| Enhanced MAPK signaling induced by CSF3R mutants confers dependence to DUSP1 for leukemic transformation. | Enhanced MAPK signaling induced by CSF3R mutants confers dependence to DUSP1 for leukemic transformation.
Kesarwani M, Kincaid Z, Azhar M, Azam M., Free PMC Article | 09/30/2024 |
| The RNA m[6]A demethylase ALKBH5 drives emergency granulopoiesis and neutrophil mobilization by upregulating G-CSFR expression. | The RNA m(6)A demethylase ALKBH5 drives emergency granulopoiesis and neutrophil mobilization by upregulating G-CSFR expression.
Liu Y, Song R, Lu Z, Zhao L, Zhan X, Li Y, Cao X., Free PMC Article | 01/5/2024 |
| G-CSF Receptor Deletion Amplifies Cortical Bone Dysfunction in Mice With STAT3 Hyperactivation in Osteocytes. | G-CSF Receptor Deletion Amplifies Cortical Bone Dysfunction in Mice With STAT3 Hyperactivation in Osteocytes.
Isojima T, Walker EC, Poulton IJ, McGregor NE, Wicks IP, Gooi JH, Martin TJ, Sims NA. | 10/29/2022 |
| Alternatively spliced CSF3R isoforms in SRSF2 P95H mutated myeloid neoplasms. | Alternatively spliced CSF3R isoforms in SRSF2 P95H mutated myeloid neoplasms.
Wang BA, Mehta HM, Penumutchu SR, Tolbert BS, Cheng C, Kimmel M, Haferlach T, Maciejewski JP, Corey SJ. | 10/8/2022 |
| Effect of the unfolded protein response and oxidative stress on mutagenesis in CSF3R: a model for evolution of severe congenital neutropenia to myelodysplastic syndrome/acute myeloid leukemia. | Effect of the unfolded protein response and oxidative stress on mutagenesis in CSF3R: a model for evolution of severe congenital neutropenia to myelodysplastic syndrome/acute myeloid leukemia.
Sapra A, Jaksik R, Mehta H, Biesiadny S, Kimmel M, Corey SJ., Free PMC Article | 08/21/2021 |
| G-CSF and G-CSFR Modulate CD4 and CD8 T Cell Responses to Promote Colon Tumor Growth and Are Potential Therapeutic Targets. | G-CSF and G-CSFR Modulate CD4 and CD8 T Cell Responses to Promote Colon Tumor Growth and Are Potential Therapeutic Targets.
Karagiannidis I, Jerman SJ, Jacenik D, Phinney BB, Yao R, Prossnitz ER, Beswick EJ., Free PMC Article | 04/24/2021 |
| beta-Catenin-TCF/LEF signaling promotes steady-state and emergency granulopoiesis via G-CSF receptor upregulation. | β-Catenin-TCF/LEF signaling promotes steady-state and emergency granulopoiesis via G-CSF receptor upregulation.
Danek P, Kardosova M, Janeckova L, Karkoulia E, Vanickova K, Fabisik M, Lozano-Asencio C, Benoukraf T, Tirado-Magallanes R, Zhou Q, Burocziova M, Rahmatova S, Pytlik R, Brdicka T, Tenen DG, Korinek V, Alberich-Jorda M., Free PMC Article | 04/13/2021 |
| Chimeric G-CSF Receptor-Mediated STAT3 Activation Contributes to Efficient Induction of Cardiomyocytes from Mouse Induced Pluripotent Stem Cells. | Chimeric G-CSF Receptor-Mediated STAT3 Activation Contributes to Efficient Induction of Cardiomyocytes from Mouse Induced Pluripotent Stem Cells.
Tsukamoto T, Sogo T, Ueyama T, Nakao S, Harada Y, Ihara D, Akagi Y, Kida YS, Hasegawa K, Nagamune T, Kawahara M, Kawamura T. | 10/24/2020 |
| T618I CSF3R mutations in chronic neutrophilic leukemia induce oncogenic signals through aberrant trafficking and constitutive phosphorylation of the O-glycosylated receptor form. | T618I CSF3R mutations in chronic neutrophilic leukemia induce oncogenic signals through aberrant trafficking and constitutive phosphorylation of the O-glycosylated receptor form.
Price A, Druhan LJ, Lance A, Clark G, Vestal CG, Zhang Q, Foureau D, Parsons J, Hamilton A, Steuerwald NM, Avalos BR. | 09/19/2020 |
| G-CSF signaling in CerS6 null bone marrow cells was not affected. In conclusion, very long chain ceramides are important for G-CSF signaling and translocation of G-CSF-R into detergent-resistant membranes. | Role of ceramide synthase 2 in G-CSF signaling and G-CSF-R translocation into detergent-resistant membranes.
Kurz J, Barthelmes J, Blum L, Ulshöfer T, Wegner MS, Ferreirós N, Roser L, Geisslinger G, Grösch S, Schiffmann S., Free PMC Article | 07/25/2020 |
| The results illustrate that Clostridium perfringens alpha-toxin disturbs G-CSF-mediated granulopoiesis by reducing the expression of G-CSFR on neutrophils while augmenting septic shock. | Clostridium perfringens α-toxin impairs granulocyte colony-stimulating factor receptor-mediated granulocyte production while triggering septic shock.
Takehara M, Seike S, Sonobe Y, Bandou H, Yokoyama S, Takagishi T, Miyamoto K, Kobayashi K, Nagahama M., Free PMC Article | 04/11/2020 |
| Activating mutations in the granulocyte colony stimulating factor receptor (CSF3R), cooperate with loss of function mutations in the transcription factor CEBPA to promote acute myeloid leukemia development. | Myeloid lineage enhancers drive oncogene synergy in CEBPA/CSF3R mutant acute myeloid leukemia.
Braun TP, Okhovat M, Coblentz C, Carratt SA, Foley A, Schonrock Z, Curtiss BM, Nevonen K, Davis B, Garcia B, LaTocha D, Weeder BR, Grzadkowski MR, Estabrook JC, Manning HG, Watanabe-Smith K, Jeng S, Smith JL, Leonti AR, Ries RE, McWeeney S, Di Genua C, Drissen R, Nerlov C, Meshinchi S, Carbone L, Druker BJ, Maxson JE., Free PMC Article | 03/14/2020 |
| this study shows that CSF3R mediates infection-dependent transition to severe asthma | CSF3R/CD114 mediates infection-dependent transition to severe asthma.
Wang H, FitzPatrick M, Wilson NJ, Anthony D, Reading PC, Satzke C, Dunne EM, Licciardi PV, Seow HJ, Nichol K, Adcock IM, Chung KF, Anderson GP, Vlahos R, Wark P, Bozinovski S. | 02/29/2020 |
| expression of the Sle2c2 Csf3r allele confers autoimmune suppression through the expansion of tolerogenic dendritic cells | Protective Role of Myeloid Cells Expressing a G-CSF Receptor Polymorphism in an Induced Model of Lupus.
Sivakumar R, Abboud G, Mathews CE, Atkinson MA, Morel L., Free PMC Article | 07/13/2019 |
| Anti-G-CSF receptor rapidly halted the progression of established disease in collagen Ab-induced arthritis in mice. Neutrophil accumulation in joints was inhibited, without rendering animals neutropenic, suggesting an effect of G-CSF receptor blockade on neutrophil homing to inflammatory sites. | Therapeutic Targeting of the G-CSF Receptor Reduces Neutrophil Trafficking and Joint Inflammation in Antibody-Mediated Inflammatory Arthritis.
Campbell IK, Leong D, Edwards KM, Rayzman V, Ng M, Goldberg GL, Wilson NJ, Scalzo-Inguanti K, Mackenzie-Kludas C, Lawlor KE, Wicks IP, Brown LE, Baz Morelli A, Panousis C, Wilson MJ, Nash AD, McKenzie BS, Andrews AE. | 07/29/2017 |
| this study shows that dorsal root ganglion neurons cultured in G-CSF failed to respond to G-CSF in vitro, and Csf3r gene expression could not be detected in dorsal root ganglion neurons by single-cell RT-PCR | G-CSF Receptor Blockade Ameliorates Arthritic Pain and Disease.
Lee MC, McCubbin JA, Christensen AD, Poole DP, Rajasekhar P, Lieu T, Bunnett NW, Garcia-Caraballo S, Erickson A, Brierley SM, Saleh R, Achuthan A, Fleetwood AJ, Anderson RL, Hamilton JA, Cook AD., Free PMC Article | 05/6/2017 |
| Neutrophil activation in postischemic brain injury is regulated via upregulation of the neutrophil activator, CSFR3. | Endothelial CD36 Contributes to Postischemic Brain Injury by Promoting Neutrophil Activation via CSF3.
Garcia-Bonilla L, Racchumi G, Murphy M, Anrather J, Iadecola C., Free PMC Article | 02/13/2016 |
| Thr-615 and Thr-618 sites of membrane-proximal mutations are part of an O-linked glycosylation cluster. Mutation at these sites prevents O-glycosylation of CSF3R and increases receptor dimerization. | Ligand independence of the T618I mutation in the colony-stimulating factor 3 receptor (CSF3R) protein results from loss of O-linked glycosylation and increased receptor dimerization.
Maxson JE, Luty SB, MacManiman JD, Abel ML, Druker BJ, Tyner JW., Free PMC Article | 04/26/2014 |
| Fbw7 together with GSK3beta negatively regulates G-CSFR expression and its downstream signaling. | E3 ubiquitin ligase Fbw7 negatively regulates granulocytic differentiation by targeting G-CSFR for degradation.
Lochab S, Pal P, Kapoor I, Kanaujiya JK, Sanyal S, Behre G, Trivedi AK. | 03/1/2014 |
| G-CSFR signaling interacts with retinoic acid receptors in the regulation of myeloid differentiation | The granulocyte-colony stimulating factor receptor (G-CSFR) interacts with retinoic acid receptors (RARs) in the regulation of myeloid differentiation.
Chee LC, Hendy J, Purton LE, McArthur GA. | 04/6/2013 |
| 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. | A truncation mutant of Csf3r cooperates with PML-RARα to induce acute myeloid leukemia in mice.
Kunter G, Woloszynek JR, Link DC., Free PMC Article | 01/7/2012 |
| 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. | Expression of the G-CSF receptor in monocytic cells is sufficient to mediate hematopoietic progenitor mobilization by G-CSF in mice.
Christopher MJ, Rao M, Liu F, Woloszynek JR, Link DC., Free PMC Article | 04/16/2011 |
| inappropriate Stat5 activation plays a key role in establishing clonal dominance by stem cells expressing mutant Csf3r. | Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5.
Liu F, Kunter G, Krem MM, Eades WC, Cain JA, Tomasson MH, Hennighausen L, Link DC., Free PMC Article | 01/21/2010 |
| Mice with truncated G-CSF receptors have neutropenia, susceptibility to infection, and bone marrow maturation arrest similar to severe congenital neutropenic humans, suggesting a role of receptor truncation mutations in SCN pathology. | Impaired neutrophil maturation in truncated murine G-CSF receptor-transgenic mice.
Mitsui T, Watanabe S, Taniguchi Y, Hanada S, Ebihara Y, Sato T, Heike T, Mitsuyama M, Nakahata T, Tsuji K. | 01/21/2010 |
| The tyrosine (Tyr) 729, located in the carboxy terminus of the G-CSF-R, controls the duration of G-CSF-stimulated activation of Stat5, Akt, and extracellular signal-regulated kinase 1/2. | Tyrosine 729 of the G-CSF receptor controls the duration of receptor signaling: involvement of SOCS3 and SOCS1.
Zhuang D, Qiu Y, Haque SJ, Dong F. | 01/21/2010 |