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Titolo:
Transforming growth factor: signal transduction pathways, cell cycle mediation, and effects on hematopoiesis
Autore:
Hu, XT; Zuckerman, KS;
Indirizzi:
Univ S Florida, Interdisciplinary Oncol Program, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 nary Oncol Program, Tampa, FL 33612 USA Univ S Florida, Dept Internal Med, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 Dept Internal Med, Tampa, FL 33612 USA Univ S Florida, Dept Biochem & Mol Biol, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 Biochem & Mol Biol, Tampa, FL 33612 USA H Lee Moffitt Canc Ctr, Tampa, FL 33612 USA H Lee Moffitt Canc Ctr Tampa FL USA 33612 t Canc Ctr, Tampa, FL 33612 USA
Titolo Testata:
JOURNAL OF HEMATOTHERAPY & STEM CELL RESEARCH
fascicolo: 1, volume: 10, anno: 2001,
pagine: 67 - 74
SICI:
1525-8165(200102)10:1<67:TGFSTP>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT-KINASE INHIBITOR; COLONY-STIMULATING FACTOR; MYELOID-LEUKEMIA CELLS; MAD-RELATED PROTEIN; TGF-BETA RECEPTOR; RETINOBLASTOMA SUSCEPTIBILITY GENE; DEOXYRIBONUCLEIC-ACID CLONING; MESSENGER RIBONUCLEIC-ACID; SERINE THREONINE KINASE; EMBRYO CHONDROCYTES;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
107
Recensione:
Indirizzi per estratti:
Indirizzo: Hu, XT Univ S Florida, Interdisciplinary Oncol Program, Tampa, FL 33612 USA Univ S Florida Tampa FL USA 33612 col Program, Tampa, FL 33612 USA
Citazione:
X.T. Hu e K.S. Zuckerman, "Transforming growth factor: signal transduction pathways, cell cycle mediation, and effects on hematopoiesis", J HEMATH ST, 10(1), 2001, pp. 67-74

Abstract

Transforming growth factor-beta (TGF-beta) is a potent growth inhibitor ofvarious cell types including hematopoietic cells. Two receptors, TGF beta RI and TGF beta RII, govern the interaction between the cell and the TGF-beta ligand. Primary binding of the ligand occurs with the RII receptor, promoting formation of a heterodimer with RI and activation of signaling. This induces transient association of Smad proteins with the receptors. Smad 3 and 4 may be involved in the TGF-beta -induced G(1) arrest. TGF-beta (1) down-regulates G(1) and G(2) cyclin-dependent kinases (cdks) and cyclins in terms of both kinase activity and protein amount. TGF-beta (1) also inhibits phosphorylation of the product of the retinoblastoma tumor suppressor gene (pRb) at multiple serine and threonine residues in human myeloid leukemia cells. The underphosphorylated pRb associates with transcription factor E2F-4 in G(1) phase, whereas the phosphorylated pRb mainly binds to E2F-1 and E2F-3. Because TGF-beta (1) up-regulates p130(pRb family member)/E2F-4 complex formation and down-regulates p107(pRb family member)/E2F-4 complex formation, with E2F-4 levels remaining constant, these results suggest that E2F-4 is switched from p107 to pRb and p130 when cells exit from the cell cycleand arrest in G(1) by the action of TGF-beta (1). The "cdk inhibitor" p27 is both a positive and a negative regulator of TGF-beta (1)-mediated cell cycle control. Although TGF-beta (1) has been reported to be a selected inhibitor of normal primitive hematopoietic stem cells, TGF-beta inhibits both primitive and more differentiated myeloid leukemia cell lines.

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Documento generato il 26/01/20 alle ore 09:46:49