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Gene Review

Csf3  -  colony stimulating factor 3 (granulocyte)

Mus musculus

Synonyms: Csfg, G-CSF, Granulocyte colony-stimulating factor, MGI-IG
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Disease relevance of Csf3

  • G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes [1].
  • Consistent with the in vitro findings, mutant mice injected with G-CSF displayed enhanced neutrophilia, progenitor cell mobilization, and splenomegaly, but unexpectedly also developed inflammatory neutrophil infiltration into multiple tissues and consequent hind-leg paresis [2].
  • These findings indicate that depending on G-CSF levels in mice, the triangle Delta715 mutation can contribute both to neutropenia and to neutrophilia [3].
  • In the casein-induced peritonitis model, the appearance of G-CSF in the casein-injected peritoneal cavity associated well with the timing of neutrophil infiltration as well as PGE2 levels in exudates, with a peak value at 6 h postinjection [4].
  • These results suggest that in P. aeruginosa infection of burn wounds: (1) up-regulation of the expression of different cytokines, locally and within the livers of burned mice, is an indication of P. aeruginosa -induced sepsis; and (2) IL-6 and G-CSF play an important role in the host response mechanism [5].
  • We suggest that G-CSF, a drug already extensively used for treating chemotherapy-induced neutropenia, should be pursued as a novel, noninvasive therapeutic agent for the treatment of AD [6].

Psychiatry related information on Csf3


High impact information on Csf3


Chemical compound and disease context of Csf3


Biological context of Csf3


Anatomical context of Csf3


Associations of Csf3 with chemical compounds


Physical interactions of Csf3

  • However, at 21 degrees C or 37 degrees C, Multi-CSF inhibits binding of the other three CSFs and GM-CSF inhibits binding of G-CSF and M-CSF [24].
  • We also identified that Fli-1 DNA binding increased in G-CSF-treated cells compared with untreated cells [25].
  • cDNA clones encoding leucine-zipper proteins which interact with G-CSF gene promoter element 1-binding protein [26].
  • Granulocyte colony-stimulating factor (G-CSF) is the major regulator of granulopoiesis and acts through binding to its specific receptor (G-CSF-R) on neutrophilic granulocytes [27].
  • Stability studies revealed that IL-17 stabilized G-CSF mRNA levels, with a t1/2 of 4 h, compared to a t1/2 of less than 2 h in medium or LPS-treated cells [28].

Enzymatic interactions of Csf3

  • Because a high concentration of G-CSF was observed in the supernatants of leukemic blast cells from these two cases, it seems likely that the soluble G-CSF receptor cut off the autocrine growth mechanism of leukemic blast cells mediated by G-CSF [29].
  • Interestingly, Tec is shown to be tyrosine phosphorylated and activated by the G-CSF stimulation in both cell growth and differentiation mechanisms [30].

Regulatory relationships of Csf3

  • When stimulated with G-CSF in vitro, SOCS3-deficient cells of the neutrophilic granulocyte lineage exhibited prolonged STAT3 activation and enhanced cellular responses to G-CSF, including an increase in cloning frequency, survival, and proliferative capacity [2].
  • 4G8 and 2F2 also enhanced G-CSF-induced proliferation of 32Dc13 and GM-CSF-induced proliferation of PT18, confirming that the effect on CFU-GM was a direct effect [31].
  • Surprisingly the perturbation of macrophage differentiation did not apply to induced expression of macrophage colony-stimulating factor (M-CSF) or granulocyte colony stimulating factor (G-CSF) receptors [32].
  • The mouse myeloid leukemic cell line (M1) transfected with G-CSF-R cDNA can be induced to differentiate into macrophages in response to G-CSF [33].
  • PGE2 and an EP2 agonist have the ability to stimulate G-CSF gene expression even in the absence of LPS [4].
  • G-CSF administration suppressed liver cell proliferation through the up-regulation of IL-1beta expression in DMN-induced liver injury [34].

Other interactions of Csf3

  • The initial proliferation of these cells can also be stimulated by two other glycoproteins, granulocyte-macrophage CSF (GM-CSF) and granulocyte CSF (G-CSF), although continued proliferation and differentiation requires the subsequent presence of multi-CSF [35].
  • Surprisingly, G-CSFR expression on neutrophils is neither necessary nor sufficient for their mobilization from the bone marrow, suggesting that G-CSF induces neutrophil mobilization indirectly through the generation of trans-acting signals [17].
  • SOCS3 is a critical physiological negative regulator of G-CSF signaling and emergency granulopoiesis [2].
  • These results indicate that the cell line 32D, originally described as predominantly a basophil/mast cell line, has retained the capacity to give rise to cells which proliferate and differentiate in response to Epo, GM-CSF, and/or G-CSF [18].
  • Purified lineage-negative progenitor cells (Lin-) did not express detectable levels of IL-1R, but 24 hours of treatment with IL-3, GM-CSF, and G-CSF stimulated IL-1--specific binding [36].

Analytical, diagnostic and therapeutic context of Csf3


  1. G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes. Harada, M., Qin, Y., Takano, H., Minamino, T., Zou, Y., Toko, H., Ohtsuka, M., Matsuura, K., Sano, M., Nishi, J., Iwanaga, K., Akazawa, H., Kunieda, T., Zhu, W., Hasegawa, H., Kunisada, K., Nagai, T., Nakaya, H., Yamauchi-Takihara, K., Komuro, I. Nat. Med. (2005) [Pubmed]
  2. SOCS3 is a critical physiological negative regulator of G-CSF signaling and emergency granulopoiesis. Croker, B.A., Metcalf, D., Robb, L., Wei, W., Mifsud, S., DiRago, L., Cluse, L.A., Sutherland, K.D., Hartley, L., Williams, E., Zhang, J.G., Hilton, D.J., Nicola, N.A., Alexander, W.S., Roberts, A.W. Immunity (2004) [Pubmed]
  3. Perturbed granulopoiesis in mice with a targeted mutation in the granulocyte colony-stimulating factor receptor gene associated with severe chronic neutropenia. Hermans, M.H., Ward, A.C., Antonissen, C., Karis, A., Löwenberg, B., Touw, I.P. Blood (1998) [Pubmed]
  4. Prostaglandin E2 stimulates granulocyte colony-stimulating factor production via the prostanoid EP2 receptor in mouse peritoneal neutrophils. Sugimoto, Y., Fukada, Y., Mori, D., Tanaka, S., Yamane, H., Okuno, Y., Deai, K., Tsuchiya, S., Tsujimoto, G., Ichikawa, A. J. Immunol. (2005) [Pubmed]
  5. The effects of infection of thermal injury by Pseudomonas aeruginosa PAO1 on the murine cytokine response. Rumbaugh, K.P., Colmer, J.A., Griswold, J.A., Hamood, A.N. Cytokine (2001) [Pubmed]
  6. G-CSF rescues the memory impairment of animal models of Alzheimer's disease. Tsai, K.J., Tsai, Y.C., Shen, C.K. J. Exp. Med. (2007) [Pubmed]
  7. Therapeutic efficacy of granulocyte colony-stimulating factor alone and in combination with antibiotics against Pseudomonas aeruginosa infections in mice. Yasuda, H., Ajiki, Y., Shimozato, T., Kasahara, M., Kawada, H., Iwata, M., Shimizu, K. Infect. Immun. (1990) [Pubmed]
  8. Signals from the sympathetic nervous system regulate hematopoietic stem cell egress from bone marrow. Katayama, Y., Battista, M., Kao, W.M., Hidalgo, A., Peired, A.J., Thomas, S.A., Frenette, P.S. Cell (2006) [Pubmed]
  9. Targeted disruption of the NF-IL6 gene discloses its essential role in bacteria killing and tumor cytotoxicity by macrophages. Tanaka, T., Akira, S., Yoshida, K., Umemoto, M., Yoneda, Y., Shirafuji, N., Fujiwara, H., Suematsu, S., Yoshida, N., Kishimoto, T. Cell (1995) [Pubmed]
  10. Expression cloning of a receptor for murine granulocyte colony-stimulating factor. Fukunaga, R., Ishizaka-Ikeda, E., Seto, Y., Nagata, S. Cell (1990) [Pubmed]
  11. G-CSF, but not corticosterone, mediates circulating neutrophilia induced by febrile-range hyperthermia. Ellis, G.S., Carlson, D.E., Hester, L., He, J.R., Bagby, G.J., Singh, I.S., Hasday, J.D. J. Appl. Physiol. (2005) [Pubmed]
  12. Osteoclast-mediated bone resorption is stimulated during short-term administration of granulocyte colony-stimulating factor but is not responsible for hematopoietic progenitor cell mobilization. Takamatsu, Y., Simmons, P.J., Moore, R.J., Morris, H.A., To, L.B., Lévesque, J.P. Blood (1998) [Pubmed]
  13. Ligand binding domain of granulocyte colony-stimulating factor receptor. Hiraoka, O., Anaguchi, H., Yamasaki, K., Fukunaga, R., Nagata, S., Ota, Y. J. Biol. Chem. (1994) [Pubmed]
  14. Granulocyte-colony stimulating factor is neuroprotective in a model of Parkinson's disease. Meuer, K., Pitzer, C., Teismann, P., Krüger, C., Göricke, B., Laage, R., Lingor, P., Peters, K., Schlachetzki, J.C., Kobayashi, K., Dietz, G.P., Weber, D., Ferger, B., Schäbitz, W.R., Bach, A., Schulz, J.B., Bähr, M., Schneider, A., Weishaupt, J.H. J. Neurochem. (2006) [Pubmed]
  15. Myeloid cell kinetics in mice treated with recombinant interleukin-3, granulocyte colony-stimulating factor (CSF), or granulocyte-macrophage CSF in vivo. Lord, B.I., Molineux, G., Pojda, Z., Souza, L.M., Mermod, J.J., Dexter, T.M. Blood (1991) [Pubmed]
  16. G-CSF-induced tyrosine phosphorylation of Gab2 is Lyn kinase dependent and associated with enhanced Akt and differentiative, not proliferative, responses. Zhu, Q.S., Robinson, L.J., Roginskaya, V., Corey, S.J. Blood (2004) [Pubmed]
  17. G-CSF is an essential regulator of neutrophil trafficking from the bone marrow to the blood. Semerad, C.L., Liu, F., Gregory, A.D., Stumpf, K., Link, D.C. Immunity (2002) [Pubmed]
  18. Selection of lineage-restricted cell lines immortalized at different stages of hematopoietic differentiation from the murine cell line 32D. Migliaccio, G., Migliaccio, A.R., Kreider, B.L., Rovera, G., Adamson, J.W. J. Cell Biol. (1989) [Pubmed]
  19. Development of a novel selective amplifier gene for controllable expansion of transduced hematopoietic cells. Ito, K., Ueda, Y., Kokubun, M., Urabe, M., Inaba, T., Mano, H., Hamada, H., Kitamura, T., Mizoguchi, H., Sakata, T., Hasegawa, M., Ozawa, K. Blood (1997) [Pubmed]
  20. Activation and proliferation signals in murine macrophages: synergistic interactions between the hematopoietic growth factors and with phorbol ester for DNA synthesis. Hamilton, J.A., Vairo, G., Nicola, N.A., Burgess, A., Metcalf, D., Lingelbach, S.R. Blood (1988) [Pubmed]
  21. "Emergency" granulopoiesis in G-CSF-deficient mice in response to Candida albicans infection. Basu, S., Hodgson, G., Zhang, H.H., Katz, M., Quilici, C., Dunn, A.R. Blood (2000) [Pubmed]
  22. Hematopoietic cytokines inhibit apoptosis induced by transforming growth factor beta 1 and cancer chemotherapy compounds in myeloid leukemic cells. Lotem, J., Sachs, L. Blood (1992) [Pubmed]
  23. Cytokines in therapy of radiation injury. Neta, R., Oppenheim, J.J. Blood (1988) [Pubmed]
  24. Hierarchical down-modulation of hemopoietic growth factor receptors. Walker, F., Nicola, N.A., Metcalf, D., Burgess, A.W. Cell (1985) [Pubmed]
  25. G-CSF induces stabilization of ETS protein Fli-1 during myeloid cell development. Mora-Garcia, P., Wei, J., Sakamoto, K.M. Pediatr. Res. (2005) [Pubmed]
  26. cDNA clones encoding leucine-zipper proteins which interact with G-CSF gene promoter element 1-binding protein. Nishizawa, M., Nagata, S. FEBS Lett. (1992) [Pubmed]
  27. Tyrosine residues of the granulocyte colony-stimulating factor receptor transmit proliferation and differentiation signals in murine bone marrow cells. Akbarzadeh, S., Ward, A.C., McPhee, D.O., Alexander, W.S., Lieschke, G.J., Layton, J.E. Blood (2002) [Pubmed]
  28. Regulation of granulocyte colony-stimulating factor gene expression by interleukin-17. Cai, X.Y., Gommoll, C.P., Justice, L., Narula, S.K., Fine, J.S. Immunol. Lett. (1998) [Pubmed]
  29. Effect of the chimeric soluble granulocyte colony-stimulating factor receptor on the proliferation of leukemic blast cells from patients with acute myeloblastic leukemia. Asano, Y., Yokoyama, T., Shibata, S., Kobayashi, S., Shimoda, K., Nakashima, H., Okamura, S., Niho, Y. Cancer Res. (1997) [Pubmed]
  30. Tec protein tyrosine kinase is involved in the signaling mechanism of granulocyte colony-stimulating factor receptor. Miyazato, A., Yamashita, Y., Hatake, K., Miura, Y., Ozawa, K., Mano, H. Cell Growth Differ. (1996) [Pubmed]
  31. Modulation of myeloid proliferation and differentiation by monoclonal antibodies directed against a protein that interacts with the interleukin-3 receptor. Tweardy, D.J., Morel, P.A., Mott, P.L., Glazer, E.W., Zeh, H.J., Sakurai, M. Blood (1992) [Pubmed]
  32. Differential regulation of macrophage differentiation in response to leukemia inhibitory factor/oncostatin-M/interleukin-6: the effect of enforced expression of the SCL transcription factor. Tanigawa, T., Nicola, N., McArthur, G.A., Strasser, A., Begley, C.G. Blood (1995) [Pubmed]
  33. Tyrosine residues in the granulocyte colony-stimulating factor (G-CSF) receptor mediate G-CSF-induced differentiation of murine myeloid leukemic (M1) cells. Nicholson, S.E., Starr, R., Novak, U., Hilton, D.J., Layton, J.E. J. Biol. Chem. (1996) [Pubmed]
  34. Granulocyte colony-stimulating factor impairs liver regeneration in mice through the up-regulation of interleukin-1beta. Ogiso, T., Nagaki, M., Takai, S., Tsukada, Y., Mukai, T., Kimura, K., Moriwaki, H. J. Hepatol. (2007) [Pubmed]
  35. Stimulation of multipotential, erythroid and other murine haematopoietic progenitor cells by adherent cell lines in the absence of detectable multi-CSF (IL-3). Li, C.L., Johnson, G.R. Nature (1985) [Pubmed]
  36. Hematopoietic growth factors upregulate the p65 type II interleukin-1 receptor on bone marrow progenitor cells in vitro. Dubois, C.M., Ruscetti, F.W., Jacobsen, S.E., Oppenheim, J.J., Keller, J.R. Blood (1992) [Pubmed]
  37. Binding of NF-Y transcription factor to one of the cis-elements in the myeloperoxidase gene promoter that responds to granulocyte colony-stimulating factor. Orita, T., Shimozaki, K., Murakami, H., Nagata, S. J. Biol. Chem. (1997) [Pubmed]
  38. The colony-stimulating factors and collagen-induced arthritis: exacerbation of disease by M-CSF and G-CSF and requirement for endogenous M-CSF. Campbell, I.K., Rich, M.J., Bischof, R.J., Hamilton, J.A. J. Leukoc. Biol. (2000) [Pubmed]
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