe myelosuppression.
Effects of interferon-γ and granulocyte colony-stimulating factor on antifungal activity of human polymorphonuclear neutrophils against Candida albicans grown as biofilms or planktonic cells.
Roilides et al., Thessaloníki, Greece. In Cytokine, 2011
Pretreatment of PMNs with IFN-gamma or G-CSF for a long-time (22 h)induced a significant lower fungal damage against biofilms compared with planktonic cells.
Expression of the G-CSF receptor in monocytic cells is sufficient to mediate hematopoietic progenitor mobilization by G-CSF in mice.
Link et al., Saint Louis, United States. In J Exp Med, 2011
G-CSFR signals in bone marrow monocytic cells inhibit the production of trophic factors required for osteoblast lineage cell maintenance, ultimately leading to hematopoietic stem and progenitor cell mobilization.
Carcinoembryonic antigen-related cell adhesion molecule-1 regulates granulopoiesis by inhibition of granulocyte colony-stimulating factor receptor.
Shively et al., Duarte, United States. In Immunity, 2010
CEACAM1 expression correlated with granulocytic differentiation, and Ceacam1(-/-) mice developed neutrophilia because of loss of the Src-homology-phosphatase-1 (SHP-1)-dependent inhibition of granulocyte colony-stimulating factor receptor (G-CSFR) signal transducer and activator of transcription (Stat3) pathway provided by CEACAM1.
[Effect of gemcitabine on granulocyte colony-stimulating factor receptor and bcr/abl mRNA in patients with chronic myeloid leukemia].
Han et al., Zhengzhou, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2010
Gemcitabine can enhance in vitro the expression rate of bone marrow G-CSFR in chronic myeloid leukemia patients at chronic or blastic phases.
Granulocyte colony-stimulating factor (G-CSF) treatment of childhood acute myeloid leukemias that overexpress the differentiation-defective G-CSF receptor isoform IV is associated with a higher incidence of relapse.
Reinhardt et al., Hannover, Germany. In J Clin Oncol, 2010
PATIENTS AND METHODS: Of 154 SR patients in the AML-BFM 98 cohort, 50 patients were tested for G-CSF receptor (G-CSFR) RNA isoform I and IV expression, G-CSFR cell surface expression, and acquired mutations in the G-CSFR gene.
G-CSF promotes the proliferation of developing cardiomyocytes in vivo and in derivation from ESCs and iPSCs.
Fukuda et al., Tokyo, Japan. In Cell Stem Cell, 2010
During a screen for humoral factors that promote cardiomyocyte differentiation from embryonic stem cells (ESCs), we found marked elevation of granulocyte colony-stimulating factor receptor (G-CSFR) mRNA in developing cardiomyocytes.
G-CSF is an essential regulator of neutrophil trafficking from the bone marrow to the blood.
Link et al., Saint Louis, United States. In Immunity, 2002
Nonredundant signals generated by the membrane-proximal 87 amino acids of the G-CSF receptor (G-CSFR) are sufficient to mediate this response.
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