Advances in understanding the biology and function of the G-CSF receptor

Current Opinion in Hematology

Volumn 3, Issue 3, 1996, Pages 180-184

  De Koning, John P ^a   Touw, Ivo R ^a,b  

^a ERASMUS UNIVERSITY ROTTERDAM   (Netherlands)

^b ERASMUS MEDICAL CENTER   (Netherlands)

Author keywords

[No Author keywords available]

Indexed keywords

COLONY STIMULATING FACTOR RECEPTOR; CYTOKINE RECEPTOR; ERYTHROPOIETIN RECEPTOR; GRANULOCYTE COLONY STIMULATING FACTOR; HEMOPOIETIC GROWTH FACTOR; MEMBRANE RECEPTOR; MITOGEN ACTIVATED PROTEIN KINASE; PROTEIN P21; PROTEIN TYROSINE KINASE;

ACUTE MYELOBLASTIC LEUKEMIA; CELL MATURATION; ENZYME ACTIVATION; GRANULOPOIESIS; HUMAN; NEUTROPENIA; PRIORITY JOURNAL; REVIEW; SOMATIC MUTATION; STRUCTURE ACTIVITY RELATION;

EID: 0029901902     PISSN: 10656251     EISSN: None     Source Type: Journal    
DOI: 10.1097/00062752-199603030-00003     Document Type: Review

References (46)

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42. De Koning JP, Schelen AM, Dong F, Van Buitenen C, Burgering BMT, Bos • JL, Löwenberg B, Touw IP: Specific involvement of tyrosine 764 of human granulocyte colony-stimulating factor receptor In signal transduction mediated by p145/Shc/GRB2 or p90/GRB2 complexes. Blood 1996, 87:132-140. G-CSF induces formation of p145/Shc/Grb2, p90/Grb2, and Syp/Grb2 complexes. Tyrosine 764 of G-CSF-R is required for formation of p145/Shc/Grb2 and p90/Grb2 complexes. G-CSF-induced Syp/Grb2 association does not depend on the presence of a single specific tyrosine residue of G-CSF-R.
43. Barge RMY, De Koning JP, Pouwels K, Dong F, Löwenberg B, Touw IP: Tryptophan 650 of human G-CSF receptor, Implicated in the activation of JAK2. is also required for G-CSF-mediated activation of signaling complexes of the p21ras route. Blood 1996, 87:2148-2153.
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46. Dong F, Brynes RK, Tidow N, Welte K, Löwenberg B, Touw IP: Mutations •• in the gene for the granulocyte-colony stimulating factor receptor in patients with acute myeloid leukemia preceded by severe congenital neutropenia. N Engl J Med 1995, 333:487-493. Point mutations in the gene for G-CSF-R were identified in two patients with acute myeloid leukemia with a history of severe congenital neutropenia. These nonsense mutations truncate the C-terminal domain essential for maturation induction. Because both normal and mutated alleles are expressed in leukemic cells, coexpression studies were performed in maturation-competent murine 32D cells, which demonstrated that the truncated receptor forms interfere with maturation signaling from the full-length (wild-type) G-CSF-R in a dominant negative fashion.